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Sample records for inflammatory syndrome tb-iris

  1. Paradoxical Tuberculosis Immune Reconstitution Inflammatory Syndrome (TB-IRIS) in HIV Patients with Culture Confirmed Pulmonary Tuberculosis in India and the Potential Role of IL-6 in Prediction

    PubMed Central

    Porter, Brian O.; Chandrasekhar, Chockalingam; Venkatesan, Perumal; Menon, Pradeep A.; Subramanian, Sudha; Anbalagan, Selvaraj; Bhavani, Kannabiran P.; Sekar, Sathiyavelu; Padmapriyadarshini, Chandrasekaran; Kumar, Satagopan; Ravichandran, Narayanan; Raja, Krishnaraj; Bhanu, Kesavamurthy; Mahilmaran, Ayyamperumal; Sekar, Lakshmanan; Sher, Alan; Sereti, Irini; Swaminathan, Soumya

    2013-01-01

    Background The incidence, manifestations, outcome and clinical predictors of paradoxical TB-IRIS in patients with HIV and culture confirmed pulmonary tuberculosis (PTB) in India have not been studied prospectively. Methods HIV+ patients with culture confirmed PTB started on anti-tuberculosis therapy (ATT) were followed prospectively after anti-retroviral therapy (ART) initiation. Established criteria for IRIS diagnosis were used including decline in plasma HIV RNA at IRIS event. Pre-ART plasma levels of interleukin (IL)-6 and C-reactive protein (CRP) were measured. Univariate and multivariate logistic regression models were used to evaluate associations between baseline variables and IRIS. Results Of 57 patients enrolled, 48 had complete follow up data. Median ATT-ART interval was 28 days (interquartile range, IQR 1447). IRIS events occurred in 26 patients (54.2%) at a median of 11 days (IQR: 716) after ART initiation. Corticosteroids were required for treatment of most IRIS events that resolved within a median of 13 days (IQR: 923). Two patients died due to CNS TB-IRIS. Lower CD4+ T-cell counts, higher plasma HIV RNA levels, lower CD4/CD8 ratio, lower hemoglobin, shorter ATT to ART interval, extra-pulmonary or miliary TB and higher plasma IL-6 and CRP levels at baseline were associated with paradoxical TB-IRIS in the univariate analysis. Shorter ATT to ART interval, lower hemoglobin and higher IL-6 and CRP levels remained significant in the multivariate analysis. Conclusion Paradoxical TBIRIS frequently complicates HIV-TB therapy in India. IL-6 and CRP may assist in predicting IRIS events and serve as potential targets for immune interventions. PMID:23691062

  2. HIV-1 tuberculosis-associated immune reconstitution inflammatory syndrome.

    PubMed

    Lai, Rachel P J; Meintjes, Graeme; Wilkinson, Robert J

    2016-03-01

    Patients co-infected with HIV-1 and tuberculosis (TB) are at risk of developing TB-associated immune reconstitution inflammatory syndrome (TB-IRIS) following commencement of antiretroviral therapy (ART). TB-IRIS is characterized by transient but severe localized or systemic inflammatory reactions against Mycobacterium tuberculosis antigens. Here, we review the risk factors and clinical management of TB-IRIS, as well as the roles played by different aspects of the immune response in contributing to TB-IRIS pathogenesis. PMID:26423994

  3. Matrix metalloproteinases and tissue damage in HIV-tuberculosis immune reconstitution inflammatory syndrome

    PubMed Central

    Tadokera, Rebecca; Meintjes, Graeme A; Wilkinson, Katalin A; Skolimowska, Keira H; Walker, Naomi; Friedland, Jon S; Maartens, Gary; Elkington, Paul T G; Wilkinson, Robert J

    2014-01-01

    The HIV-TB-associated immune reconstitution inflammatory syndrome (TB-IRIS) can complicate combined treatments for HIV-1 and TB. Little is known about tissue damage in TB-IRIS. Matrix metalloproteinases (MMPs) degrade components of the extracellular matrix and consequently may play a role in such immunopathology. Here we investigated the involvement of MMPs in TB-IRIS. We determined MMP transcript abundance and secreted protein in Mycobacterium tuberculosis stimulated PBMCs from 22 TB-IRIS patients and 22 non-IRIS controls. We also measured MMP protein levels in corresponding serum and the effect of prednisone — which reduces the duration of symptoms in IRIS patients — or placebo treatment on MMP transcript and circulating MMP protein levels. PBMCs from TB-IRIS had increased MMP-1,-3,-7, and-10 transcript levels when compared with those of controls at either 6 or 24 h. Similarly, MMP-1,-3,-7, and-10 protein secretion in stimulated cultures was higher in TB-IRIS than in controls. Serum MMP-7 concentration was elevated in TB-IRIS and 2 weeks of corticosteroid therapy decreased this level, although not significantly. TB-IRIS is associated with a distinct pattern of MMP gene and protein activation. Modulation of dysregulated MMP activity may represent a novel therapeutic approach to alleviate TB-IRIS in HIV-TB patients undergoing treatment. PMID:24136296

  4. Lower Pre-Treatment T Cell Activation in Early- and Late-Onset Tuberculosis-Associated Immune Reconstitution Inflammatory Syndrome

    PubMed Central

    Goovaerts, Odin; Jennes, Wim; Massinga-Loemb, Marguerite; Ondoa, Pascale; Ceulemans, Ann; Vereecken, Chris; Worodria, William; Mayanja-Kizza, Harriet; Colebunders, Robert; Kestens, Luc

    2015-01-01

    Background Tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) is an inflammatory complication in HIV-TB co-infected patients receiving antiretroviral therapy (ART). The role of disturbed T cell reconstitution in TB-IRIS is not well understood. We investigated T cell activation and maturation profiles in patients who developed TB-IRIS at different intervals during ART. Methods Twenty-two HIV-TB patients who developed early-onset TB-IRIS and 10 who developed late-onset TB-IRIS were matched for age, sex and CD4 count to equal numbers of HIV-TB patients who did not develop TB-IRIS. Flow cytometry analysis was performed on fresh blood, drawn before and after ART initiation and during TB-IRIS events. T cell activation and maturation was measured on CD4+ and CD8+ T cells using CD45RO, CD38, HLA-DR, CCR7 and CD27 antibodies. Results CD8+ T cell activation before ART was decreased in both early-onset (77% vs. 82%, p = 0.014) and late-onset (71% vs. 83%, p = 0.012) TB-IRIS patients compared to non-IRIS controls. After ART initiation, the observed differences in T cell activation disappeared. During late-onset, but not early-onset TB-IRIS, we observed a skewing from memory to terminal effector CD4+ and CD8+ T cell populations (p?0.028). Conclusion Our data provide evidence of reduced CD8+ T cell activation before ART as a common predisposing factor of early- and late-onset TB-IRIS. The occurrence of TB-IRIS itself was not marked by an over-activated CD8+ T cell compartment. Late- but not early-onset TB-IRIS was characterized by a more terminally differentiated T cell phenotype. PMID:26208109

  5. Tuberculosis associated immune reconstitution inflammatory syndrome in patients infected with HIV: meningitis a potentially life threatening manifestation

    PubMed Central

    2012-01-01

    Background Tuberculosis (TB) is the most common co infection in HIV-infected persons in India, requiring concomitant administration of anti TB and antiretroviral therapies. Paradoxical worsening of tuberculosis after anti-retroviral therapy (ART) initiation is frequently seen. Objective To study the frequency, clinical presentation and outcome of paradoxical tuberculosis associated immune reconstitution inflammatory syndrome (TB-IRIS) in HIV infected patients in a TB hospital in North India. Design A retrospective chart review of HIV-infected TB patients on anti-tubercular treatment (ATT) at time of ART initiation over a 3?year period. Medical records were reviewed for clinical manifestations and outcome in patients who developed TB-IRIS. Results 514 HIV-infected patients were enrolled between January 2006 and December 2008. Thirteen (12.6%) of 103 patients who had received ART and ATT simultaneously developed paradoxical TB-IRIS. Clinical presentations of paradoxical TB-IRIS included new lymphadenopathy (n?=?3), increase in size of existing lymphadenopathy (n?=?3), worsening of existing pulmonary lesions (n?=?2), appearance of new pleural effusion (n?=?1) and prolonged high grade fever (n?=?2). Four patients developed new tubercular meningitis as manifestation of TB-IRIS. Our cases developed TB-IRIS a median of 15?days after starting ART (IQR 1536). TB-IRIS patients were older (> 35?years) than those with no IRIS (P?=?0.03), but were not distinguishable by CD4 T-cell count, duration of ATT before ART or the outcome of TB treatment. Eight (62%) patients had a complete recovery while 5 (38%) patients with TB-IRIS died, of which majority (n?=?3) had meningitis. Conclusions Paradoxical TB-IRIS is a frequent problem during concomitant ATT and ART in HIV-TB co infected patients in north India. Meningitis is a potentially life threatening manifestation of TB-IRIS. PMID:22620862

  6. HIV–tuberculosis-associated immune reconstitution inflammatory syndrome is characterized by Toll-like receptor and inflammasome signalling

    PubMed Central

    Lai, Rachel P. J.; Meintjes, Graeme; Wilkinson, Katalin A.; Graham, Christine M.; Marais, Suzaan; Van der Plas, Helen; Deffur, Armin; Schutz, Charlotte; Bloom, Chloe; Munagala, Indira; Anguiano, Esperanza; Goliath, Rene; Maartens, Gary; Banchereau, Jacques; Chaussabel, Damien; O'Garra, Anne; Wilkinson, Robert J.

    2015-01-01

    Patients with HIV-associated tuberculosis (TB) initiating antiretroviral therapy (ART) may develop immune reconstitution inflammatory syndrome (TB-IRIS). No biomarkers for TB-IRIS have been identified and the underlying mechanisms are unclear. Here we perform transcriptomic profiling of the blood samples of patients with HIV-associated TB. We identify differentially abundant transcripts as early as week 0.5 post ART initiation that predict downstream activation of proinflammatory cytokines in patients who progress to TB-IRIS. At the characteristic time of TB-IRIS onset (week 2), the signature is characterized by over-representation of innate immune mediators including TLR signalling and TREM-1 activation of the inflammasome. In keeping with the transcriptional data, concentrations of plasma cytokines and caspase-1/5 are elevated in TB-IRIS. Inhibition of MyD88 adaptor and group 1 caspases reduces secretion of cytokines including IL-1 in TB-IRIS patients. These data provide insight on the pathogenesis of TB-IRIS and may assist the development of specific therapies. PMID:26399326

  7. Corticosteroid-modulated Immune Activation in the Tuberculosis Immune Reconstitution Inflammatory Syndrome

    PubMed Central

    Skolimowska, Keira H.; Wilkinson, Katalin A.; Matthews, Kerryn; Tadokera, Rebecca; Conesa-Botella, Anali; Seldon, Ronnett; Rangaka, Molebogeng X.; Rebe, Kevin; Pepper, Dominique J.; Morroni, Chelsea; Colebunders, Robert; Maartens, Gary; Wilkinson, Robert J.

    2012-01-01

    Rationale: HIV–tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) is an immunopathological reaction to mycobacterial antigens induced by antiretroviral therapy. Prednisone reduces morbidity in TB-IRIS, but the mechanisms are unclear. Objectives: To determine the effect of prednisone on the inflammatory response in TB-IRIS (antigen-specific effector T cells, cytokines, and chemokines). Methods: Blood was taken from participants in a randomized placebo-controlled trial of prednisone for TB-IRIS, at 0, 2, and 4 weeks. Participants received prednisone at a dosage of 1.5 mg/kg/day for 2 weeks followed by 0.75 mg/kg/day for 2 weeks, or placebo at identical dosages. Measurements and Main Results: Analyses included IFN-γ enzyme-linked immunospot (ELISPOT), reverse transcription-polymerase chain reaction on peripheral blood mononuclear cells after restimulation with heat-killed Mycobacterium tuberculosis, Luminex multiplex cytokine analysis of corresponding tissue culture supernatants, and Luminex multiplex cytokine analysis of serum. Fifty-eight participants with TB-IRIS (31 receiving prednisone, 27 receiving placebo) were included. In serum, significant decreases in IL-6, IL-10, IL-12 p40, tumor necrosis factor-α, IFN-γ, and IFN-γ–induced protein-10 concentrations during prednisone, but not placebo, treatment were observed. No differences in ELISPOT responses comparing prednisone and placebo groups were shown in response to ESAT-6 (early secreted antigen target-6), Acr1, Acr2, 38-kD antigen, or heat-killed H37Rv M. tuberculosis. Purified protein derivative ELISPOT responses increased over 4 weeks in the prednisone group and decreased in the placebo group (P = 0.007). Conclusions: The beneficial effects of prednisone in TB-IRIS appear to be mediated via suppression of predominantly proinflammatory cytokine responses of innate immune origin, not via a reduction of the numbers of antigen-specific T cells in peripheral blood. PMID:22700860

  8. Type 1 Helper T Cells and FoxP3-positive T Cells in HIVTuberculosis-associated Immune Reconstitution Inflammatory Syndrome

    PubMed Central

    Meintjes, Graeme; Wilkinson, Katalin Andrea; Rangaka, Molebogeng Xheeda; Skolimowska, Keira; van Veen, Kerryn; Abrahams, Musaed; Seldon, Ronnett; Pepper, Dominique J.; Rebe, Kevin; Mouton, Priscilla; van Cutsem, Gilles; Nicol, Mark Patrick; Maartens, Gary; Wilkinson, Robert John

    2008-01-01

    Rationale: Tuberculosis-associated immune reconstitution inflammatory syndrome (TBIRIS) induced by combination antiretroviral therapy (cART) has been attributed to dysregulated expansion of tuberculin PPDspecific IFN-?secreting CD4+ T cells. Objectives: To investigate the role of type 1 helper T cell expansions and regulatory T cells in HIVTB IRIS. Methods: Longitudinal and cross-sectional studies of Mycobacterium tuberculosisspecific IFN-? enzyme-linked immunospot responses and flow cytometric analysis of blood cells from a total of 129 adults with HIV-1associated tuberculosis, 98 of whom were prescribed cART. Measurements and Main Results: In cross-sectional analysis the frequency of IFN-?secreting T cells recognizing early secretory antigenic target (ESAT)-6, ?-crystallins 1 and 2, and PPD of M. tuberculosis was higher in patients with TBIRIS than in similar patients treated for both HIV-1 and tuberculosis who did not develop IRIS (non-IRIS; P ? 0.03). The biggest difference was in the recognition of ?-crystallin molecules: peptide mapping indicated a polyclonal response. Flow cytometric analysis indicated equal proportions of CD4+ and CD8+ cells positive for activation markers HLA-DR and CD71 in both patients with TBIRIS and non-IRIS patients. The percentage of CD4+ cells positive for FoxP3 (Forkhead box P3) was low in both groups (TBIRIS, 5.3 4.5; non-IRIS, 2.46 2.46; P = 0.13). Eight weeks of longitudinal analysis of patients with tuberculosis who were starting cART showed dynamic changes in antigen-specific IFN-?secreting T cells in both the TBIRIS and non-IRIS groups: the only significant trend was an increased response to PPD in the TBIRIS group (P = 0.041). Conclusions: There is an association between helper T-cell type 1 expansions and TBIRIS, but the occurrence of similar expansions in non-IRIS brings into question whether these are causal. The defect in immune regulation responsible for TBIRIS remains to be fully elucidated. PMID:18755923

  9. Mycobacterial Antigen Driven Activation of CD14++CD16? Monocytes Is a Predictor of Tuberculosis-Associated Immune Reconstitution Inflammatory Syndrome

    PubMed Central

    Andrade, Bruno B.; Singh, Amrit; Narendran, Gopalan; Schechter, Melissa E.; Nayak, Kaustuv; Subramanian, Sudha; Anbalagan, Selvaraj; Jensen, Stig M. R.; Porter, Brian O.; Antonelli, Lis R.; Wilkinson, Katalin A.; Wilkinson, Robert J.; Meintjes, Graeme; van der Plas, Helen; Follmann, Dean; Barber, Daniel L.; Swaminathan, Soumya; Sher, Alan; Sereti, Irini

    2014-01-01

    Paradoxical tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) is an aberrant inflammatory response occurring in a subset of TB-HIV co-infected patients initiating anti-retroviral therapy (ART). Here, we examined monocyte activation by prospectively quantitating pro-inflammatory plasma markers and monocyte subsets in TB-HIV co-infected patients from a South Indian cohort at baseline and following ART initiation at the time of IRIS, or at equivalent time points in non-IRIS controls. Pro-inflammatory biomarkers of innate and myeloid cell activation were increased in plasma of IRIS patients pre-ART and at the time of IRIS; this association was confirmed in a second cohort in South Africa. Increased expression of these markers correlated with elevated antigen load as measured by higher sputum culture grade and shorter duration of anti-TB therapy. Phenotypic analysis revealed the frequency of CD14++CD16? monocytes was an independent predictor of TB-IRIS, and was closely associated with plasma levels of CRP, TNF, IL-6 and tissue factor during IRIS. In addition, production of inflammatory cytokines by monocytes was higher in IRIS patients compared to controls pre-ART. These data point to a major role of mycobacterial antigen load and myeloid cell hyperactivation in the pathogenesis of TB-IRIS, and implicate monocytes and monocyte-derived cytokines as potential targets for TB-IRIS prevention or treatment. PMID:25275318

  10. Transient expansion of activated CD8+ T cells characterizes tuberculosis-associated immune reconstitution inflammatory syndrome in patients with HIV: a case control study

    PubMed Central

    2013-01-01

    Background CD4+ T cell activation indicators have been reported to be a common phenomenon underlying diverse manifestations of immune reconstitution inflammatory syndrome (IRIS). However, we have found that a high frequency of circulating CD8+ T cells is a specific risk factor for mycobacterial IRIS. Therefore, we investigated whether CD8+ T cells from patients who develop TB IRIS were specifically activated. Methods We obtained PBMCs from HIV+?patients prior to and 4, 8, 12, 24, 52 and 104weeks after initiating antiretroviral therapy. CD38 and HLADR expression on naive, central memory and effector memory CD8+ and CD4+ T cells were determined by flow cytometry. Absolute counts and frequencies of CD8+ T cell subsets were compared between patients who developed TB IRIS, who developed other IRIS forms and who remained IRIS-free. Results TB IRIS patients showed significantly higher counts of naive CD8+ T cells than the other groups at most time points, with a contraction of the effector memory subpopulation occurring later in the follow-up period. Activated (CD38+ HLADR+) CD8+ T cells from all groups decreased with treatment but transiently peaked in TB IRIS patients. This increase was due to an increase in activated naive CD8+ T cell counts during IRIS. Additionally, the CD8+ T cell subpopulations of TB IRIS patients expressed HLADR without CD38 more frequently and expressed CD38 without HLADR less frequently than cells from other groups. Conclusions CD8+ T cell activation is specifically relevant to TB IRIS. Different IRIS forms may involve different alterations in T cell subsets, suggesting different underlying inflammatory processes. PMID:23688318

  11. Thoracic manifestations of paradoxical immune reconstitution inflammatory syndrome during or after antituberculous therapy in HIV-negative patients.

    PubMed

    Pornsuriyasak, Prapaporn; Suwatanapongched, Thitiporn

    2015-01-01

    Immune reconstitution inflammatory syndrome (IRIS) is a consequence of exaggerated and dysregulated host's inflammatory response to invading microorganism, leading to uncontrolled inflammatory reactions. IRIS associated with tuberculosis (TB) is well recognized among human immunodeficiency virus (HIV)-infected patients receiving highly active antiretroviral therapy, but it is less common among HIV-negative patients. IRIS can manifest as a paradoxical worsening or recurring of preexisting tuberculous lesions or development of new lesions despite successful antituberculous treatment. Hence, the condition might be misdiagnosed as superimposed infections, treatment failure, or relapse of TB. This pictorial essay reviewed diagnostic criteria and various thoracic manifestations of the paradoxical form of TB-associated IRIS (TB-IRIS) that might aid in early recognition of this clinical entity among HIV-negative patients. The treatment and outcomes of TB-IRIS were also discussed. PMID:25698091

  12. Matrix Metalloproteinases in Tuberculosis-Immune Reconstitution Inflammatory Syndrome and Impaired Lung Function Among Advanced HIV/TB Co-infected Patients Initiating Antiretroviral Therapy

    PubMed Central

    Ravimohan, Shruthi; Tamuhla, Neo; Kung, Shiang-Ju; Nfanyana, Kebatshabile; Steenhoff, Andrew P.; Gross, Robert; Weissman, Drew; Bisson, Gregory P.

    2015-01-01

    Background HIV-infected patients with pulmonary TB (pTB) can have worsening of respiratory symptoms as part of TB-immune reconstitution inflammatory syndrome (TB-IRIS) following antiretroviral therapy (ART) initiation. Thus, reconstitution of immune function on ART could drive incident lung damage in HIV/TB. Methods We hypothesized that increases in matrix metalloproteinases (MMPs), which can degrade lung matrix, on ART are associated with TB-IRIS among a cohort of advanced, ART naïve, HIV-infected adults with pTB. Furthermore, we related early changes in immune measures and MMPs on ART to lung function in an exploratory subset of patients post-TB cure. This study was nested within a prospective cohort study. Rank sum and chi-square tests, Spearman's correlation coefficient, and logistic regression were used for analyses. Results Increases in MMP-8 following ART initiation were independently associated with TB-IRIS (p = 0.04; adjusted odds ratio 1.5 [95% confidence interval: 1.0–2.1]; n = 32). Increases in CD4 counts and MMP-8 on ART were also associated with reduced forced expiratory volume in one-second post-TB treatment completion (r = − 0.7, p = 0.006 and r = − 0.6, p = 0.02, respectively; n = 14). Conclusions ART-induced MMP increases are associated with TB-IRIS and may affect lung function post-TB cure. End-organ damage due to TB-IRIS and mechanisms whereby immune restoration impairs lung function in pTB deserve further investigation. PMID:27014741

  13. Central Nervous System Immune Reconstitution Inflammatory Syndrome

    PubMed Central

    Boulware, David R.; Marais, Suzaan; Scriven, James; Wilkinson, Robert J.; Meintjes, Graeme

    2013-01-01

    Central nervous system immune reconstitution inflammatory syndrome (CNS-IRIS) develops in 9 %–47 % of persons with HIV infection and a CNS opportunistic infection who start antiretroviral therapy and is associated with a mortality rate of 13 %–75 %. These rates vary according to the causative pathogen. Common CNS-IRIS events occur in relation to Cryptococcus, tuberculosis (TB), and JC virus, but several other mycobacteria, fungi, and viruses have been associated with IRIS. IRIS symptoms often mimic the original infection, and diagnosis necessitates consideration of treatment failure, microbial resistance, and an additional neurological infection. These diagnostic challenges often delay IRIS diagnosis and treatment. Corticosteroids have been used to treat CNS-IRIS, with variable responses; the best supportive evidence exists for the treatment of TB-IRIS. Pathogenic mechanisms vary: Cryptococcal IRIS is characterized by a paucity of cerebrospinal inflammation prior to antiretroviral therapy, whereas higher levels of inflammatory markers at baseline predispose to TB meningitis IRIS. This review focuses on advances in the understanding of CNS-IRIS over the past 2 years. PMID:24173584

  14. [Ocular immune reconstitution inflammatory syndrome].

    PubMed

    Ma, N; Ye, J J

    2016-02-11

    Immune reconstitution inflammatory syndrome (IRIS) is a collection of inflammatory disorders associated with paradoxical worsening of preexisting infectious processes or emerging diseases or even dead after the initiation of highly active antiretroviral therapy (HAART) in human immunodeficiency virus (HIV) infected individuals in a period of recovery of immune function. Ocular immune reconstitution inflammatory syndrome is mainly caused by cytomegalovirus which performing a series of ocular inflammation accompanied with the increase of CD4+ T lymphocytes, such as cytomegalovirus retinitis, after HAART. With HAART widely used, the patients of IRIS gradually increased. But the clinical presentations of IRIS were various because of different pathogens. This review summarized the clinical manifestations, risk factors, diagnosis and treatment of ocular IRIS.(Chin J Ophthalmol, 2016, 51: 150-153). PMID:26906710

  15. NCI scientists identify new inflammatory syndrome

    Cancer.gov

    NCI scientists have identified a new inflammatory condition called interleukin-6 syndrome caused by Kaposis sarcoma-associated herpesvirus (KSHV) in some people with HIV/AIDS. This syndrome will be added to three existing types of KSHV-linked illnesses i

  16. HIV & immune reconstitution inflammatory syndrome (IRIS)

    PubMed Central

    Sharma, Surendra K.; Soneja, Manish

    2011-01-01

    Antiretroviral therapy (ART) initiation in HIV-infected patients leads to recovery of CD4+T cell numbers and restoration of protective immune responses against a wide variety of pathogens, resulting in reduction in the frequency of opportunistic infections and prolonged survival. However, in a subset of patients, dysregulated immune response after initiation of ART leads to the phenomenon of immune reconstitution inflammatory syndrome (IRIS). The hallmark of the syndrome is paradoxical worsening of an existing infection or disease process or appearance of a new infection/disease process soon after initiation of therapy. The overall incidence of IRIS is unknown, but is dependent on the population studied and the burden of underlying opportunistic infections. The immunopathogenesis of the syndrome is unclear and appears to be result of unbalanced reconstitution of effector and regulatory T-cells, leading to exuberant inflammatory response in patients receiving ART. Biomarkers, including interferon-γ (INF-γ), tumour necrosis factor-α (TNF-α), C-reactive protein (CRP) and inter leukin (IL)-2, 6 and 7, are subject of intense investigation at present. The commonest forms of IRIS are associated with mycobacterial infections, fungi and herpes viruses. Majority of patients with IRIS have a self-limiting disease course. ART is usually continued and treatment for the associated condition optimized. The overall mortality associated with IRIS is low; however, patients with central nervous system involvement with raised intracranial pressures in cryptococcal and tubercular meningitis, and respiratory failure due to acute respiratory distress syndrome (ARDS) have poor prognosis and require aggressive management including corticosteroids. Paradigm shifts in management of HIV with earlier initiation of ART is expected to decrease the burden of IRIS in developed countries; however, with enhanced rollout of ART in recent years and the enormous burden of opportunistic infections in developing countries like India, IRIS is likely to remain an area of major concern. PMID:22310819

  17. Vitamin D, d-dimer, Interferon γ, and sCD14 Levels are Independently Associated with Immune Reconstitution Inflammatory Syndrome: A Prospective, International Study☆

    PubMed Central

    Musselwhite, Laura W.; Andrade, Bruno B.; Ellenberg, Susan S.; Tierney, Ann; Belaunzaran-Zamudio, Pablo F.; Rupert, Adam; Lederman, Michael M.; Sanne, Ian; Sierra Madero, Juan G.; Sereti, Irini

    2016-01-01

    To determine the immunological profile most important for IRIS prediction, we evaluated 20 baseline plasma biomarkers in Acquired Immunodeficiency Syndrome (AIDS) patients initiating antiretroviral therapy (ART). Patients were enrolled in a randomized, placebo-controlled ART initiation trial in South Africa and Mexico to test whether maraviroc could prevent IRIS. Participants were classified prospectively as having IRIS within 6 months of ART initiation. Twenty plasma biomarkers were measured at study enrollment for 267 participants. Biomarkers were tested for predicting IRIS with adjustment for covariates chosen through forward stepwise selection. Sixty-two participants developed IRIS and of these 19 were tuberculosis (TB)-IRIS. Baseline levels of vitamin D and higher d-dimer, interferon gamma (IFNγ), and sCD14 were independently associated with risk of IRIS in multivariate analyses. TB-IRIS cases exhibited a distinct biosignature from IRIS related to other pathogens, with increased levels of C-reactive protein (CRP), sCD14, IFNγ, and lower levels of Hb that could be captured by a composite risk score. Elevated markers of Type 1 T helper (Th1) response, monocyte activation, coagulation and low vitamin D were independently associated with IRIS risk. Interventions that decrease immune activation and increase vitamin D levels warrant further study. PMID:26981576

  18. Vitamin D, d-dimer, Interferon γ, and sCD14 Levels are Independently Associated with Immune Reconstitution Inflammatory Syndrome: A Prospective, International Study.

    PubMed

    Musselwhite, Laura W; Andrade, Bruno B; Ellenberg, Susan S; Tierney, Ann; Belaunzaran-Zamudio, Pablo F; Rupert, Adam; Lederman, Michael M; Sanne, Ian; Sierra Madero, Juan G; Sereti, Irini

    2016-02-01

    To determine the immunological profile most important for IRIS prediction, we evaluated 20 baseline plasma biomarkers in Acquired Immunodeficiency Syndrome (AIDS) patients initiating antiretroviral therapy (ART). Patients were enrolled in a randomized, placebo-controlled ART initiation trial in South Africa and Mexico to test whether maraviroc could prevent IRIS. Participants were classified prospectively as having IRIS within 6 months of ART initiation. Twenty plasma biomarkers were measured at study enrollment for 267 participants. Biomarkers were tested for predicting IRIS with adjustment for covariates chosen through forward stepwise selection. Sixty-two participants developed IRIS and of these 19 were tuberculosis (TB)-IRIS. Baseline levels of vitamin D and higher d-dimer, interferon gamma (IFNγ), and sCD14 were independently associated with risk of IRIS in multivariate analyses. TB-IRIS cases exhibited a distinct biosignature from IRIS related to other pathogens, with increased levels of C-reactive protein (CRP), sCD14, IFNγ, and lower levels of Hb that could be captured by a composite risk score. Elevated markers of Type 1 T helper (Th1) response, monocyte activation, coagulation and low vitamin D were independently associated with IRIS risk. Interventions that decrease immune activation and increase vitamin D levels warrant further study. PMID:26981576

  19. Subclinical inflammatory status in Rett syndrome.

    PubMed

    Cortelazzo, Alessio; De Felice, Claudio; Guerranti, Roberto; Signorini, Cinzia; Leoncini, Silvia; Pecorelli, Alessandra; Zollo, Gloria; Landi, Claudia; Valacchi, Giuseppe; Ciccoli, Lucia; Bini, Luca; Hayek, Joussef

    2014-01-01

    Inflammation has been advocated as a possible common central mechanism for developmental cognitive impairment. Rett syndrome (RTT) is a devastating neurodevelopmental disorder, mainly caused by de novo loss-of-function mutations in the gene encoding MeCP2. Here, we investigated plasma acute phase response (APR) in stage II (i.e., "pseudo-autistic") RTT patients by routine haematology/clinical chemistry and proteomic 2-DE/MALDI-TOF analyses as a function of four major MECP2 gene mutation types (R306C, T158M, R168X, and large deletions). Elevated erythrocyte sedimentation rate values (median 33.0?mm/h versus 8.0?mm/h, P < 0.0001) were detectable in RTT, whereas C-reactive protein levels were unchanged (P = 0.63). The 2-DE analysis identified significant changes for a total of 17 proteins, the majority of which were categorized as APR proteins, either positive (n = 6 spots) or negative (n = 9 spots), and to a lesser extent as proteins involved in the immune system (n = 2 spots), with some proteins having overlapping functions on metabolism (n = 7 spots). The number of protein changes was proportional to the severity of the mutation. Our findings reveal for the first time the presence of a subclinical chronic inflammatory status related to the "pseudo-autistic" phase of RTT, which is related to the severity carried by the MECP2 gene mutation. PMID:24511209

  20. Inflammatory Lung Disease in Rett Syndrome

    PubMed Central

    De Felice, Claudio; Rossi, Marcello; Chisci, Glauco; Lonetti, Giuseppina; Vannuccini, Laura; Spina, Donatella; Iacona, Ingrid; Cortelazzo, Alessio; Ciccoli, Lucia; Pizzorusso, Tommaso; Hayek, Joussef

    2014-01-01

    Rett syndrome (RTT) is a pervasive neurodevelopmental disorder mainly linked to mutations in the gene encoding the methyl-CpG-binding protein 2 (MeCP2). Respiratory dysfunction, historically credited to brainstem immaturity, represents a major challenge in RTT. Our aim was to characterize the relationships between pulmonary gas exchange abnormality (GEA), upper airway obstruction, and redox status in patients with typical RTT (n = 228) and to examine lung histology in a Mecp2-null mouse model of the disease. GEA was detectable in ~80% (184/228) of patients versus ~18% of healthy controls, with high (39.8%) and low (34.8%) patterns dominating over mixed (19.6%) and simple mismatch (5.9%) types. Increased plasma levels of non-protein-bound iron (NPBI), F2-isoprostanes (F2-IsoPs), intraerythrocyte NPBI (IE-NPBI), and reduced and oxidized glutathione (i.e., GSH and GSSG) were evidenced in RTT with consequently decreased GSH/GSSG ratios. Apnea frequency/severity was positively correlated with IE-NPBI, F2-IsoPs, and GSSG and negatively with GSH/GSSG ratio. A diffuse inflammatory infiltrate of the terminal bronchioles and alveoli was evidenced in half of the examined Mecp2-mutant mice, well fitting with the radiological findings previously observed in RTT patients. Our findings indicate that GEA is a key feature of RTT and that terminal bronchioles are a likely major target of the disease. PMID:24757286

  1. Subclinical Inflammatory Status in Rett Syndrome

    PubMed Central

    Cortelazzo, Alessio; De Felice, Claudio; Guerranti, Roberto; Landi, Claudia; Valacchi, Giuseppe; Ciccoli, Lucia; Hayek, Joussef

    2014-01-01

    Inflammation has been advocated as a possible common central mechanism for developmental cognitive impairment. Rett syndrome (RTT) is a devastating neurodevelopmental disorder, mainly caused by de novo loss-of-function mutations in the gene encoding MeCP2. Here, we investigated plasma acute phase response (APR) in stage II (i.e., “pseudo-autistic”) RTT patients by routine haematology/clinical chemistry and proteomic 2-DE/MALDI-TOF analyses as a function of four major MECP2 gene mutation types (R306C, T158M, R168X, and large deletions). Elevated erythrocyte sedimentation rate values (median 33.0 mm/h versus 8.0 mm/h, P < 0.0001) were detectable in RTT, whereas C-reactive protein levels were unchanged (P = 0.63). The 2-DE analysis identified significant changes for a total of 17 proteins, the majority of which were categorized as APR proteins, either positive (n = 6 spots) or negative (n = 9 spots), and to a lesser extent as proteins involved in the immune system (n = 2 spots), with some proteins having overlapping functions on metabolism (n = 7 spots). The number of protein changes was proportional to the severity of the mutation. Our findings reveal for the first time the presence of a subclinical chronic inflammatory status related to the “pseudo-autistic” phase of RTT, which is related to the severity carried by the MECP2 gene mutation. PMID:24511209

  2. Hansen's disease in association with immune reconstitution inflammatory syndrome

    PubMed Central

    George, Anju; Vidyadharan, Suja

    2016-01-01

    Immune reconstitution inflammatory syndrome is characterized by a paradoxical worsening of an existing infection or disease process, soon after initiation of highly active antiretroviral therapy. The first case of leprosy presenting as immune reconstitution inflammatory syndrome was published in 2003. Here we report a case of Hansen's disease borderline tuberculoid presenting with type 1 lepra reaction 5 months after initiation of highly active antiretroviral therapy. PMID:26955584

  3. Hansen's disease in association with immune reconstitution inflammatory syndrome.

    PubMed

    George, Anju; Vidyadharan, Suja

    2016-01-01

    Immune reconstitution inflammatory syndrome is characterized by a paradoxical worsening of an existing infection or disease process, soon after initiation of highly active antiretroviral therapy. The first case of leprosy presenting as immune reconstitution inflammatory syndrome was published in 2003. Here we report a case of Hansen's disease borderline tuberculoid presenting with type 1 lepra reaction 5 months after initiation of highly active antiretroviral therapy. PMID:26955584

  4. Obesity-Driven Gut Microbiota Inflammatory Pathways to Metabolic Syndrome

    PubMed Central

    Cavalcante-Silva, Luiz H. A.; Galvão, José G. F. M.; da Silva, Juliane Santos de França; de Sales-Neto, José M.; Rodrigues-Mascarenhas, Sandra

    2015-01-01

    The intimate interplay between immune system, metabolism, and gut microbiota plays an important role in controlling metabolic homeostasis and possible obesity development. Obesity involves impairment of immune response affecting both innate and adaptive immunity. The main factors involved in the relationship of obesity with inflammation have not been completely elucidated. On the other hand, gut microbiota, via innate immune receptors, has emerged as one of the key factors regulating events triggering acute inflammation associated with obesity and metabolic syndrome. Inflammatory disorders lead to several signaling transduction pathways activation, inflammatory cytokine, chemokine production and cell migration, which in turn cause metabolic dysfunction. Inflamed adipose tissue, with increased macrophages infiltration, is associated with impaired preadipocyte development and differentiation to mature adipose cells, leading to ectopic lipid accumulation and insulin resistance. This review focuses on the relationship between obesity and inflammation, which is essential to understand the pathological mechanisms governing metabolic syndrome. PMID:26635627

  5. Therapeutics targeting inflammation in the immune reconstitution inflammatory syndrome.

    PubMed

    Shahani, Lokesh; Hamill, Richard J

    2016-01-01

    Immune reconstitution inflammatory syndrome (IRIS) is characterized by improvement in a previously incompetent human immune system manifesting as worsening of clinical symptoms secondary to the ability of the immune system to now mount a vigorous inflammatory response. IRIS was first recognized in the setting of human immunodeficiency virus, and this clinical setting continues to be where it is most frequently encountered. Hallmarks of the pathogenesis of IRIS, independent of the clinical presentation and the underlying pathogen, include excessive activation of the immune system, with increased circulating effector memory T cells, and elevated levels of serum cytokines and inflammatory markers. Patients with undiagnosed opportunistic infections remain at risk for unmasking IRIS at the time of active antiretroviral therapy (ART) initiation. Systematic screening for opportunistic infections before starting ART is a key element to prevent this phenomenon. Appropriate management of IRIS requires prompt recognition of the syndrome and exclusion of alternative diagnoses, particularly underlying infections and drug resistance. Controlled studies supporting the use of pharmacologic interventions in IRIS are scare, and recommendations are based on case series and expert opinions. The only controlled trial published to date, showed reduction in morbidity in patients with paradoxical tuberculosis-related IRIS with the use of oral corticosteroids. There are currently limited data to recommend other anti-inflammatory or immunomodulatory therapies that are discussed in this review, and further research is needed. Ongoing research regarding the immune pathogenesis of IRIS will likely direct future rational therapeutic approaches and clinical trials. PMID:26303886

  6. [Non-infectious inflammatory fasciitis: a borderline syndrome].

    PubMed

    Hachulla, E; Janin, A

    1995-01-01

    Inflammatory fasciitis without infection include different entity like eosinophilic fasciitis, the syndrome of eosinophilia-myalgia after tryptophan ingestion, toxic oil syndrome, exposure to trichlorethylene, phenylketonuria skin changes, the syndrome of palmar fasciitis, fasciitis in chronic graft-versus-host disease and fasciitis secondary to an adjacence process. The diagnosis of all these scleroderma-like skin changes is sometimes not easy because the clinical and sometimes the histopathological changes are bordeline manifestations with scleroderma. The most characteristic markers for non infectious fasciitis is eosinophilia and the infiltration of the fascia with eosinophilis, but it may be unremarkable or absent, only frequently present at the onset of the disease. Anamnesis is most important to guide the diagnosis. The eosinophils, but not only, may play a major role in the pathogenesis of this entity. PMID:7597318

  7. Electrophysiological features of POEMS syndrome and chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Guo, Xiuming; Qin, Xinyue; Zhang, Yuping; Huang, Cheng; Yu, Gang

    2014-04-01

    Polyneuropathy is often an initial manifestation of polyneuropathy, organomegaly, endocrinopathy, M protein and skin changes (POEMS) syndrome and therefore this disorder is frequently misdiagnosed as chronic inflammatory demyelinating polyneuropathy (CIDP). We reviewed electrophysiological data in 20 patients with POEMS syndrome and 36 matched patients with CIDP to compare the electrophysiological features of POEMS syndrome and CIDP. Compared with CIDP controls, POEMS patients demonstrated (1) less prolonged distal motor latency and less reduced motor nerve and sensory nerve conduction velocities, (2) greater reduction of amplitudes of compound motor action potentials (CMAP) in distal stimulation, and similar reduction of amplitudes of CMAP in proximal stimulation, (3) similar reduction of amplitudes of sensory nerve action potentials (SNAP) in median and ulnar nerves, and a greater reduction of amplitudes of SNAP in tibial and peroneal nerves, (4) less temporal dispersion, (5) less frequent conduction block, (6) more frequent neurogenic injury in the muscles of the upper and lower limbs, and more frequent neurogenic injury in the muscles of the lower than upper limbs, (7) similar F wave and H reflex abnormalities, and (8) less frequent skin sympathetic response abnormalities. We concluded that before development of typical clinical manifestations, POEMS neuropathy can be distinguished from CIDP by neural electrophysiological examination. These electrophysiological features can be used for early diagnosis and initiating correct treatment of POEMS syndrome. PMID:24268501

  8. Irritable bowel syndrome, inflammatory bowel disease and the microbiome

    PubMed Central

    Major, Giles; Spiller, Robin

    2014-01-01

    Purpose of review The review aims to update the reader on current developments in our understanding of how the gut microbiota impact on inflammatory bowel disease and the irritable bowel syndrome. It will also consider current efforts to modulate the microbiota for therapeutic effect. Recent findings Gene polymorphisms associated with inflammatory bowel disease increasingly suggest that interaction with the microbiota drives pathogenesis. This may be through modulation of the immune response, mucosal permeability or the products of microbial metabolism. Similar findings in irritable bowel syndrome have reinforced the role of gut-specific factors in this ‘functional’ disorder. Metagenomic analysis has identified alterations in pathways and interactions with the ecosystem of the microbiome that may not be recognized by taxonomic description alone, particularly in carbohydrate metabolism. Treatments targeted at the microbial stimulus with antibiotics, probiotics or prebiotics have all progressed in the past year. Studies on the long-term effects of treatment on the microbiome suggest that dietary intervention may be needed for prolonged efficacy. Summary The microbiome represents ‘the other genome’, and to appreciate its role in health and disease will be as challenging as with our own genome. Intestinal diseases occur at the front line of our interaction with the microbiome and their future treatment will be shaped as we unravel our relationship with it. PMID:24296462

  9. [Unidentified Inflammatory Disease Induced by Azacitidine Therapy for Myelodysplastic Syndrome].

    PubMed

    Inagaki, Shunichiro; Tamai, Yotaro; Yoshizawa, Masaki; Sato, Shuku; Kanbe, Emiko; Tanaka, Eri

    2015-11-01

    We report a 73-year-old woman with myelodysplastic syndromes (MDS) of the refractory anemia with excess of blasts-1 subtype, which was diagnosed in April 2014 on the basis of cytopenia for two cell types. After completing 3cycles of azacitidine (AZA) therapy, the patient was admitted to our hospital based on an initial presentation of high fever. During hospitalization, the high fever and increasing inflammatory reaction persisted. We reevaluated the effect of MDS in this patient and concluded that the AZA administration was successful and the MDS was extremely stable. On medical examination and inspection, the patient had an unidentified inflammatory disease. First, we treated her with high-dose steroid pulse therapy. However, the effect of the treatment was transient. Furthermore, the effects of cyclosporin A and oral steroid therapy were poor; therefore, we initiated tocilizumab administration. Nevertheless, she died of multiorgan failure. An increasing serum IL- 6 level induced by the AZA therapy was later confirmed. Recent studies have reported the immunomodulatory effects stimulated by AZA therapy in MDS. This case is a valuable reminder that an unidentified inflammatory disease can be induced in the course of AZA therapy for MDS. PMID:26602409

  10. Irritable bowel syndrome in quiescent inflammatory bowel disease: a review.

    PubMed

    Burgell, R E; Asthana, A K; Gibson, P R

    2015-12-01

    Ongoing troublesome bowel symptoms despite quiescent inflammatory disease are a frequent management challenge when caring for patients with inflammatory bowel disease (IBD). Even when active disease has been excluded the prevalence of residual gastrointestinal symptoms is surprisingly high and the cause often obscure. The presence of a concurrent functional disorder such as irritable bowel syndrome (IBS) is associated with worse quality of life, worse physical functioning, higher prevalence of anxiety and greater health care utilization. Potential etiological mechanisms leading to the development of IBS like symptoms include the development of visceral hypersensitivity following the original inflammatory insult, alteration in cortical processing, dysbiosis and residual subacute inflammation. Therapeutic options for managing IBS in patients with IBD include dietary modification, interventions targeted at correction of visceral sensory dysfunction or cortical processing and modulation of the gut microbiota. As there are few studies specifically examining the treatment of IBS in patients with IBD, the majority of therapeutic interventions are extrapolated from the IBS literature. Given the frequency of residual functional symptoms in IBS, significantly more research is warranted in this field. PMID:26426460

  11. Immune reconstitution inflammatory syndrome in HIV-infected patients

    PubMed Central

    Walker, Naomi F; Scriven, James; Meintjes, Graeme; Wilkinson, Robert J

    2015-01-01

    Access to antiretroviral therapy (ART) is improving worldwide. Immune reconstitution inflammatory syndrome (IRIS) is a common complication of ART initiation. In this review, we provide an overview of clinical and epidemiological features of HIV-associated IRIS, current understanding of pathophysiological mechanisms, available therapy, and preventive strategies. The spectrum of HIV-associated IRIS is described, with a particular focus on three important pathogen-associated forms: tuberculosis-associated IRIS, cryptococcal IRIS, and Kaposi’s sarcoma IRIS. While the clinical features and epidemiology are well described, there are major gaps in our understanding of pathophysiology and as a result therapeutic and preventative strategies are suboptimal. Timing of ART initiation is critical to reduce IRIS-associated morbidity. Improved understanding of the pathophysiology of IRIS will hopefully enable improved diagnostic modalities and better targeted treatments to be developed. PMID:25709503

  12. Deregulation of innate immune and inflammatory signaling in myelodysplastic syndromes.

    PubMed

    Gan-Gmez, I; Wei, Y; Starczynowski, D T; Colla, S; Yang, H; Cabrero-Calvo, M; Bohannan, Z S; Verma, A; Steidl, U; Garcia-Manero, G

    2015-07-01

    Myelodysplastic syndromes (MDSs) are a group of heterogeneous clonal hematologic malignancies that are characterized by defective bone marrow (BM) hematopoiesis and by the occurrence of intramedullary apoptosis. During the past decade, the identification of key genetic and epigenetic alterations in patients has improved our understanding of the pathophysiology of this disease. However, the specific molecular mechanisms leading to the pathogenesis of MDS have largely remained obscure. Recently, essential evidence supporting the direct role of innate immune abnormalities in MDS has been obtained, including the identification of multiple key regulators that are overexpressed or constitutively activated in BM hematopoietic stem and progenitor cells. Mounting experimental results indicate that the dysregulation of these molecules leads to abnormal hematopoiesis, unbalanced cell death and proliferation in patients' BM, and has an important role in the pathogenesis of MDS. Furthermore, there is compelling evidence that the deregulation of innate immune and inflammatory signaling also affects other cells from the immune system and the BM microenvironment, which establish aberrant associations with hematopoietic precursors and contribute to the MDS phenotype. Therefore, the deregulation of innate immune and inflammatory signaling should be considered as one of the driving forces in the pathogenesis of MDS. In this article, we review and update the advances in this field, summarizing the results from the most recent studies and discussing their clinical implications. PMID:25761935

  13. Irritable bowel syndrome - An inflammatory disease involving mast cells

    PubMed Central

    Philpott, Hamish; Gibson, Peter

    2011-01-01

    Irritable bowel syndrome (IBS) is traditionally defined as a functional disorder - that is the presence of symptoms in the absence of demonstrable pathological abnormalities. In recent times, low grade inflammatory infiltrates in both the small and large bowel of some patients with IBS - often rich in mast cells, along with serological markers of low grade inflammation have focussed attention on IBS as an inflammatory disease. The observation that mast cells often lie in close association to enteric neurons, and in-vitro and in-vivo animal studies demonstrating that mast cell mediators may influence enteric motility provides a biologically plausible causal mechanism in IBS. Pilot studies on patients with IBS using the mast cell stabiliser sodium cromoglycate ('proof of concept') have been encouraging. The essential question remains why mast cells infiltrate the bowel of IBS patients. A disturbance of the 'brain-gut axis' is the current favoured hypothesis, whereby childhood stress or psychiatric comorbidity act via neuro-immune mechanisms to modulate low grade inflammation. An alternative hypothesis is that food allergy may be responsible. Serum specific IgE, and skin prick tests are not elevated in IBS patients, suggesting type 1 IgE mediated food allergy is not the cause. However questionnaire based studies indicate IBS patients have higher rates of atopic disease, and increased bronchial reactivity to methacholine has been demonstrated. In this review, we highlight the potential role of mast cells in IBS, and current and future research directions into this intriguing condition. PMID:22053295

  14. The spectrum of post-vaccination inflammatory CNS demyelinating syndromes.

    PubMed

    Karussis, Dimitrios; Petrou, Panayiota

    2014-03-01

    A wide variety of inflammatory diseases temporally associated with the administration of various vaccines, has been reported in the literature. A PubMed search from 1979 to 2013 revealed seventy one (71) documented cases. The most commonly reported vaccinations that were associated with CNS demyelinating diseases included influenza (21 cases), human papilloma virus (HPV) (9 cases), hepatitis A or B (8 cases), rabies (5 cases), measles (5 cases), rubella (5 cases), yellow fever (3 cases), anthrax (2 cases),meningococcus (2 cases) and tetanus (2 cases). The vast majority of post-vaccination CNS demyelinating syndromes, are related to influenza vaccination and this could be attributed to the high percentage of the population that received the vaccine during the HI1N1 epidemia from 2009 to 2012. Usually the symptoms of the CNS demyelinating syndrome appear few days following the immunization (mean: 14.2 days) but there are cases where the clinical presentation was delayed (more than 3 weeks or even up to 5 months post-vaccination) (approximately a third of all the reported cases). In terms of the clinical presentation and the affected CNS areas, there is a great diversity among the reported cases of post-vaccination acute demyelinating syndromes. Optic neuritis was the prominent clinical presentation in 38 cases, multifocal disseminated demyelination in 30, myelitis in 24 and encephalitis in 17. Interestingly in a rather high proportion of the patients (and especially following influenza and human papiloma virus vaccination-HPV) the dominant localizations of demyelination were the optic nerves and the myelon, presenting as optic neuritis and myelitis (with or without additional manifestations of ADEM), reminiscent to neuromyelitic optica (or, more generally, the NMO-spectrum of diseases). Seven patients suffered an NMO-like disease following HPV and we had two similar cases in our Center. One patient with post-vaccination ADEM, subsequently developed NMO. Overall, the risk of a demyelinating CNS disease following vaccination, although non-negligible, is relatively low. The risk of onset or relapse of CNS demyelination following infections against which the vaccines are aimed to protect, is substantially higher and the benefits of vaccinations surpass the potential risks of CNS inflammation. This does not in any way exempt us fromlearning the lessons taught by the reported cases and searching new and safer ways to improve vaccination techniques and increase their safety profile. PMID:24514081

  15. Progressive multifocal leukoencephalopathy and immune reconstitution inflammatory syndrome (IRIS).

    PubMed

    Bauer, Jan; Gold, Ralf; Adams, Ortwin; Lassmann, Hans

    2015-12-01

    Progressive multifocal leukoencephalopathy is a viral encephalitis induced by the John Cunningham (JC) virus, an ubiquitous neurotropic papovavirus of the genus polyomavirus that in healthy people in latency resides in kidney and bone marrow cells. Activation and entry into the CNS were first seen in patients with malignancies of the hematopoietic system and an impaired immune system. During the 1980 and the 1990s with the appearance of human immunodeficiency virus infection in humans, PML was found to be the most important opportunistic infection of the central nervous system. As a result of highly efficient immunosuppressive and immunomodulatory treatments, in recent years, the number of PML cases again increased. PML is prevented by an intact cellular immune response and accordingly immune reconstitution can terminate established disease in the CNS. However, forced immune reconstitution can lead to massive destruction of virus-infected cells. This may result in clinical exacerbation associated with high morbidity and mortality and referred to as PML with immune reconstitution inflammatory syndrome (PML-IRIS). In the present review, we discuss virological properties and routes of infection in the CNS, but mostly focus on the pathology of PML and PML-IRIS and on the role of the immune system in these disorders. We show that PML and PML-IRIS result from predominant JC virus infection of oligodendrocytes and, to a lesser extent, of infected neurons. Inflammation in these encephalitides seems to be driven by a dominant cytotoxic T cell response which is massively exaggerated during IRIS. PMID:26323992

  16. Irritable bowel syndrome and inflammatory bowel disease: interrelated diseases?

    PubMed

    Quigley, Eamonn M M

    2005-01-01

    In the past inflammatory bowel disease (IBD), celiac disease and irritable bowel syndrome (IBS) were regarded as completely separate disorders. Now, with the description of inflammation, albeit low-grade, in IBS, and of symptom overlap between IBS and celiac disease, this contention has come under question. Is there true overlap between these disorders? Despite the limitations of available data one cannot but be struck by some areas of apparent convergence: IBD and celiac disease in remission, lymphocytic colitis and microscopic inflammation in IBS, in general, and, especially, in the post-infectious IBS category. The convergence between latent celiac disease and sub-clinical IBD, on the one hand, and IBS, on the other, appears, based on available evidence, to be somewhat spurious and may largely relate to misdiagnosis, a phenomenon which may also explain the apparent evolution of IBS into IBD in some studies. Similarities between IBS and lymphocytic colitis are more striking and less readily dismissed; as for IBS, well documented instances of progression of lymphocytic colitis to full-blown IBD are infrequent, suggesting a true separation between this disorder and classical IBD. Do IBS and lymphocytic colitis represent different responses to similar triggers? Will some of the 'inflamed' IBS subgroup be reclassified as part of the spectrum of lymphocytic colitis in the future? Will inflammation emerge as a common underlying factor in the pathogenesis of IBS? The answer to these and many questions must await further study of this fascinating area. PMID:16045602

  17. Immune reconstitution inflammatory syndrome: incidence and implications for mortality

    PubMed Central

    Novak, Richard M.; Richardson, James T.; Buchacz, Kate; Chmiel, Joan S.; Durham, Marcus D.; Palella, Frank J.; Wendrow, Andrea; Wood, Kathy; Young, Benjamin; Brooks, John T.

    2015-01-01

    Objective To describe incidence of immune reconstitution inflammatory syndrome (IRIS) and its association with mortality in a large multisite US HIV-infected cohort applying an objective, comprehensive definition. Design We studied 2 610 patients seen during 1996–2007 who initiated or resumed highly active combination antiretroviral therapy (cART) and, during the next 6 months, demonstrated a decline in plasma HIV-RNA viral load of at least 0.5 log10 copies/ml or an increase of at least 50% in CD4 cell count per microliter. We defined IRIS as the diagnosis of a type B or C condition [as per the Centers for Disease Control and Prevention (CDC) 1993 AIDS case definition] or any new mucocutaneous disorder during this same 6-month period. Methods We assessed the incidence of IRIS and evaluated risk factors for IRIS using conditional logistic regression and for all-cause mortality using proportional hazards models. Results We identified 370 cases of IRIS (in 276 patients). Median and nadir CD4 cell counts at cART initiation were 90 and 43 cells/μl, respectively; median viral load was 2.7 log10 copies/ml. The most common IRIS-defining diagnoses were candidiasis (all forms), cytomegalovirus infection, disseminated Mycobacterium avium intracellulare, Pneumocystis pneumonia, varicella zoster, Kaposi’s sarcoma and non-Hodgkin lymphoma. Only one case of Mycobacterium tuberculosis was observed. IRIS was independently associated with CD4 cell count less than 50 cells/μl vs. at least 200 cells/μl [odds ratio (OR) 5.0] and a viral load of at least 5.0 log10 copies vs. less than 4.0 log10 copies (OR 2.3). IRIS with a type B-defining or type C-defining diagnosis approximately doubled the risk for all-cause mortality. Conclusion In this large US-based HIV-infected cohort, IRIS occurred in 10.6% of patients who responded to effective ART and contributed to increased mortality. PMID:22233655

  18. Sepsis: a pro- and anti-inflammatory disequilibrium syndrome.

    PubMed

    Pinsky, M R

    2001-01-01

    Severe sepsis and probably most prolonged critical illnesses reflect a paradox of combined increased activation and depression of the immune apparatus. The increased activation of the inflammatory response is evidenced from the increased levels of circulating proinflammatory cytokines in the blood, increased endothelial activation with increased expression of inducible nitric oxide synthase, and increased de novo CD11b expression on circulating immune effector cells, such as PMNs, monocytes and lymphocytes. However, coexisting with this proinflammatory process is a profound anti-inflammatory state characterized by increased circulating levels of anti-inflammatory species that both directly block the binding of proinflammatory stimuli to their cell surface receptors (IL-1ra, soluble TNF receptors) and also induce an anti-inflammatory state on their own (IL-10, TFG-beta). This humoral anti-inflammatory state is mirrored at the cellular levels by decreased monocyte ability to process antigen, characterized by a reduced HLA-DR expression and impaired PMN upregulation in response to clearly proinflammatory stimuli. Accordingly, severe sepsis reflects a combined pro- and anti-inflammatory state. Both the pro- and anti-inflammatory arms have protective and destructive aspects, making their modulation by treatment less predictable than if their actions were purely beneficial or detrimental. PMID:11395903

  19. Syndromic and sporadic inflammatory/hyperplastic small-bowel polyps: a comparative study

    PubMed Central

    Liu, Xiuli; Chen, Derrick; Dugum, Mohannad; Horvath, Bela; Yuan, Lisi; Xiao, Shu-Yuan

    2015-01-01

    Background: Inflammatory/hyperplastic small-bowel polyps (SBPs) occur either sporadically or in patients with a polyposis syndrome; however, comparison between these two settings of the histological features of SBPs has not been reported and the etiology of sporadic inflammatory/hyperplastic SBPs remains unclear. Method: Twenty-eight cases of sporadic inflammatory/hyperplastic SBPs and nine cases of syndromic SBPs were retrieved from the Department of Anatomic Pathology at the Cleveland Clinic. Clinico-demographics and histological features were compared between the two groups. Results: Patients with syndromic inflammatory/hyperplastic SBPs were younger (48 vs. 63 years; P?=?0.007) and had higher rates of hemorrhagic telangiectasia (55.6% vs. 0%; P?=?0.000), gastric polyps (87.5% vs. 21.4%; P?=?0.001), and family history of colon cancer (62.5% vs. 11.1%; P?=?0.014). Sporadic cases were more frequently associated with gastro-esophageal reflux (35.7% vs. 0%; P?=?0.079) and anti-reflux medication use (55.6% vs. 11.1%; P?=?0.026). Histologically, the syndromic SBPs were more often of pure intestinal type (45.4% vs. 3.8%; P?=?0.005) and had prominent vessels (81.8% vs. 42.3%; P?=?0.036). Conclusions: Patients with syndromic SBPs are younger and have higher rates of hemorrhagic telangiectasia, gastric polyps, and family history of colon cancer. Histologically, syndromic inflammatory/hyperplastic SBPs are more likely to be of pure intestinal type and to have prominent vessels. PMID:26049720

  20. Acute Cryptococcal Immune Reconstitution Inflammatory Syndrome in a Patient on Natalizumab

    PubMed Central

    Gundacker, Nathan D.; Jordan, Stephen J.; Jones, Benjamin A.; Drwiega, Joseph C.; Pappas, Peter G.

    2016-01-01

    Presented is the first case of acute immune reconstitution inflammatory syndrome (IRIS)-associated cryptococcal meningoencephalitis in a patient on natalizumab for multiple sclerosis. The patient developed acute cerebral edema after initiation of amphotericin B. We propose several mechanisms that explain the acuity of IRIS in this specific patient population and suggest possible therapies. PMID:27006962

  1. Staphylococcus pseudintermedius infection associated with nodular skin lesions and systemic inflammatory response syndrome in a dog.

    PubMed

    Min, Sa-Hee; Kang, Min-Hee; Sur, Jung-Hyang; Park, Hee-Myung

    2014-05-01

    A 10-year-old Pekingese dog with atopic dermatitis was referred due to pyrexia, multiple skin nodules, anorexia, and depression. The dog was diagnosed as having systemic inflammatory response syndrome (SIRS) induced by bacterial dermatitis. This case presents diagnosis and treatment of SIRS with staphylococcal skin infection in a dog that was immunosuppressed due to long-term use of corticosteroid. PMID:24790236

  2. Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome.

    PubMed

    Bhatia, Madhav; Moochhala, Shabbir

    2004-02-01

    Inflammatory response leading to organ dysfunction and failure continues to be the major problem after injury in many clinical conditions such as sepsis, severe burns, acute pancreatitis, haemorrhagic shock, and trauma. In general terms, systemic inflammatory response syndrome (SIRS) is an entirely normal response to injury. Systemic leukocyte activation, however, is a direct consequence of a SIRS and if excessive, can lead to distant organ damage and multiple organ dysfunction syndrome (MODS). When SIRS leads to MODS and organ failure, the mortality becomes high and can be more than 50%. Acute lung injury that clinically manifests as acute respiratory distress syndrome (ARDS) is a major component of MODS of various aetiologies. Inflammatory mediators play a key role in the pathogenesis of ARDS, which is the primary cause of death in these conditions. This review summarizes recent studies that demonstrate the critical role played by inflammatory mediators such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, platelet activating factor (PAF), IL-10, granulocyte macrophage-colony stimulating factor (GM-CSF), C5a, intercellular adhesion molecule (ICAM)-1, substance P, chemokines, VEGF, IGF-I, KGF, reactive oxygen species (ROS), and reactive nitrogen species (RNS) in the pathogenesis of ARDS. It is reasonable to speculate that elucidation of the key mediators in ARDS coupled with the discovery of specific inhibitors would make it possible to develop clinically effective anti-inflammatory therapy. PMID:14743496

  3. A review of the neuro- and systemic inflammatory responses in post concussion symptoms: Introduction of the "post-inflammatory brain syndrome" PIBS.

    PubMed

    Rathbone, Alasdair Timothy Llewelyn; Tharmaradinam, Surejini; Jiang, Shucui; Rathbone, Michel P; Kumbhare, Dinesh A

    2015-05-01

    Post-concussion syndrome is an aggregate of symptoms that commonly present together after head injury. These symptoms, depending on definition, include headaches, dizziness, neuropsychiatric symptoms, and cognitive impairment. However, these symptoms are common, occurring frequently in non-head injured controls, leading some to question the existence of post-concussion syndrome as a unique syndrome. Therefore, some have attempted to explain post-concussion symptoms as post-traumatic stress disorder, as they share many similar symptoms and post-traumatic stress disorder does not require head injury. This explanation falls short as patients with post-concussion syndrome do not necessarily experience many key symptoms of post-traumatic stress disorder. Therefore, other explanations must be sought to explain the prevalence of post-concussion like symptoms in non-head injury patients. Many of the situations in which post-concussion syndrome like symptoms may be experienced such as infection and post-surgery are associated with systemic inflammatory responses, and even neuroinflammation. Post-concussion syndrome itself has a significant neuroinflammatory component. In this review we examine the evidence of neuroinflammation in post-concussion syndrome and the potential role systemic inflammation plays in post-concussion syndrome like symptoms. We conclude that given the overlap between these conditions and the role of inflammation in their etiologies, a new term, post-inflammatory brain syndromes (PIBS), is necessary to describe the common outcomes of many different inflammatory insults. The concept of post-concussion syndrome is in its evolution therefore, the new term post-inflammatory brain syndromes provides a better understanding of etiology of its wide-array of symptoms and the wide array of conditions they can be seen in. PMID:25736063

  4. POEMS Syndrome in a Juvenile Initially Diagnosed as Treatment Resistant Chronic Inflammatory Demyelinating Polyneuropathy.

    PubMed

    Krish, Sonia N; Nguyen, Thy; Biliciler, Suur; Kumaravel, Manickam; Wahed, Amer; Risin, Semyon; Sheikh, Kazim A

    2015-12-01

    POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, skin changes) is a disorder that mainly affects adults. We report a pediatric patient, initially considered to have Guillain-Barr syndrome, who continued to have progression of neuropathic disease leading to the diagnosis of chronic inflammatory demyelinating polyneuropathy. Diagnosis of POEMS was established by an abnormal bone marrow biopsy, prompted by laboratory and imaging findings, which became abnormal later in the course of the disease. POEMS syndrome is extremely rare in children, and neuropathic features in this age group have not been previously described. This case illustrates that "Guillain-Barr syndrome-like" initial presentation for POEMS, which has not been previously reported. It also emphasizes that in children with progressive acquired neuropathies that are treatment unresponsive, POEMS syndrome should be considered. PMID:26583497

  5. Inflammatory activation: cardiac, renal, and cardio-renal interactions in patients with the cardiorenal syndrome.

    PubMed

    Colombo, Paolo C; Ganda, Anjali; Lin, Jeffrey; Onat, Duygu; Harxhi, Ante; Iyasere, Julia E; Uriel, Nir; Cotter, Gad

    2012-03-01

    Although inflammation is a physiologic response designed to protect us from infection, when unchecked and ongoing it may cause substantial harm. Both chronic heart failure (CHF) and chronic kidney disease (CKD) are known to cause elaboration of several pro-inflammatory mediators that can be detected at high concentrations in the tissues and blood stream. The biologic sources driving this chronic inflammatory state in CHF and CKD are not fully established. Traditional sources of inflammation include the heart and the kidneys which produce a wide range of pro-inflammatory cytokines in response to neurohormones and sympathetic activation. However, growing evidence suggests that non-traditional biomechanical mechanisms such as venous and tissue congestion due to volume overload are also important as they stimulate endotoxin absorption from the bowel and peripheral synthesis and release of pro-inflammatory mediators. Both during the chronic phase and, more rapidly, during acute exacerbations of CHF and CKD, inflammation and congestion appear to amplify each other resulting in a downward spiral of worsening cardiac, vascular, and renal functions that may negatively impact patients' outcome. Anti-inflammatory treatment strategies aimed at attenuating end organ damage and improving clinical prognosis in the cardiorenal syndrome have been disappointing to date. A new therapeutic paradigm may be needed, which involves different anti-inflammatory strategies for individual etiologies and stages of CHF and CKD. It may also include specific (short-term) anti-inflammatory treatments that counteract inflammation during the unsettled phases of clinical decompensation. Finally, it will require greater focus on volume overload as an increasingly significant source of systemic inflammation in the cardiorenal syndrome. PMID:21688186

  6. Expression of pro-inflammatory TACE-TNF-?-amphiregulin axis in Sjgren's syndrome salivary glands.

    PubMed

    Sisto, Margherita; Lisi, Sabrina; Lofrumento, Dario Domenico; Ingravallo, Giuseppe; Mitolo, Vincenzo; D'Amore, Massimo

    2010-10-01

    The tumor-necrosis-factor-converting-enzyme (TACE)-TNF-?-Amphiregulin (AREG) axis plays an important pathogenic role in inflammatory and autoimmune disorders. However, the pathological roles of these proteins in the chronic autoimmune disease Sjgren's syndrome (SS) remain to be elucidated. It is known that the TACE-AREG axis is clearly part of a larger cascade of signals that starts with the activation of Furin, responsible for maturation of TACE that, in turn, determines the production of active TNF-?, directly involved in the up-regulation of AREG expression. This study showed that Furin, TACE, TNF-?, and AREG proteins, detected in acinar and ductal cells of human salivary glands from SS patients, increased remarkably in comparison with biopsies of labial salivary glands from healthy controls. The changes in Furin, TACE, TNF- ?, and AREG proteins' level detected in salivary glands biopsies of SS patients could be responsible for pro-inflammatory cytokines overexpression characterizing Sjgren's syndrome. PMID:20811902

  7. Anti-inflammatory properties of culinary herbs and spices that ameliorate the effects of metabolic syndrome.

    PubMed

    Jungbauer, Alois; Medjakovic, Svjetlana

    2012-03-01

    Obesity and metabolic syndrome are increasing global health problems. In addition to the malnutrition of a sedentary lifestyle, high calorie intake leads to obesity with many negative health consequences. Macrophages infiltrate adipose tissue and induce chronic inflammation by secreting pro-inflammatory cytokines, including COX-2 and iNOS, among other mediators of inflammation. Free fatty acids mediate adipose tissue signalling through toll-like receptor 4 and the expression of these pro-inflammatory mediators via NF-?B or JNK. PPAR ? activators can inhibit the activation of NF-?B, down-regulating the expression of pro-inflammatory cytokines. Here we provide an overview of how different culinary herbs and spices exert anti-inflammatory activities and the extent to which they activate PPAR ? and PPAR ?, inhibit the activation of NF-?B, and enhance expression of anti-inflammatory cytokines. Spices can play essential roles as anti-inflammatory agents in our diet, acting as pan PPAR activators and improving insulin sensitivity, counteracting dyslipidaemia and weight gain. The effects of chronic inflammation caused by obesity are counteracted and, consequently, the progression of diseases associated with chronic inflammation slowed. PMID:22226987

  8. Immune Reconstitution Inflammatory Syndrome Secondary to Mycobacterium kansasii Infection in a Kidney Transplant Recipient.

    PubMed

    Lemoine, M; Laurent, C; Hanoy, M; Leporrier, J; Franois, A; Guerrot, D; Godin, M; Bertrand, D

    2015-12-01

    Nontuberculous mycobacteria (NTM) infection is a challenging diagnosis for clinicians in solid organ transplantation. Immune reconstitution inflammatory syndrome (IRIS) is so far unreported in this context. We report here the case of a renal transplant recipient who developed Mycobacterium kansasii-associated lymphadenitis complicated by IRIS while undergoing reduction of his immunosuppressive therapy. For IRIS, the patient required low-dose steroids and an increase in global immunosuppression, in association with NTM antibiotherapy. PMID:26372924

  9. Point prevalence of general ward patients fulfilling criteria for systemic inflammatory response syndrome.

    PubMed

    Douglas, L; Casamento, A; Jones, D

    2016-02-01

    The systemic inflammatory response syndrome (SIRS) is defined by abnormal temperature, heart rate, minute ventilation or white cell count and can be due to infectious or non-infectious causes. In a single day, 23% of hospital ward patients fulfilled SIRS criteria. Patients with SIRS were more likely to be under medical than surgical units. One-third of the patients had evidence of infection. There was no association between SIRS criteria and increased mortality or hospital length of stay. PMID:26899889

  10. Quantitative Risk-Benefit Analysis of Probiotic Use for Irritable Bowel Syndrome and Inflammatory Bowel Disease.

    PubMed

    Bennett, William E

    2016-04-01

    Probiotics have seen widespread use for a variety of gastrointestinal problems, especially in two common disorders: irritable bowel syndrome and inflammatory bowel disease. Since a wide variety of probiotic preparations has been used, and despite a large number of studies performed, a great deal of heterogeneity exists among them. Straightforward evidence-based recommendations for the use of probiotics in irritable bowel syndrome and inflammatory bowel disease have thus been difficult to formulate. In an effort to improve understanding of the risk-benefit balance of probiotics in these conditions, this study (1) queried the US FDA Adverse Event Reporting System (FAERS) database for all reported adverse drug events related to probiotics in 2013, and (2) constructed risk-benefit planes for both irritable bowel syndrome and inflammatory bowel disease using a geometric approximation of the confidence region between risk and benefit. The results show that adverse events from probiotics vary widely by disease, and when they occur, they are mild and may be difficult to distinguish from the natural history of the underlying disorders they are used to treat. The risk-benefit plane for irritable bowel syndrome straddles the risk-benefit threshold, so patients can expect a balance between a low chance of risk and also a low chance of benefit. The risk-benefit plane for inflammatory bowel disease largely lies above the risk-benefit threshold, so patients may expect more benefit than risk in most cases. More standardized and high-quality research is needed to improve our understanding of risk and benefit for these complex biopharmaceuticals. PMID:26467550

  11. Inflammatory Markers of the Systemic Capillary Leak Syndrome (Clarkson Disease)

    PubMed Central

    Xie, Zhihui; Chan, Eunice; Yin, Yuzhi; Ghosh, Chandra C.; Wisch, Laura; Nelson, Celeste; Young, Michael; Parikh, Samir M.; Druey, Kirk M.

    2014-01-01

    Objectives The Systemic Capillary Leak Syndrome (SCLS) is a rare and potentially fatal disorder resembling systemic anaphylaxis that is characterized by transient episodes of hypotensive shock and peripheral edema. The pathogenesis of SCLS is unknown, and triggers for attacks are apparent only in a minority of patients. We introduce a clinical algorithm for the diagnosis of SCLS, and we investigated potential serum biomarkers of acute SCLS episodes. Methods We analyzed serum cytokines in a cohort of 35 patients with an established diagnosis of SCLS and characterized the effects of SCLS sera on endothelial cell function. We investigated the cellular source(s) of CXCL10, a chemokine that was significantly elevated in both basal and acute SCLS sera, by flow cytometry. Results Several cytokines were elevated in acute SCLS sera compared to baseline or sera from healthy controls, including CXCL10, CCL2, IL-1?, IL-6, IL-8, IL-12 and TNF?. The majority of acute sera failed to activate endothelial cells as assessed by surface adhesion marker expression. Monocytes appear to be the major source of serum CXCL10, and the percentage of CXLC10+ monocytes in response to IFN? stimulation was increased in SCLS subjects compared to controls. Conclusions The presence of proinflammatory cytokines in acute SCLS sera suggests that inflammation or infection may have a role in triggering episodes. The enhanced capacity of monocytes from SCLS patients to produce CXCL10 suggests a new therapeutic avenue for SCLS. PMID:25405070

  12. Pathology in euthermic bats with white nose syndrome suggests a natural manifestation of immune reconstitution inflammatory syndrome.

    PubMed

    Meteyer, Carol U; Barber, Daniel; Mandl, Judith N

    2012-11-15

    White nose syndrome, caused by Geomyces destructans, has killed more than 5 million cave hibernating bats in eastern North America. During hibernation, the lack of inflammatory cell recruitment at the site of fungal infection and erosion is consistent with a temperature-induced inhibition of immune cell trafficking. This immune suppression allows G. destructans to colonize and erode the skin of wings, ears and muzzle of bat hosts unchecked. Yet, paradoxically, within weeks of emergence from hibernation an intense neutrophilic inflammatory response to G. destructans is generated, causing severe pathology that can contribute to death. We hypothesize that the sudden reversal of immune suppression in bats upon the return to euthermia leads to a form of immune reconstitution inflammatory syndrome (IRIS). IRIS was first described in HIV-infected humans with low helper T lymphocyte counts and bacterial or fungal opportunistic infections. IRIS is a paradoxical and rapid worsening of symptoms in immune compromised humans upon restoration of immunity in the face of an ongoing infectious process. In humans with HIV, the restoration of adaptive immunity following suppression of HIV replication with anti-retroviral therapy (ART) can trigger severe immune-mediated tissue damage that can result in death. We propose that the sudden restoration of immune responses in bats infected with G. destructans results in an IRIS-like dysregulated immune response that causes the post-emergent pathology. PMID:23154286

  13. Pathology in euthermic bats with white nose syndrome suggests a natural manifestation of immune reconstitution inflammatory syndrome

    USGS Publications Warehouse

    Meteyer, Carol U.; Barber, Daniel; Mandl, Judith N.

    2012-01-01

    White nose syndrome, caused by Geomyces destructans, has killed more than 5 million cave hibernating bats in eastern North America. During hibernation, the lack of inflammatory cell recruitment at the site of fungal infection and erosion is consistent with a temperature-induced inhibition of immune cell trafficking. This immune suppression allows G. destructans to colonize and erode the skin of wings, ears and muzzle of bat hosts unchecked. Yet, paradoxically, within weeks of emergence from hibernation an intense neutrophilic inflammatory response to G. destructans is generated, causing severe pathology that can contribute to death. We hypothesize that the sudden reversal of immune suppression in bats upon the return to euthermia leads to a form of immune reconstitution inflammatory syndrome (IRIS), which was first described in HIV-infected humans with low helper T lymphocyte counts and bacterial or fungal opportunistic infections. IRIS is a paradoxical and rapid worsening of symptoms in immune compromised humans upon restoration of immunity in the face of an ongoing infectious process. In humans with HIV, the restoration of adaptive immunity following suppression of HIV replication with anti-retroviral therapy (ART) can trigger severe immune-mediated tissue damage that can result in death. We propose that the sudden restoration of immune responses in bats infected with G. destructans results in an IRIS-like dysregulated immune response that causes the post-emergent pathology.

  14. Pathology in euthermic bats with white nose syndrome suggests a natural manifestation of immune reconstitution inflammatory syndrome

    PubMed Central

    Meteyer, Carol U.; Barber, Daniel; Mandl, Judith N.

    2012-01-01

    White nose syndrome, caused by Geomyces destructans, has killed more than 5 million cave hibernating bats in eastern North America. During hibernation, the lack of inflammatory cell recruitment at the site of fungal infection and erosion is consistent with a temperature-induced inhibition of immune cell trafficking. This immune suppression allows G. destructans to colonize and erode the skin of wings, ears and muzzle of bat hosts unchecked. Yet, paradoxically, within weeks of emergence from hibernation an intense neutrophilic inflammatory response to G. destructans is generated, causing severe pathology that can contribute to death. We hypothesize that the sudden reversal of immune suppression in bats upon the return to euthermia leads to a form of immune reconstitution inflammatory syndrome (IRIS). IRIS was first described in HIV-infected humans with low helper T lymphocyte counts and bacterial or fungal opportunistic infections. IRIS is a paradoxical and rapid worsening of symptoms in immune compromised humans upon restoration of immunity in the face of an ongoing infectious process. In humans with HIV, the restoration of adaptive immunity following suppression of HIV replication with anti-retroviral therapy (ART) can trigger severe immune-mediated tissue damage that can result in death. We propose that the sudden restoration of immune responses in bats infected with G. destructans results in an IRIS-like dysregulated immune response that causes the post-emergent pathology. PMID:23154286

  15. Multiphasic and multifocal cryptococcal immune reconstitution inflammatory syndrome in an HIV-infected patient: interplay of infection and immunity.

    PubMed

    Katchanov, Juri; Zimmermann, Ulrike; Branding, Gordian; Tintelnot, Kathrin; Mller, Markus; Arasth, Keikawus; Stocker, Hartmut

    2014-01-01

    We report a case of cryptococcal immune reconstitution inflammatory syndrome affecting the lungs, and 10 months later the cervical lymph nodes, in the absence of cryptococcal meningitis, in advanced HIV infection. Our report demonstrates the organ-specificity of the timing of the inflammatory response and illustrates the organ-specific interplay of immunity and infection in cryptococcal disease. PMID:24161208

  16. Neovascularization is prominent in the chronic inflammatory lesions of Sjgren's syndrome

    PubMed Central

    Sisto, Margherita; Lisi, Sabrina; Ingravallo, Giuseppe; Lofrumento, Dario Domenico; D'Amore, Massimo; Ribatti, Domenico

    2014-01-01

    Angiogenesis is a common finding in chronic inflammatory diseases; however, its role in Sjgren's syndrome (SS) remains to be elucidated. Previous SS studies have demonstrated an increase in VEGF-A/VEGFR-2 system expression in minor salivary gland (MSG) biopsies from patients with SS, but differences in the new blood vessel formation between the different grades of disease severity have not been reported. Therefore, experiments were performed to demonstrate angiogenesis during different phases of primary SS (pSS) and to define the relationship between the microvessel density (MVD), macrophage infiltration and histiocyte distribution in SS MSG inflammatory lesions. In this series of experiments, immunohistochemistry was used to examine angiogenesis in serial sections of pSS MSG. Patients with pSS were classified accordingly with the grade of inflammatory lesions as I?=?low-grade (low focus score of 1 or 2), II?=?intermediate-grade (focus score of 36) and III?=?extensive inflammation in the MSG (high focus score of 12). Histological examination demonstrated that the MVD increased with the severity of the inflammatory lesions, and in addition, we found an increased infiltration of inflammatory and pro-angiogenic cells.These findings reveal that angiogenesis is intimately involved in the progression of pSS, may be central to the propagation of the chronic immune response observed in pSS and could represent a novel potential biomarker of pSS disease activity. PMID:24772480

  17. Human adjuvant-related syndrome or autoimmune/inflammatory syndrome induced by adjuvants. Where have we come from? Where are we going? A proposal for new diagnostic criteria.

    PubMed

    Alijotas-Reig, J

    2015-09-01

    In 1964, Miyoshi reported a series of patients with diverse symptoms after receiving treatment with silicone or paraffin fillers. Miyoshi named this condition 'human adjuvant disease'. Since then, the literature has been flooded with case reports and case series of granulomatous and systemic autoimmune disorders related to vaccines, infection or other adjuvants such as silicone and other biomaterials. A new term -autoimmune/inflammatory syndrome induced by adjuvants--has recently been coined for a process that includes several clinical features previously described by Miyoshi plus other clinical and laboratory parameters related to exposure to diverse external stimuli. Disorders such as siliconosis, Gulf War syndrome, macrophagic myofasciitis syndrome, sick building syndrome and post-vaccination syndrome have been included in autoimmune/inflammatory syndrome induced by adjuvants. Disorders such as Spanish toxic oil syndrome and Ardystil syndrome could also be included. Furthermore, biomaterials other than silicone should also be considered as triggering factors for these adjuvant-related syndromes. New diagnostic criteria in this field have been proposed. Nevertheless, many of these criteria are too subjective, leading to some patients being diagnosed with chronic fatigue syndrome or other 'central sensitization syndromes'. Diagnostic criteria based only on objective clinical and laboratory data to be further discussed and validated are proposed herein. PMID:25813870

  18. Inflammatory cause of metabolic syndrome via brain stress and NF-κB

    PubMed Central

    Cai, Dongsheng; Liu, Tiewen

    2012-01-01

    Metabolic syndrome, a network of medical disorders that greatly increase the risk for developing metabolic and cardiovascular diseases, has reached epidemic levels in many areas of today's world. Despite this alarming medicare situation, scientific understandings on the root mechanisms of metabolic syndrome are still limited, and such insufficient knowledge contributes to the relative lack of effective treatments or preventions for related diseases. Recent interdisciplinary studies from neuroendocrinology and neuroimmunology fields have revealed that overnutrition can trigger intracellular stresses to cause inflammatory changes mediated by molecules that control innate immunity. This type of nutrition-related molecular inflammation in the central nervous system, particularly in the hypothalamus, can form a common pathogenic basis for the induction of various metabolic syndrome components such as obesity, insulin resistance, and hypertension. Proinflammatory NF-κB pathway has been revealed as a key molecular system for pathologic induction of brain inflammation, which translates overnutrition and resulting intracellular stresses into central neuroendocrine and neural dysregulations of energy, glucose, and cardiovascular homeostasis, collectively leading to metabolic syndrome. This article reviews recent research advances in the neural mechanisms of metabolic syndrome and related diseases from the perspective of pathogenic induction by intracellular stresses and NF-κB pathway of the brain. PMID:22328600

  19. Role of PPARs in inflammatory processes associated with metabolic syndrome (Review).

    PubMed

    Fuentes, Eduardo; Guzmán-Jofre, Luis; Moore-Carrasco, Rodrigo; Palomo, Iván

    2013-12-01

    Metabolic syndrome (MS) includes the presence of arterial hypertension, insulin resistance, dyslipidemia, cardiovascular disease (CVD) and abdominal obesity, which is associated with a chronic inflammatory response, characterized by abnormal adipokine production, and the activation of certain pro-inflammatory signaling pathways. Furthermore, the changes presented by the adipose tissue in MS favors the secretion of several molecular mediators capable of activating or suppressing a number of transcription factors, such as the peroxisome proliferator-activated receptors (PPARs), whose main functions include storage regulation and fatty acid catabolization. When they are activated by their ligands (synthetic or endogenous), they control several genes involved in intermediate metabolism, which make them, together with the PPAR gamma coactivator-1-α (PGC-1) and the silent information regulator T1 (SIRT1), good targets for treating metabolic diseases and their cardiovascular complications. PMID:24100795

  20. Porcine reproductive and respiratory syndrome virus infection triggers HMGB1 release to promote inflammatory cytokine production

    SciTech Connect

    Duan, Erzhen; Wang, Dang; Luo, Rui; Luo, Jingyi; Gao, Li; Chen, Huanchun; Fang, Liurong Xiao, Shaobo

    2014-11-15

    The high mobility group box 1 (HMGB1) protein is an endogenous damage-associated molecular pattern (DAMP) molecule involved in the pathogenesis of various infectious agents. Based on meta-analysis of all publicly available microarray datasets, HMGB1 has recently been proposed as the most significant immune modulator during the porcine response to porcine reproductive and respiratory syndrome virus (PRRSV) infection. However, the function of HMGB1 in PRRSV pathogenesis is unclear. In this study, we found that PRRSV infection triggers the translocation of HMGB1 from the nucleus to the extracellular milieu in MARC-145 cells and porcine alveolar macrophages. Although HMGB1 has no effect on PRRSV replication, HMGB1 promotes PRRSV-induced NF-κB activation and subsequent expression of inflammatory cytokines through receptors RAGE, TLR2 and TLR4. Our findings show that HMGB1 release, triggered by PRRSV infection, enhances the efficiency of virus-induced inflammatory responses, thereby providing new insights into the pathogenesis of PRRSV infection. - Highlights: • PRRSV infection triggers HMGB1 release from MARC-145 cells and PAMs. • HMGB1 does not significantly affect PRRSV proliferation. • HMGB1 is involved in PRRSV-induced NF-κB activation and inflammatory responses. • HMGB1 promotes PRRSV-induced inflammatory responses through TLR2/4 and RAGE.

  1. Bullous disorders as a manifestation of immune reconstitution inflammatory syndrome: A series of three cases

    PubMed Central

    Das, Rama; Sarkar, Somenath; Besra, Mrinal

    2013-01-01

    Bullous disorders such as pemphigus vulgaris, bullous pemphigoid after the initiation of highly active antiretroviral therapy in certain human immunodeficiency virus reactive individuals have been described in this case series as a manifestation of an immune reconstitution inflammatory syndrome. This phenomenon should be suspected in individuals who present with bullous lesions within 3-8 weeks after initiation of therapy despite of improved immunological response. Strong clinical suspicion, through clinical examination, appropriate laboratory investigation such as CD4 T-cell count, histopathological examinations with H and E stain, direct immunofluorescence test are required for diagnosis. PMID:24339465

  2. [Metabolic and inflammatory profiles in polycystic ovary syndrome associated to weight excess].

    PubMed

    Chaabouni, Khansa; Lahyani, Amina; Turki, Mouna; Messedi, Mariem; Louati, Doulira; Jamoussi, Kamel; Ayedi, Fatma

    2014-01-01

    Polycystic ovary syndrome (PCOS) and weight excess exhibited metabolic abnormalities and elevated cardiovascular risk. Our objective was to assess metabolic and inflammatory profiles in women with PCOS associated to weight excess; 85 women were enrolled. Four groups were then identified with and without PCOS and/or weight excess. Hyperlipidemia was significantly more observed in the two groups with weight excess. In whom insulinresistance and high sensitive C reactive protein were also elevated. Abnormalities observed when PCOS and weight excess are associated would mimic these observed in isolated weight excess with some particularities. PMID:25119811

  3. [Clinical assessment of immune parameters at surgical patients with syndrome of systemic inflammatory reaction].

    PubMed

    Abakumov, M M; Bulava, G V; Borovkova, N V; Khvatov, V B

    2007-01-01

    Results of immunological examination of 423 patients with syndrome of systemic inflammatory reaction of different ethiology (mediastinitis--78 patients, peritonitis--85, severe acute pancreatitis--91, trauma of thorax and abdomen complicated with massive hemorrhage--111, severe burn trauma--40 patients) are analyzed. For complex and objective assessment of immune reaction the system of scores has been developed. This scale permitted to detect the immune disorders, to diagnose the degree of immune insufficiency at early stages of disease, to predict the purulent complications and to start timely immune therapy. PMID:17828122

  4. SYSTEM-WIDE MAPPING OF ACTIVATED CIRCUITRY IN EXPERIMENTAL SYSTEMIC INFLAMMATORY RESPONSE SYNDROME.

    PubMed

    Gharib, Sina A; Mar, Daniel; Bomsztyk, Karol; Denisenko, Oleg; Dhanireddy, Shireesha; Liles, W Conrad; Altemeier, William A

    2016-02-01

    Sepsis-induced multiple organ dysfunction syndrome (MODS) is a major cause of morbidity and mortality in critically ill patients and remains impervious to most therapeutic interventions. We utilized a clinically relevant murine model of systemic inflammatory response syndrome (SIRS) during early MODS induced by ventilator-associated pneumonia to systematically delineate pathways dysregulated in lung, liver, and kidney. We focused on processes commonly activated across at-risk organs and constructed an SIRS-associated network based on connectivity among the gene members of these functionally coherent pathways. Our analyses led to the identification of several putative drivers of early MODS whose expression was regulated by epidermal growth factor receptor. Our unbiased, integrative method is a promising approach to unravel mechanisms in system-wide disorders afflicting multiple compartments such as sepsis-induced MODS, and identify putative therapeutic targets. PMID:26536201

  5. Elevated white cell count in acute coronary syndromes: relationship to variants in inflammatory and thrombotic genes

    PubMed Central

    Byrne, Connie E; Fitzgerald, Anthony; Cannon, Christopher P; Fitzgerald, Desmond J; Shields, Denis C

    2004-01-01

    Background Elevated white blood cell counts (WBC) in acute coronary syndromes (ACS) increase the risk of recurrent events, but it is not known if this is exacerbated by pro-inflammatory factors. We sought to identify whether pro-inflammatory genetic variants contributed to alterations in WBC and C-reactive protein (CRP) in an ACS population. Methods WBC and genotype of interleukin 6 (IL-6 G-174C) and of interleukin-1 receptor antagonist (IL1RN intronic repeat polymorphism) were investigated in 732 Caucasian patients with ACS in the OPUS-TIMI-16 trial. Samples for measurement of WBC and inflammatory factors were taken at baseline, i.e. Within 72 hours of an acute myocardial infarction or an unstable angina event. Results An increased white blood cell count (WBC) was associated with an increased C-reactive protein (r = 0.23, p < 0.001) and there was also a positive correlation between levels of ?-fibrinogen and C-reactive protein (r = 0.42, p < 0.0001). IL1RN and IL6 genotypes had no significant impact upon WBC. The difference in median WBC between the two homozygote IL6 genotypes was 0.21/mm3 (95% CI = -0.41, 0.77), and -0.03/mm3 (95% CI = -0.55, 0.86) for IL1RN. Moreover, the composite endpoint was not significantly affected by an interaction between WBC and the IL1 (p = 0.61) or IL6 (p = 0.48) genotype. Conclusions Cytokine pro-inflammatory genetic variants do not influence the increased inflammatory profile of ACS patients. PMID:15171792

  6. Therapeutic Role of Innovative Anti-Inflammatory Medications in the Prevention of Acute Coronary Syndrome.

    PubMed

    Pashun, Raymond Anthony; Frishman, William H

    2015-01-01

    An improved understanding of the pathogenesis of acute coronary syndromes and its relationship to atherosclerotic plaque rupture and thrombosis has contributed to the investigation of novel therapies for prevention and treatment. New data ascribe an increasingly important role of active inflammation in contributing to thinning of the atherosclerotic fibrous cap and plaque instability. Despite this understanding, there are currently no therapeutic approaches to specifically target the unstable plaque. Multiple randomized trials investigating treatment strategies have recently been completed or are currently being conducted, using anti-inflammatory medications, such as methotrexate, colchicine, darapladib, varespladib, losmapimod, and canakinumab, to reduce the incidence of cardiovascular events including acute coronary syndromes. These anti-inflammatory medications differ in their mechanism of action from having widespread targets (as is the case for methotrexate and colchicine) to having specific targets (as is the case for darapladib, varespladib, losmapimod, and canakinumab). The trials investigating the efficacy of darapladib in reducing cardiovascular events revealed no significant benefit when compared with the current standard of care. The varespladib studies were terminated early because of adverse outcomes. However, the outcomes of the remaining drug studies may still contribute to novel therapeutic approaches in the treatment of patients with unstable coronary artery disease. PMID:25741604

  7. Anti-Inflammatory Dietary Combo in Overweight and Obese Women with Polycystic Ovary Syndrome

    PubMed Central

    Salama, Amany Alsayed; Amine, Ezzat Khamis; Salem, Hesham Abd Elfattah; Abd El Fattah, Nesrin Kamal

    2015-01-01

    Background: Polycystic ovary syndrome (PCOS) is of clinical and public health importance, affecting up to one in five women of reproductive age. It has significant and diverse clinical implications including reproductive, metabolic, and psychological features. Aim: The study was to investigate the effect of anti-inflammatory dietary combo on metabolic, endocrine, inflammatory, and reproductive profiles in overweight and obese women with PCOS. Materials and Methods: A total of 100 nonpregnant, overweight, and obese adult females with PCOS according to the Rotterdam criteria, were screened during the year 2012, and 75 completed the trial. At baseline and study end, fasting blood samples were drawn to measure biological markers, body fat percent (BFP), and visceral fat area (VFA) were assessed by the InBody720 device and anthropometric measurements were done for all participants who were subjected to an anti-inflammatory hypocaloric diet and physical activity for 12 weeks. Results: At study completion, we achieved moderate weight loss of (± 7%) and significant improvements in body composition, hormones and menstrual cyclicity, blood pressure, glucose homeostasis, dyslipidemia, C-reactive protein (CRP), and serum amyloid A (SAA) (surrogate measures of cardiovascular risk (CVR)). This was a clinically relevant weight loss that is associated with a reduced prevalence of type 2 diabetes mellitus (DM2) and metabolic syndrome (MS) in the general population and improved fertility outcomes in PCOS. We achieved 63% regain of menstrual cyclicity and 12% spontaneous pregnancy rate within 12 week. Conclusions: We have explored an additional dietary treatment option with good prognostic metabolic and reproductive responses to weight loss that occur in overweight and obese PCOS. PMID:26258078

  8. Elevated Circulating Levels of Inflammatory Markers in Patients with Acute Coronary Syndrome

    PubMed Central

    Al Shahi, Hamad; Shimada, Kazunori; Miyauchi, Katsumi; Yoshihara, Takuma; Sai, Eiryu; Shiozawa, Tomoyuki; Naito, Ryo; Aikawa, Tatsuro; Ouchi, Shohei; Kadoguchi, Tomoyasu; Miyazaki, Tetsuro; Daida, Hiroyuki

    2015-01-01

    Objective. We evaluated inflammatory cytokines and chemokine in peripheral blood mononuclear cells (PBMCs) in patients with either acute coronary syndrome (ACS) or stable coronary artery disease (CAD). Methods. We enrolled 20 ACS patients and 50 stable CAD patients without previous history of ACS who underwent cardiac catheterization. Patients with an estimated glomerular filtration rate of ?30?mL/min/1.73?m2 and C-reactive protein of ?1.0?mg/dL were excluded. Blood samples were collected from the patients just before catheterization, and PBMCs were isolated from the whole blood. The levels of inflammatory cytokines and chemokine were measured by using real-time quantitative polymerase chain reaction and immunoassays. Results. The expression of tumor necrosis factor alpha (TNF-?), interleukin- (IL-) 6, IL-10, IL-23A, IL-27, and IL-37 was significantly higher in the ACS group than in the CAD group (P < 0.05). In contrast, the expression of IL-33 was significantly lower in the ACS group than in the CAD group (P < 0.05). The ACS patients had higher plasma levels of TNF-?, IL-6, and IL-10 in the ACS group than in the CAD group. Conclusion. Circulating levels of pro-/anti-inflammatory cytokines, including IL-23A, IL-27, IL-33, and IL-37, may be associated with the pathogenesis of atherosclerosis in ACS patients. PMID:26504600

  9. Inflammatory and Antioxidant Pattern Unbalance in Clopidogrel-Resistant Patients during Acute Coronary Syndrome

    PubMed Central

    Gori, Anna Maria; Cecchettini, Antonella; Parodi, Guido; Marcucci, Rossella; Parolini, Marina; Romagnuolo, Ilaria; Citti, Lorenzo; Abbate, Rosanna

    2015-01-01

    Background. In acute coronary syndrome (ACS), inflammation and redox response are associated with increased residual platelet reactivity (RPR) on clopidogrel therapy. We investigated whether clopidogrel interaction affects platelet function and modulates factors related to inflammation and oxidation in ACS patients differently responding to clopidogrel. Material and Methods. Platelet aggregation was measured in 29 ACS patients on dual (aspirin/clopidogrel) antiplatelet therapy. Nonresponders (NR) were defined as RPR ?70% by ADP. Several inflammatory and redox parameters were assayed and platelet proteome was determined. Results. Eight (28%) out of 29 ACS patients resulted NR to clopidogrel. At 24 hours, the levels of Th2-type cytokines IL-4, IFN?, and MCP-1 were higher in NR, while blood GSH (r-GSHbl) levels were lower in NR than responders (R). Proteomic analysis evidenced an upregulated level of platelet adhesion molecule, CD226, and a downregulation of the antioxidant peroxiredoxin-4. In R patients the proinflammatory cytokine IL-6 decreased, while the anti-inflammatory cytokine IL-1Ra increased. Conclusions. In patients with high RPR on clopidogrel therapy, an unbalance of inflammatory factors, platelet adhesion molecules, and circulatory and platelet antioxidant molecules was observed during the acute phase. Proinflammatory milieu persists in nonresponders for a long time after the acute event while antioxidant blood factors tend to conform to normal responsiveness. PMID:25873769

  10. Acute cytomegalovirus colitis presenting during primary HIV infection: an unusual case of an immune reconstitution inflammatory syndrome.

    PubMed

    von Both, Ulrich; Laffer, Reto; Grube, Christina; Bossart, Walter; Gaspert, Ariana; Gnthard, Huldrych F

    2008-02-15

    Severe ulcerous cytomegalovirus pancolitis developed during primary human immunodeficiency virus (HIV) infection in a patient who underwent early combination antiretroviral treatment. This massive inflammatory process led to acute colon perforation. Serological testing demonstrated cytomegalovirus reactivation. Severe immunosuppression caused by primary HIV infection resulted in cytomegalovirus colitis, and initiation of early combination antiretroviral therapy triggered an immune reconstitution inflammatory syndrome potentially leading to colonic perforation. PMID:18199043

  11. Immunoglobulin A nephropathy in association with generalized inflammatory peeling skin syndrome.

    PubMed

    Srinivasaraghavan, Rangan; Krishnamurthy, Sriram; Chandar, Rumesh; Mahadevan, Subramanian; Chandrashekar, Laxmisha; Rajesh, Nachiappa Ganesh

    2015-01-01

    We describe an 8-year-old girl born to second-degree consanguineous parents with complaints of recurrent episodes of hematuria for 6months. She had generalized peeling of the skin since birth and recurrent purulent cutaneous infections. The clinical presentation and histopathology of the skin biopsy specimen were consistent with the inflammatory variant of peeling skin syndrome (PSS). She also had a single ventricle with pulmonary stenosis, for which a bidirectional Glenn shunt had been placed. The renal biopsy specimen showed immunoglobulin A (IgA) nephropathy. She responded well to enalapril and steroids, with a decrease in proteinuria. IgA nephropathy has not been previously reported in PSS. Complications such as IgA nephropathy in children with PSS would help to further delineate the diverse clinical presentations and the clinical course of this rare dermatosis. We discuss the mechanisms that could explain this hitherto unreported association. PMID:25196305

  12. Is circulating endotoxin the trigger for the systemic inflammatory response syndrome seen after injury?

    PubMed Central

    Kelly, J L; O'Sullivan, C; O'Riordain, M; O'Riordain, D; Lyons, A; Doherty, J; Mannick, J A; Rodrick, M L

    1997-01-01

    OBJECTIVE: Patients with severe traumatic or burn injury and a mouse model of burn injury were studied early after injury to determine the relation of plasma endotoxin (lipopolysaccharide [LPS]) to the production of proinflammatory cytokines and subsequent resistance to infection. SUMMARY BACKGROUND DATA: Elevated levels of plasma LPS have been reported in patients after serious injury. It has been suggested that circulating LPS may be a trigger for increased proinflammatory cytokine production and may play a role in the septic syndromes seen in a substantial portion of such patients. Yet, despite multiple reports of leakage of LPS from the gut and bacterial translocation after injury in animal models, there is little direct evidence linking circulating LPS with production of inflammatory mediators. METHODS: The authors studied serial samples of peripheral blood from 10 patients with 25% to 50% surface area burns and 8 trauma patients (injury Severity Score, 25-57). Patients were compared with 18 healthy volunteers. The study was focused on the first 10 days after injury before the onset of sepsis or the systemic inflammatory response syndrome. Plasma samples were assayed for LPS, and adherent cells from the blood were studied for basal and LPS-stimulated production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6). The correlation of increased plasma LPS with TNF-alpha production was studied as was the association of increased plasma LPS and increased TNF-alpha production with subsequent septic complications. We also studied a mouse model of 25% burn injury. Burn mice were compared with sham burn control subjects. Plasma samples were assayed at serial intervals for LPS, and adherent cells from the spleens were studied for basal- and LPS-stimulated production of TNF-alpha, IL-1 beta, and IL-6. Expression of the messenger RNAs for IL-1 beta and TNF-alpha also was measured. The relation of increased TNF-alpha production with mortality from a septic challenge, cecal ligation and puncture (CLP), was determined. Finally, the effect of administration of LPS to normal mice on subsequent mortality after CLP and on TNF-alpha production was studied. RESULTS: Elevated plasma LPS (> 1 pg/mL) was seen in 11 of the 18 patients within 10 days of injury and in no normal control subjects. In this period, patients as compared with control subjects showed increased stimulated production of TNF-alpha, IL-1 beta, and IL-6. Increased TNF-alpha production was not correlated with elevated plasma LPS in the same patients. Neither increased plasma LPS nor increased TNF-alpha production early after injury was correlated with subsequent development of systemic inflammatory response syndrome or sepsis in the patients. Burn mice, as compared with sham burn control subjects, showed elevated plasma LPS levels chiefly in the first 3 days after injury. Increased stimulated production of proinflammatory cytokines by adherent splenocytes from the burn mice also was seen at multiple intervals after injury and did not correlate with mortality from CLP. Increased production of TNF-alpha and IL-1 beta was associated with increased expression of messenger RNAs for these cytokines. Finally, two doses of 1 ng LPS administered 24 hours apart to normal mice had no effect on mortality from CLP performed 7 days later nor on the production of TNF-alpha at the time of CLP. CONCLUSIONS: These findings call into question the idea that circulating LPS is the trigger for increased proinflammatory cytokine production, systemic inflammatory response syndrome, and septic complications in injured patients. Images Figure 6. Figure 7. PMID:9193181

  13. Persistent inflammatory, immunosuppressed, catabolic syndrome (PICS): A new phenotype of multiple organ failure

    PubMed Central

    Rosenthal, Martin D.; Moore, Frederick A.

    2015-01-01

    A new phenotype of multiple organ failure has appeared: Persistent Inflammatory, Immunosuppressed, Catabolic Syndrome (PICS). Comorbidities and age >65 years have been established as the leading risk factors for PICS. As the percentage of elderly people continues to increase the prevalence of PICS in our ICUs will surely grow. Malnutrition (despite appropriate supplementation), recurrent nosocomial infections, frailty, ventilator dependence, and an indolent death depicts the central theme that plagues PICS patients. Aligned with the recently awarded P50 grant by NIGMS entitled, “PICS: A New Horizon for Surgical Critical Care”, and the University Of Florida’s Sepsis and Critical Illness Research Center will investigate the genetic make-up of PICS patients, better understand frailty and the implication in trauma patients, and hopefully elucidate new therapies. Currently, there are no therapies to combat PICS aside from nutritional inference elaborated after reviewing the literature on Burns, Cachexia, and Sarcopenia. PMID:26086042

  14. Periplaneta americana extract used in patients with systemic inflammatory response syndrome

    PubMed Central

    Zhang, Hong-wei; Wei, Li-you; Zhao, Gang; Yang, Ya-jing; Liu, Shu-zheng; Zhang, Zhen-yu; Jing, Zhang; Hu, Yan-ling

    2016-01-01

    BACKGROUND: Periplaneta americana extract is recognized to have a positive effect on gastrointestinal mucosa. This study aimed to investigate the effects of periplaneta americana extract on immune function, nutrition status and gastrointestinal complications of early enteral nutrition patients with systemic inflammatory response syndrome (SIRS). METHODS: Patients with SIRS were randomly divided into two groups: treatment and control groups. All patients in the two groups received conventional therapy including enteral nutrition, but periplaneta americana extract, an additional Chinese medicine, was given to the patients in the treatment group. At the beginning of treatment (0 day) and 1, 3, and 7 days after treatment, the levels of immunoglobulin (IgA), total lymphocyte count (TLC), total protein (TP) and prealbumin (PA) were respectively tested in patients’ venous blood. The incidences of bloating, diarrhea, aspiration pneumonia and high blood sugar at 7 days after treatment were recorded. The mortality of the patients in 28 days was recorded. RESULTS: At 3 and 7 days after treatment, the levels of IgA and TLC in the treatment group were higher than those in the control group (P<0.05). At 7 days after treatment, the levels of TP and PA in the treatment group were higher than those in the control group (P<0.05). The incidences of bloating and diarrhea in the treatment group were lower than those in the control group, the differences were significant (P<0.05). The mortality of treatment group was lower than that of the control group (P>0.05). CONCLUSION: Periplaneta americana extract could reduce gastrointestinal complications and improve immune function and nutritional status in patients with systemic inflammatory response syndrome.

  15. Surgical management of malignant cerebral edema secondary to immune reconstitution inflammatory syndrome from natalizumab-associated progressive multifocal encephalopathy.

    PubMed

    Tan, Lee A; Lopes, Demetrius K

    2015-10-01

    We report a rare multiple sclerosis (MS) patient who developed malignant cerebral edema related to progressive multifocal encephalopathy (PML) immune reconstitution inflammatory syndrome (IRIS) after natalizumab discontinuation. The patient subsequently required a decompressive hemicraniectomy to reduce intracranial pressure and to avoid uncal herniation. PML is a demyelinating disease of the central nervous system (CNS) which affects oligodendrocytes and is caused by reactivation of latent John Cunningham virus. Natalizumab is a known risk factor (1 in 1000) for MS patients treated with this drug. Discontinuation of natalizumab treatment decreases the risk of PML progression, but a massive inflammatory response can occur after cell-mediated immune surveillance is reestablished in the CNS, causing immune reconstitution inflammatory syndrome (IRIS). Treatment of IRIS usually consists of steroids and plasma exchange to lessen the immune response, however, mortality has been reported at up to 29.4%, despite aggressive medical treatment. We discuss our management strategy with a review of the pertinent literature. PMID:26115897

  16. Porcine reproductive and respiratory syndrome virus infection triggers HMGB1 release to promote inflammatory cytokine production.

    PubMed

    Duan, Erzhen; Wang, Dang; Luo, Rui; Luo, Jingyi; Gao, Li; Chen, Huanchun; Fang, Liurong; Xiao, Shaobo

    2014-11-01

    The high mobility group box 1 (HMGB1) protein is an endogenous damage-associated molecular pattern (DAMP) molecule involved in the pathogenesis of various infectious agents. Based on meta-analysis of all publicly available microarray datasets, HMGB1 has recently been proposed as the most significant immune modulator during the porcine response to porcine reproductive and respiratory syndrome virus (PRRSV) infection. However, the function of HMGB1 in PRRSV pathogenesis is unclear. In this study, we found that PRRSV infection triggers the translocation of HMGB1 from the nucleus to the extracellular milieu in MARC-145 cells and porcine alveolar macrophages. Although HMGB1 has no effect on PRRSV replication, HMGB1 promotes PRRSV-induced NF-?B activation and subsequent expression of inflammatory cytokines through receptors RAGE, TLR2 and TLR4. Our findings show that HMGB1 release, triggered by PRRSV infection, enhances the efficiency of virus-induced inflammatory responses, thereby providing new insights into the pathogenesis of PRRSV infection. PMID:25129433

  17. Cardiorenal syndrome type 5: in vitro cytotoxicity effects on renal tubular cells and inflammatory profile.

    PubMed

    Brocca, Alessandra; Virz, Grazia Maria; Pasqualin, Chiara; Pastori, Silvia; Marcante, Stefano; de Cal, Massimo; Ronco, Claudio

    2015-01-01

    Background. Cardiorenal Syndrome Type 5 (CRS Type 5) reflects concomitant cardiac and renal dysfunctions in the setting of a wide spectrum of systemic disorders. Our aim was to study in vitro effects of CRS Type 5 plasma on renal tubular cells (RTCs), in terms of cellular death and the characterization of inflammatory plasma profile in these patients. Material and Methods. We enrolled 11 CRS Type 5 patients from ICU and 16 healthy controls. Plasma from patients and controls was incubated with renal tubular cells (RTCs) and cell death was evaluated. Plasma cytokines were detected. Results. RTCs incubated with CRS Type 5 plasma showed significantly higher apoptosis and necrosis with respect to controls. Plasma cytokine profile of CRS Type 5 patients was significantly different from controls: we observed the production of pro- and anti-inflammatory mediators in these patients. Caspase-3, caspase-8, and caspase-9 were activated in cells treated with CRS Type 5 plasma compared to controls. Conclusions. Our results underline the cytotoxic effect of CRS Type 5 mediators on RTC viability, probably due to the activation of both intrinsic and extrinsic pathways of apoptosis and to the deregulation of cytokine release. The consequence may be the damage of distant organs which lead to the worsening of condition of patients. PMID:26266085

  18. [Phenotypes of Charcot-Marie-Tooth Syndrome and Differential Diagnosis Focused in Inflammatory Neuropathies].

    PubMed

    Iijima, Masahiro

    2016-01-01

    Charcot-Marie-Tooth disease (CMT), the most frequent form of inherited neuropathy, is a genetically heterogeneous syndrome of the peripheral nervous system with a rather homologous clinical phenotype (slowly progressive distal weakness and muscle atrophy, skeletal deformities, and areflexia in each limb). CMT1 is the autosomal-dominant demyelinating form, and CMT1A (mostly PMP22 duplication) is the most frequent subtype, followed by CMTX1, HNPP (hereditary neuropathy with liability to pressure palsies), CMT1B, or CMT2. As CMT is characterized by slowly progressive motor and sensory disturbances in each limb, it could be misdiagnosed as chronic inflammatory demyelinating polyneuropathy (CIDP) occasionally. Some points can distinguish demyelinating CMT from CIDP. CMT1 patients do not show the conduction block that is frequent in CIDP. In addition, ultrasonographic findings are useful because CMT1 suggests diffuse enlargement of peripheral nerves, whereas CIDP is characterized by asymmetrical or focal enlargement of peripheral nerves. Some CMT1 cases show favorable responses to immunomodulating therapeutics such as corticosteroids, IVIg, and plasma exchange. Such CIDP-like CMT1 (especially CMT1B or CMT2A) shows moderate to high levels of cerebrospinal fluid protein and infiltrated inflammatory macrophages. PMID:26764297

  19. Symptomatology of irritable bowel syndrome and inflammatory bowel disease during the menstrual cycle.

    PubMed

    Bharadwaj, Shishira; Barber, Matthew D; Graff, Lesley A; Shen, Bo

    2015-08-01

    Gender-related physiological variations in gastrointestinal (GI) symptomatology have been observed in women of reproductive age. Many women experience cyclical changes in GI symptomatology during their menstrual cycle, particularly alteration in their bowel habits. Physiological studies of healthy women during the menstrual cycle showed a prolonged GI transit time during the luteal phase, either in the oro-cecum route or in the colon. Worsened GI symptoms, such as abdominal pain, bloating or diarrhea are observed in patients with irritable bowel syndrome (IBS) during menses. This may be due to elevated prostaglandin levels during menses, with an enhanced perception of viscera-somatic stimuli resulting in nausea, abdominal distension and pain. Also patients with IBS or IBD demonstrate a cyclical pattern more closely related to their bowel habits than healthy controls. Women with inflammatory bowel disease (IBD) also have exacerbated symptoms during menses; however, it is unclear whether this relates to physiological variation or disease exacerbation in IBS or IBD. Studies examining the association of the menstrual cycle and GI symptomatology in patients with IBS or IBD, have not yet clarified the underlying mechanisms. Moreover medications-such as non-steroidal anti-inflammatory drugs and oral contraceptive pills used for dysmenorrhea and menstrual migraine in those patients have not well been controlled for in the previous studies, which can contribute to further bias. Understanding changes in GI symptomatology during the menstrual cycle may help to determine the true extent of disease exacerbation and proper management strategy. PMID:25788484

  20. Elevated pro-inflammatory and lipotoxic mucosal lipids characterise irritable bowel syndrome

    PubMed Central

    Kajander, Kajsa; Myllyluoma, Eveliina; Kyrnpalo, Sinikka; Rasmussen, Martin; Sipponen, Pentti; Mattila, Ismo; Seppnen-Laakso, Tuulikki; Vapaatalo, Heikki; Orei?, Matej; Korpela, Riitta

    2009-01-01

    AIM: To investigate the pathophysiology of irritable bowel syndrome (IBS) by comparing the global mucosal metabolic profiles of IBS patients with those of healthy controls. METHODS: Fifteen IBS patients fulfilling the Rome II criteria, and nine healthy volunteers were included in the study. A combined lipidomics (UPLC/MS) and metabolomics (GC GC-TOF) approach was used to achieve global metabolic profiles of mucosal biopsies from the ascending colon. RESULTS: Overall, lipid levels were elevated in patients with IBS. The most significant upregulation was seen for pro-inflammatory lysophosphatidylcholines. Other lipid groups that were significantly upregulated in IBS patients were lipotoxic ceramides, glycosphingolipids, and di- and triacylglycerols. Among the metabolites, the cyclic ester 2(3H)-furanone was almost 14-fold upregulated in IBS patients compared to healthy subjects (P = 0.03). CONCLUSION: IBS mucosa is characterised by a distinct pro-inflammatory and lipotoxic metabolic profile. Especially, there was an increase in several lipid species such as lysophospholipids and ceramides. PMID:20027679

  1. Cardiorenal Syndrome Type 5: In Vitro Cytotoxicity Effects on Renal Tubular Cells and Inflammatory Profile

    PubMed Central

    Brocca, Alessandra; Virz, Grazia Maria; Pasqualin, Chiara; Pastori, Silvia; Marcante, Stefano; de Cal, Massimo; Ronco, Claudio

    2015-01-01

    Background. Cardiorenal Syndrome Type 5 (CRS Type 5) reflects concomitant cardiac and renal dysfunctions in the setting of a wide spectrum of systemic disorders. Our aim was to study in vitro effects of CRS Type 5 plasma on renal tubular cells (RTCs), in terms of cellular death and the characterization of inflammatory plasma profile in these patients. Material and Methods. We enrolled 11 CRS Type 5 patients from ICU and 16 healthy controls. Plasma from patients and controls was incubated with renal tubular cells (RTCs) and cell death was evaluated. Plasma cytokines were detected. Results. RTCs incubated with CRS Type 5 plasma showed significantly higher apoptosis and necrosis with respect to controls. Plasma cytokine profile of CRS Type 5 patients was significantly different from controls: we observed the production of pro- and anti-inflammatory mediators in these patients. Caspase-3, caspase-8, and caspase-9 were activated in cells treated with CRS Type 5 plasma compared to controls. Conclusions. Our results underline the cytotoxic effect of CRS Type 5 mediators on RTC viability, probably due to the activation of both intrinsic and extrinsic pathways of apoptosis and to the deregulation of cytokine release. The consequence may be the damage of distant organs which lead to the worsening of condition of patients. PMID:26266085

  2. Metabolism of Albumin after Continuous Venovenous Hemofiltration in Patients with Systemic Inflammatory Response Syndrome

    PubMed Central

    Chen, Yu; Qin, Xiaodong; Li, Guanwei; Zhou, Bo; Gu, Guosheng; Hong, Zhiwu; Aa, JiYe; Li, Jieshou

    2015-01-01

    Background. The systemic inflammatory response syndrome (SIRS) is characterized by a hypercatabolic state induced by inflammatory mediators. Continuous venovenous hemofiltration (CVVH) stabilizes the internal environment but also aggravates loss of amino acids. The effect of CVVH on protein dynamics is largely unknown. We adopted the stable isotopic tracer technology to investigate how CVVH changed serum albumin metabolism. Methods. Twenty SIRS patients were randomized into low- (2000?mL/h) and high- (4000?mL/h) volume CVVH groups according to the rate of replacement fluid. Eight patients with abdominal infection matched for age, sex, and laboratory index served as controls. Consecutive arterial blood samples were drawn during a primed-constant infusion of two stable isotopes to determine the albumin fractional synthesis rate (FSR) and fractional breakdown rate (FBR). Results. Before treatment, there was no significant difference of FSR and FBR among 3 groups. After CVVH, the albumin FSR in high- and low-volume groups was 7.75??1.08% and 7.30??0.89%, respectively, both higher than in the control (5.83??0.94%). There was no significant difference in albumin FBR after treatment. Conclusions. Protein dynamic indicators could reflect protein synthesis and breakdown state directly and effectively. CVVH increased albumin synthesis, while the breakdown rate remained at a high level independently of the CVVH rate. PMID:25650044

  3. Symptomatology of irritable bowel syndrome and inflammatory bowel disease during the menstrual cycle

    PubMed Central

    Bharadwaj, Shishira; Barber, Matthew D.; Graff, Lesley A.; Shen, Bo

    2015-01-01

    Gender-related physiological variations in gastrointestinal (GI) symptomatology have been observed in women of reproductive age. Many women experience cyclical changes in GI symptomatology during their menstrual cycle, particularly alteration in their bowel habits. Physiological studies of healthy women during the menstrual cycle showed a prolonged GI transit time during the luteal phase, either in the oro-cecum route or in the colon. Worsened GI symptoms, such as abdominal pain, bloating or diarrhea are observed in patients with irritable bowel syndrome (IBS) during menses. This may be due to elevated prostaglandin levels during menses, with an enhanced perception of viscera-somatic stimuli resulting in nausea, abdominal distension and pain. Also patients with IBS or IBD demonstrate a cyclical pattern more closely related to their bowel habits than healthy controls. Women with inflammatory bowel disease (IBD) also have exacerbated symptoms during menses; however, it is unclear whether this relates to physiological variation or disease exacerbation in IBS or IBD. Studies examining the association of the menstrual cycle and GI symptomatology in patients with IBS or IBD, have not yet clarified the underlying mechanisms. Moreover medicationssuch as non-steroidal anti-inflammatory drugs and oral contraceptive pills used for dysmenorrhea and menstrual migraine in those patients have not well been controlled for in the previous studies, which can contribute to further bias. Understanding changes in GI symptomatology during the menstrual cycle may help to determine the true extent of disease exacerbation and proper management strategy. PMID:25788484

  4. Non-steroidal anti-inflammatory drugs attenuate the vascular responses in aging metabolic syndrome rats

    PubMed Central

    Rubio-Ruiz, María Esther; Pérez-Torres, Israel; Diaz-Diaz, Eulises; Pavón, Natalia; Guarner-Lans, Verónica

    2014-01-01

    Aim: Metabolic syndrome (MS) and aging are low-grade systemic inflammatory conditions, and inflammation is a key component of endothelial dysfunction. The aim of this study was to investigate the effects of non-steroidal anti-inflammatory drugs (NSAIDs) upon the vascular reactivity in aging MS rats. Methods: MS was induced in young male rats by adding 30% sucrose in drinking water over 6, 12, and 18 months. When the treatment was finished, the blood samples were collected, and aortas were dissected out. The expression of COX isoenzymes and PLA2 in the aortas was analyzed using Western blot analysis. The contractile responses of aortic rings to norepinephrine (1 μmol/L) were measured in the presence or absence of different NSAIDs (10 μmol/L for each). Results: Serum levels of pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β) in control rats were remained stable during the aging process, whereas serum IL-6 in MS rats were significantly increased at 12 and 18 months. The levels of COX isoenzyme and PLA2 in aortas from control rats increased with the aging, whereas those in aortas from MS rats were irregularly increased with the highest levels at 6 months. Pretreatment with acetylsalicylic acid (a COX-1 preferential inhibitor), indomethacin (a non-selective COX inhibitor) or meloxicam (a COX-2 preferential inhibitor) decreased NE-induced contractions of aortic rings from MS rats at all the ages, with meloxicam being the most potent. Acetylsalicylic acid also significantly reduced the maximum responses of ACh-induced vasorelaxation of aortic rings from MS rats, but indomethacin and meloxicam had no effect. Conclusion: NSAIDs can directly affect vascular responses in aging MS rats. Understanding the effects of NSAIDs on blood vessels may improve the treatment of cardiovascular diseases and MS in the elders. PMID:25263337

  5. Colchicine Acutely Suppresses Local Cardiac Production of Inflammatory Cytokines in Patients With an Acute Coronary Syndrome

    PubMed Central

    Martnez, Gonzalo J; Robertson, Stacy; Barraclough, Jennifer; Xia, Qiong; Mallat, Ziad; Bursill, Christina; Celermajer, David S; Patel, Sanjay

    2015-01-01

    Background Interleukin (IL)-1?, IL-18, and downstream IL-6 are key inflammatory cytokines in the pathogenesis of coronary artery disease. Colchicine is believed to block the NLRP3 inflammasome, a cytosolic complex responsible for the production of IL-1? and IL-18. In vivo effects of colchicine on cardiac cytokine release have not been previously studied. This study aimed to (1) assess the local cardiac production of inflammatory cytokines in patients with acute coronary syndromes (ACS), stable coronary artery disease and in controls; and (2) determine whether acute administration of colchicine inhibits their production. Methods and Results Forty ACS patients, 33 with stable coronary artery disease, and 10 controls, were included. ACS and stable coronary artery disease patients were randomized to oral colchicine treatment (1mg followed by 0.5mg 1hour later) or no colchicine, 6 to 24hours prior to cardiac catheterization. Blood samples from the coronary sinus, aortic root (arterial), and lower right atrium (venous) were collected and tested for IL-1?, IL-18, and IL-6 using ELISA. In ACS patients, coronary sinus levels of IL-1?, IL-18, and IL-6 were significantly higher than arterial and venous levels (P=0.017, <0.001 and <0.001, respectively). Transcoronary (coronary sinus-arterial) gradients for IL-1?, IL-18, and IL-6 were highest in ACS patients and lowest in controls (P=0.077, 0.033, and 0.014, respectively). Colchicine administration significantly reduced transcoronary gradients of all 3 cytokines in ACS patients by 40% to 88% (P=0.028, 0.032, and 0.032, for IL-1?, IL-18, and IL-6, respectively). Conclusions ACS patients exhibit increased local cardiac production of inflammatory cytokines. Short-term colchicine administration rapidly and significantly reduces levels of these cytokines. PMID:26304941

  6. New Insights into immune Reconstitution Inflammatory Syndrome of the Central Nervous System

    PubMed Central

    Johnson, Tory P.; Nath, Avindra

    2014-01-01

    Purpose of review To highlight the importance of immune reconstitution inflammatory syndrome (IRIS) affecting the brain in HIV-infected individuals in the absence of opportunistic infections. To describe the varied clinical manifestations, unifying pathophysiological features and discuss the principles of management of this syndrome. Recent Findings IRIS within the brain is commonly seen in patients with HIV infection upon initiation of antiretroviral drugs. The fulminant forms occur in the face of opportunistic infections or uncontrolled viral replication within the brain. In this case the enhanced immune response is targeted against the microbial agent, and the brain suffers bystander damage. Treatment requires the combination of the antimicrobial agent, continued antiretrovirals and in some cases corticosteroids. It is increasingly being recognized that despite adequate control of viral replication in the brain some patients develop a chronic form of T cell encephalitis which appears to be driven by continued production of HIV-Tat protein. In others the immune response may be targeted against the host antigens in the brain. Summary In patients with CNS-IRIS the use of corticosteroids and strategies that prevent T cell migration into the brain may be needed. Extreme caution is necessary if viral eradication strategies are to employed that involve activation of viral reservoirs, since these patients may be at risk for developing CNS-IRIS. PMID:25275706

  7. Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes

    PubMed Central

    Tuttolomondo, Antonino; Maida, Carlo; Pinto, Antonio

    2015-01-01

    Diabetic foot ulcerations have been extensively reported as vascular complications of diabetes mellitus associated with a high degree of morbidity and mortality. Diabetic foot syndrome (DFS), as defined by the World Health Organization, is an ulceration of the foot (distally from the ankle and including the ankle) associated with neuropathy and different grades of ischemia and infection. Pathogenic events able to cause diabetic foot ulcers are multifactorial. Among the commonest causes of this pathogenic pathway its possible to consider peripheral neuropathy, foot deformity, abnormal foot pressures, abnormal joint mobility, trauma, peripheral artery disease. Several studies reported how diabetic patients show a higher mortality rate compared to patients without diabetes and in particular these studies under filled how cardiovascular mortality and morbidity is 2-4 times higher among patients affected by type 2 diabetes mellitus. This higher degree of cardiovascular morbidity has been explained as due to the observed higher prevalence of major cardiovascular risk factor, of asymptomatic findings of cardiovascular diseases, and of prevalence and incidence of cardiovascular and cerebrovascular events in diabetic patients with foot complications. In diabetes a fundamental pathogenic pathway of most of vascular complications has been reported as linked to a complex interplay of inflammatory, metabolic and procoagulant variables. These pathogenetic aspects have a direct interplay with an insulin resistance, subsequent obesity, diabetes, hypertension, prothrombotic state and blood lipid disorder. Involvement of inflammatory markers such as IL-6 plasma levels and resistin in diabetic subjects as reported by Tuttolomondo et al confirmed the pathogenetic issue of the a adipo-vascular axis that may contribute to cardiovascular risk in patients with type 2 diabetes. This adipo-vascular axis in patients with type 2 diabetes has been reported as characterized by lower plasma levels of adiponectin and higher plasma levels of interleukin-6 thus linking foot ulcers pathogenesis to microvascular and inflammatory events. The purpose of this review is to highlight the immune inflammatory features of DFS and its possible role as a marker of cardiovascular risk in diabetes patients and to focus the management of major complications related to diabetes such as infections and peripheral arteriopathy. PMID:25621212

  8. Effect of lornoxicam in lung inflammatory response syndrome after operations for cardiac surgery with cardiopulmonary bypass

    PubMed Central

    Tsakiridis, Kosmas; Vretzkakis, Giorgos; Mikroulis, Dimitris; Mpakas, Andreas; Kesisis, Georgios; Arikas, Stamatis; Kolettas, Alexandros; Moschos, Giorgios; Katsikogiannis, Nikolaos; Machairiotis, Nikolaos; Tsiouda, Theodora; Siminelakis, Stavros; Beleveslis, Thomas; Zarogoulidis, Konstantinos

    2014-01-01

    Background The establishment of Extracorporeal Circulation (EC) significantly contributed to improvement of cardiac surgery, but this is accompanied by harmful side-effects. The most important of them is systemic inflammatory response syndrome. Many efforts have been undertaken to minimize this problem but unfortunately without satisfied solution to date. Materials and methods Lornoxicam is a non steroid anti-inflammatory drug which temporally inhibits the cycloxygenase. In this clinical trial we study the effect of lornoxicam in lung inflammatory response after operations for cardiac surgery with cardiopulmonary bypass. In our study we conclude 14 volunteers patients with ischemic coronary disease undergoing coronary artery bypass grafting with EC. In seven of them 16 mg lornoxicam was administered iv before the anesthesia induction and before the connection in heart-lung machine. In control group (7 patients) we administered the same amount of normal saline. Results Both groups are equal regarding pro-operative and intra-operative parameters. The inflammatory markers were calculated by Elisa method. We measured the levels of cytokines (IL-6, IL-8, TNF-a), adhesion molecules (ICAM-1, e-Selectin, p-Selectin) and matrix metaloproteinase-3 (MMP-3) just after anesthesia induction, before and after cardiopulmonary bypass, just after the patients administration in ICU and after 8 and 24 hrs. In all patients we estimated the lung’s inflammatory reaction with lung biopsy taken at the begging and at the end of the operation. We calculated hemodynamics parameters: Cardiac Index (CI), Systemic Vascular Resistance Index (SVRI), Pulmonary Vascular Resistance Index (PVRI), Left Ventricular Stroke Work Index (LVSWI), Right Ventricular Stroke Work Index (RVSWI), and the Pulmonary arterial pressure, and respiratory parameters too: alveolo-arterial oxygen difference D (A-a), intrapulmonary shunt (Qs/Qt) and pulmonary Compliance. IL-6 levels of lornoxicam group were statistical significant lower at 1st postoperative day compared to them of control group (113±49 and 177±20 respectively, P=0.008). ICAM-1 levels were statistical significant lower at the patient admission in ICU, compared to them of control group (177±29 and 217±22 respectively, P=0.014), and the 1st postoperative day compared to them in control group (281±134 and 489±206 respectively, P=0.045). P-selectin levels were statistical significant lower, compared to them in control group in four measurements (97±23 and 119±7 respectively, P=0.030, 77±19 and 101±20 respectively, P=0.044, 86±4 and 105±13 respectively, P=0.06, 116±13 and 158±17 respectively, P=0.000). Conclusions Hemodynamics and respiratory parameters were improved compared to control group, but these differences was not statistical significant. Eosinofil adhesion and sequestration in intermediate tissue of lung parenchyma were significantly lower compared to control group. Also, alveolar edema was not noted in lornoxicam’s group. Lornoxicam reduce the inflammatory response in patients undergone coronary artery bypass grafting with extracorporeal circulation. This calculated from levels reduction of IL-6, ICAM-1 και p-Selectin, and from lung pathologoanatomic examination (absence of alveolar edema, reduce in eosinofil adhesion and sequestration in intermediate tissues). Despite the favorable effect of lornoxicam on the hemodinamics and respiratory parameters these improvement did not seem to be statistical significant. PMID:24672701

  9. The impact of inflammatory rheumatic diseases on the presentation, severity, and outcome of acute coronary syndrome.

    PubMed

    Ben-Zvi, Ilan; Goldenberg, Ilan; Matetzky, Shlomi; Grossman, Chagai; Elis, Avishay; Gavrielov-Yusim, Natalie; Livneh, Avi

    2016-01-01

    Patients with inflammatory rheumatic diseases (IRD) have a high burden of cardiovascular disease (CVD), leading to increased mortality and morbidity. However, it is not clear whether increased CVD mortality in IRD is due to a higher incidence or worse outcome of cardiovascular events (higher case fatality). In this observational case-control study, we assessed the outcome of acute coronary syndrome (ACS) in patients with IRDs compared to matched controls without IRD, using data from the Acute Coronary Syndrome Israeli Survey (ACSIS), a large, national, real-life registry detailing the extent, severity, and outcome of ACS. Of 2,193 subjects enrolled to the ACSIS, 20 (nine men) were identified with IRD, including 11 patients with rheumatoid arthritis, five patients with systemic lupus erythematosus (SLE), three patients with ankylosing spondylitis (AS), and one patient with psoriatic arthritis (PsA). The study patients were compared to 120 matched control patients (adjusted for age and risk factors for CVD) without IRD. Compared to controls, IRD patients had similar clinical presentation and similar type of ACS and received identical initial treatment at the ER. The two groups had comparable rates of complications including major adverse cardiovascular events (death, recurrent myocardial infarction, stroke, major bleeding, and definite stent thrombosis) (10 vs. 11.7% in the study and control group, respectively, p?>?0.05), re-hospitalization (20 vs. 21.1%, respectively, p?>?0.05), and severe congestive heart failure (7.7 vs. 6.9%, respectively, p?>?0.05) within 30days. The outcome and prognosis of ACS in patients with IRD is not worse than that of control, supporting the higher prevalence of CVD in this population as the cause for their excess mortality. PMID:24928341

  10. Comparison of anti-inflammatory effect of atorvastatin with rosuvastatin in patients of acute coronary syndrome

    PubMed Central

    Khurana, Sushant; Gupta, Surabhi; Bhalla, HiraLal; Nandwani, Shefali; Gupta, Varad

    2015-01-01

    Objectives: To compare anti-inflammatory effect of atorvastatin and rosuvastatin in patients of acute coronary syndrome. Materials and Methods: The study was a prospective, open-labeled, randomized and single-center study conducted on 100 patients of acute coronary syndrome. Patients were assigned to atorvastatin 40 mg daily or rosuvastatin 20 mg daily for 4 weeks. C-reactive protein (CRP) levels, lipid profiles, erythrocyte sedimentation rate (ESR) and adverse effects were measured at beginning and at the end of 4 weeks. Results: Baseline parameters and clinical profile did not differ between the two groups. CRP levels significantly decreased from beginning to the end of 4 weeks in both atorvastatin and rosuvastatin groups (from 35.48 to 23.07 mg/l and from 35.88 to 19.91 mg/l respectively, both P < 0.001). However, there was significant difference between the levels of CRP in patients of the rosuvastatin group as compared to the atorvastatin group (19.91 6.32 vs 23.07 7.47, P < 0.05). In addition, both the drugs were associated with a reduction in total cholesterol, LDL levels and ESR at the end of 4 weeks as compared to the beginning (P < 0.001 for all comparisons). Conclusion: Both atorvastatin (40 mg) and rosuvastatin (20 mg) are effective in decreasing CRP and LDL cholesterol levels even in a short duration of 4 weeks. Rosuvastatin was found to be more effective in decreasing CRP levels. PMID:26311995

  11. Docosahexaenoic Acid, Inflammation, and Bacterial Dysbiosis in Relation to Periodontal Disease, Inflammatory Bowel Disease, and the Metabolic Syndrome

    PubMed Central

    Tabbaa, Maria; Golubic, Mladen; Roizen, Michael F.; Bernstein, Adam M.

    2013-01-01

    Docosahexaenoic acid (DHA), a long-chain omega-3 polyunsaturated fatty acid, has been used to treat a range of different conditions, including periodontal disease (PD) and inflammatory bowel disease (IBD). That DHA helps with these oral and gastrointestinal diseases in which inflammation and bacterial dysbiosis play key roles, raises the question of whether DHA may assist in the prevention or treatment of other inflammatory conditions, such as the metabolic syndrome, which have also been linked with inflammation and alterations in normal host microbial populations. Here we review established and investigated associations between DHA, PD, and IBD. We conclude that by beneficially altering cytokine production and macrophage recruitment, the composition of intestinal microbiota and intestinal integrity, lipopolysaccharide- and adipose-induced inflammation, and insulin signaling, DHA may be a key tool in the prevention of metabolic syndrome. PMID:23966110

  12. Correlation Between Bladder Pain Syndrome/Interstitial Cystitis and Pelvic Inflammatory Disease

    PubMed Central

    Chung, Shiu-Dong; Chang, Chao-Hsiang; Hung, Peir-Haur; Chung, Chi-Jung; Muo, Chih-Hsin; Huang, Chao-Yuan

    2015-01-01

    Abstract Pelvic inflammatory disease (PID) has been investigated in Western countries and identified to be associated with chronic pelvic pain and inflammation. Bladder pain syndrome/interstitial cystitis (BPS/IC) is a complex syndrome that is significantly more prevalent in women than in men. Chronic pelvic pain is a main symptom of BPS/IC, and chronic inflammation is a major etiology of BPS/IC. This study aimed to investigate the correlation between BPS/IC and PID using a population-based dataset. We constructed a case–control study from the Taiwan National Health Insurance program. The case cohort comprised 449 patients with BPS/IC, and 1796 randomly selected subjects (about 1:4 matching) were used as controls. A Multivariate logistic regression model was constructed to estimate the association between BPS/IC and PID. Of the 2245 sampled subjects, a significant difference was observed in the prevalence of PID between BPS/IC cases and controls (41.7% vs 15.4%, P < 0.001). Multivariate logistic regression analysis revealed that the odds ratio (OR) for PID among cases was 3.69 (95% confidence interval [CI]: 2.89–4.71). Furthermore, the ORs for PID among BPS/IC cases were 4.52 (95% CI: 2.55–8.01), 4.31 (95% CI: 2.91–6.38), 3.00 (95% CI: 1.82–4.94), and 5.35 (95% CI: 1.88–15.20) in the <35, 35–49, 50–64, and >65 years age groups, respectively, after adjusting for geographic region, irritable bowel syndrome, and hypertension. Joint effect was also noted, specifically when patients had both PID and irritable bowel disease with OR of 10.5 (95% CI: 4.88–22.50). This study demonstrated a correlation between PID and BPS/IC. Clinicians treating women with PID should be alert to BPS/IC-related symptoms in the population. PMID:26579800

  13. Correlation Between Bladder Pain Syndrome/Interstitial Cystitis and Pelvic Inflammatory Disease.

    PubMed

    Chung, Shiu-Dong; Chang, Chao-Hsiang; Hung, Peir-Haur; Chung, Chi-Jung; Muo, Chih-Hsin; Huang, Chao-Yuan

    2015-11-01

    Pelvic inflammatory disease (PID) has been investigated in Western countries and identified to be associated with chronic pelvic pain and inflammation. Bladder pain syndrome/interstitial cystitis (BPS/IC) is a complex syndrome that is significantly more prevalent in women than in men. Chronic pelvic pain is a main symptom of BPS/IC, and chronic inflammation is a major etiology of BPS/IC. This study aimed to investigate the correlation between BPS/IC and PID using a population-based dataset.We constructed a case-control study from the Taiwan National Health Insurance program. The case cohort comprised 449 patients with BPS/IC, and 1796 randomly selected subjects (about 1:4 matching) were used as controls. A Multivariate logistic regression model was constructed to estimate the association between BPS/IC and PID.Of the 2245 sampled subjects, a significant difference was observed in the prevalence of PID between BPS/IC cases and controls (41.7% vs 15.4%, P < 0.001). Multivariate logistic regression analysis revealed that the odds ratio (OR) for PID among cases was 3.69 (95% confidence interval [CI]: 2.89-4.71). Furthermore, the ORs for PID among BPS/IC cases were 4.52 (95% CI: 2.55-8.01), 4.31 (95% CI: 2.91-6.38), 3.00 (95% CI: 1.82-4.94), and 5.35 (95% CI: 1.88-15.20) in the <35, 35-49, 50-64, and >65 years age groups, respectively, after adjusting for geographic region, irritable bowel syndrome, and hypertension. Joint effect was also noted, specifically when patients had both PID and irritable bowel disease with OR of 10.5 (95% CI: 4.88-22.50).This study demonstrated a correlation between PID and BPS/IC. Clinicians treating women with PID should be alert to BPS/IC-related symptoms in the population. PMID:26579800

  14. Inflammatory Biomarkers, Death, and Recurrent Nonfatal Coronary Events After an Acute Coronary Syndrome in the MIRACL Study

    PubMed Central

    Zamani, Payman; Schwartz, Gregory G.; Olsson, Anders G.; Rifai, Nader; Bao, Weihang; Libby, Peter; Ganz, Peter; Kinlay, Scott

    2013-01-01

    Background In acute coronary syndromes, C‐reactive protein (CRP) strongly relates to subsequent death, but surprisingly not to recurrent myocardial infarction. Other biomarkers may reflect different processes related to these outcomes. We assessed 8 inflammatory and vascular biomarkers and the risk of death and recurrent nonfatal cardiovascular events in the 16 weeks after an acute coronary syndrome. Methods and Results We measured blood concentrations of CRP, serum amyloid A (SAA), interleukin‐6 (IL‐6), soluble intercellular adhesion molecule (ICAM), soluble vascular cell adhesion molecule (VCAM), E‐selectin, P‐selectin, and tissue plasminogen activator antigen (tPA) 24 to 96 hours after presentation with acute coronary syndrome in 2925 subjects participating in a multicenter study. Biomarkers were related to the risk of death, and recurrent nonfatal acute coronary syndromes (myocardial infarction or unstable angina) over 16 weeks using Cox proportional hazard models. On univariate analyses, baseline CRP (P=0.006), SAA (P=0.012), and IL‐6 (P<0.001) were related to death, but not to recurrent nonfatal acute coronary syndromes. VCAM and tPA related to the risk of death (P<0.001, P=0.021, respectively) and to nonfatal acute coronary syndromes (P=0.021, P=0.049, respectively). Adjusting for significant covariates reduced the strength of the associations; however, CRP and SAA continued to relate to death. Conclusions In acute coronary syndromes, the CRP inflammatory axis relates to the risk of death and may reflect myocardial injury. VCAM and tPA may have greater specificity for processes reflecting inflammation and thrombosis in the epicardial arteries, which determine recurrent coronary events. PMID:23525424

  15. Managing Sjögren’s Syndrome and non-Sjögren Syndrome dry eye with anti-inflammatory therapy

    PubMed Central

    Coursey, Terry G; de Paiva, Cintia S

    2014-01-01

    Dry eye from Sjögren’s syndrome is a multifactorial disease that results in dysfunction of the lacrimal functional unit. Studies have shown changes in tear composition, including inflammatory cytokines, chemokines, and metalloproteinase. T-lymphocytes have been shown to increase in the conjunctiva and lacrimal glands in patient and animal models. This inflammation is in part responsible for the pathogenesis of the disease, which results in symptoms of eye irritation, ocular surface epithelial disease, and loss of corneal barrier function. There are a number of anti-inflammatory approaches for treating this disease. The current study reviews details of immune response and anti–inflammatory therapies used to control this disease. PMID:25120351

  16. Cellular Immune Activation in Cerebrospinal Fluid From Ugandans With Cryptococcal Meningitis and Immune Reconstitution Inflammatory Syndrome

    PubMed Central

    Meya, David B.; Okurut, Samuel; Zziwa, Godfrey; Rolfes, Melissa A.; Kelsey, Melander; Cose, Steve; Joloba, Moses; Naluyima, Prossy; Palmer, Brent E.; Kambugu, Andrew; Mayanja-Kizza, Harriet; Bohjanen, Paul R.; Eller, Michael A.; Wahl, Sharon M.; Boulware, David R.; Manabe, Yuka C.; Janoff, Edward N.

    2015-01-01

    Background.?Human immunodeficiency virus (HIV)-associated cryptococcal meningitis (CM) is characterized by high fungal burden and limited leukocyte trafficking to cerebrospinal fluid (CSF). The immunopathogenesis of CM immune reconstitution inflammatory syndrome (IRIS) after initiation of antiretroviral therapy at the site of infection is poorly understood. Methods.?We characterized the lineage and activation status of mononuclear cells in blood and CSF of HIV-infected patients with noncryptococcal meningitis (NCM) (n = 10), those with CM at day 0 (n = 40) or day 14 (n = 21) of antifungal therapy, and those with CM-IRIS (n = 10). Results.?At diagnosis, highly activated CD8+ T cells predominated in CSF in both CM and NCM. CM-IRIS was associated with an increasing frequency of CSF CD4+ T cells (increased from 2.2% to 23%; P = .06), a shift in monocyte phenotype from classic to an intermediate/proinflammatory, and increased programmed death ligand 1 expression on natural killer cells (increased from 11.9% to 61.6%, P = .03). CSF cellular responses were distinct from responses in peripheral blood. Conclusions.?After CM, T cells in CSF tend to evolve with the development of IRIS, with increasing proportions of activated CD4+ T cells, migration of intermediate monocytes to the CSF, and declining fungal burden. These changes provide insight into IRIS pathogenesis and could be exploited to more effectively treat CM and prevent CM-IRIS. PMID:25492918

  17. Fecal lactoferrin in discriminating inflammatory bowel disease from Irritable bowel syndrome: a diagnostic meta-analysis

    PubMed Central

    2014-01-01

    Background To perform a meta-analysis evaluating the diagnostic ability of fecal lactoferrin (FL) to distinguish inflammatory bowel disease (IBD) from irritable bowel syndrome (IBS). Methods The Medline, EMBASE, Web of Science, Cochrane library and CNKI databases were systematically searched for studies that used FL concentrations to distinguish between IBD and IBS. The sensitivity, specificity, and other diagnostic indexes of FL were pooled using a random-effects model. Results Seven studies, involving 1012 patients, were eligible for inclusion. In distinguishing IBD from IBS, FL had a pooled sensitivity of 0.78 (95% confidence interval [CI]: 0.75, 0.82), a specificity of 0.94 (95% CI: 0.91, 0.96), a positive likelihood ratio of 12.31 (95% CI: 5.93, 29.15), and a negative likelihood ratio of 0.23 (95% CI: 0.18, 0.29). The area under the summary receiver-operating characteristic curve was 0.94 (95% CI: 0.90, 0.98) and the diagnostic odds ratio was 52.65 (95% CI: 25.69, 107.91). Conclusions FL, as a noninvasive and simple marker, is useful in differentiating between IBD and IBS. PMID:25002150

  18. Predictors of immune reconstitution inflammatory syndrome associated with Kaposi's sarcoma: a case report.

    PubMed

    Cattelan, Anna Maria; Mattiolo, Adriana; Grassi, Angela; Piano, Maria Assunta; Sasset, Lolita; Trevenzoli, Marco; Zanovello, Paola; Calabrò, Maria Luisa

    2016-01-01

    We present here a case of immune reconstitution inflammatory syndrome associated with Kaposi's sarcoma (KS-IRIS) developed in an AIDS patient two months after initiation of antiretroviral therapy (ART). Baseline characteristics of this IRIS-KS case, within a cohort of 12 naïve AIDS-KS patients, were analyzed. No statistically significant differences in CD4 cell counts, plasma HIV RNA load, KS clinical staging, human herpesvirus 8 (HHV8) antibody titers and HHV8 load in peripheral blood mononuclear cells and saliva were evidenced. HHV8 load in plasma was found to be significantly higher in the KS-IRIS patient (> 6 log10 genome equivalents/ml, p = 0.01, t-test) compared to the 11 patients with KS regression. This case highlights that measurement of HHV8 load in plasma may be useful to identify patients at risk for KS-IRIS, and that this parameter should be included in the design of larger studies to define KS-IRIS risk predictors. PMID:26848307

  19. Risk factors for immune reconstitution inflammatory syndrome under combination antiretroviral therapy can be aetiology-specific.

    PubMed

    Espinosa, E; Ormsby, C E; Vega-Barrientos, R S; Ruiz-Cruz, M; Moreno-Coutio, G; Pea-Jimnez, A; Peralta-Prado, A B; Cantoral-Daz, M; Romero-Rodrguez, D P; Reyes-Tern, G

    2010-08-01

    In order to discriminate general from aetiology-specific risk factors for immune reconstitution inflammatory syndrome (IRIS), we followed up, during six months, 99 patients with advanced HIV infection commencing antiretroviral therapy (ART) without active opportunistic infections or evident inflammation. IRIS predictors were determined by univariate analysis using clinical data from 76 ART-responding patients either completing follow-up or developing IRIS, and by multivariate analysis of inflammation, disease progression and nutrition status variables. We identified 23 primary IRIS events (30.3%). Univariate predictors for all IRIS events were higher platelet counts and lower CD4/CD8 ratio, whereas subclinical inflammation was the multivariate predictor. Platelets, alkaline phosphatase levels and %CD8 T-cells in univariate analysis also predicted mycobacteria-associated IRIS independently, remaining elevated during follow-up. Herpesvirus IRIS was predicted by platelets and inflammation. Indicators of advanced HIV disease and subclinical inflammation jointly predict IRIS, and some are specific of the underlying microbial aetiology, possibly explaining previous reports. PMID:20975091

  20. Experimental Human Endotoxemia: A Model of the Systemic Inflammatory Response Syndrome?

    PubMed Central

    Coyle, Susette M.

    2012-01-01

    Abstract Background The normal human intravenous endotoxin model has been used for more than 50 years. It was once considered a possible model of sepsis, but, because no infection is present, it is better described as a model of systemic inflammation. We demonstrate herein that at least three of four systemic inflammatory response syndrome (SIRS) criteria are achieved with the model. Methods Otherwise healthy human volunteers were given Escherichia coli endotoxin 2?ng/kg intravenously. Vital signs were monitored, and blood samples were collected over time for assessment of white blood cells (WBCs), cytokines, counter-regulatory hormones, and monocyte receptors. Results The means of three variables (core temperature, heart rate, WBC) met the SIRS criteria. Compared with baseline, cytokines were elevated acutely, with tumor necrosis factor-alpha (TNF?) exhibiting temporal primacy over the other cytokines. Counter-regulatory hormones (cortisol, epinephrine) also were elevated acutely. Finally, the monocyte cell-surface receptors cluster of differentiation molecule (CD) 11b and TNF receptor-II were elevated and decreased, respectively. Conclusions The experimental human endotoxin model satisfies SIRS criteria and probably is best described as a model of Toll-like receptor 4 agonist-induced systemic inflammation. PMID:23072275

  1. DNAemia Detection by Multiplex PCR and Biomarkers for Infection in Systemic Inflammatory Response Syndrome Patients

    PubMed Central

    Fitting, Catherine; Parlato, Marianna; Adib-Conquy, Minou; Memain, Nathalie; Philippart, Franois; Misset, Benot; Monchi, Mehran; Cavaillon, Jean-Marc; Adrie, Christophe

    2012-01-01

    Fast and reliable assays to precisely define the nature of the infectious agents causing sepsis are eagerly anticipated. New molecular biology techniques are now available to define the presence of bacterial or fungal DNA within the bloodstream of sepsis patients. We have used a new technique (VYOO) that allows the enrichment of microbial DNA before a multiplex polymerase chain reaction (PCR) for pathogen detection provided by SIRS-Lab (Jena, Germany). We analyzed 72 sepsis patients and 14 non-infectious systemic inflammatory response syndrome (SIRS) patients. Among the sepsis patients, 20 had a positive blood culture and 35 had a positive microbiology in other biological samples. Of these, 51.4% were positive using the VYOO test. Among the sepsis patients with a negative microbiology and the non-infectious SIRS, 29.4% and 14.2% were positive with the VYOO test, respectively. The concordance in bacterial identification between microbiology and the VYOO test was 46.2%. This study demonstrates that these new technologies offer great hopes, but improvements are still needed. PMID:22719987

  2. Idiopathic Inflammatory Myopathies and the Anti-Synthetase Syndrome: A Comprehensive Review

    PubMed Central

    Mahler, Michael; Miller, Frederick W.; Fritzler, Marvin J.

    2014-01-01

    Autoantibodies are a hallmark in the diagnosis of many systemic autoimmune rheumatic diseases (SARD) including idiopathic inflammatory myopathies (IIM). Based on their specificity, autoantibodies in IIM are grouped into myositis specific (MSA) and myositis associated autoantibodies (MAA). Among the MSA, autoantibodies against aminoacyl-tRNA synthetases (ARS) represent the most common antibodies and can be detected in 2535 % of patients. The presence of ARS and other autoantibodies have become a key feature for classification and diagnosis of IIM and are increasingly used to define clinically distinguishable IIM subsets. For example, anti-ARS autoantibodies are the key features of what has become known as anti-synthetase syndrome (aSS), characterized by multiple organ involvement, primarily interstitial lung disease, often accompanied by myositis, non-erosive arthritis, Raynauds phenomenon, fever, and mechanics hands. Autoantibodies directed to eight different ARS have been described: Jo-1 (histidyl), PL-7 (threonyl), PL-12 (alanyl), OJ (isoleucyl), EJ (glycyl), KS (asparaginyl), Zo (phenylalanyl) and Ha (tyrosyl). Each anti-ARS antibody seems to define a distinctive clinical phenotype. Although several research methods and commercial tests are available, routine testing for anti-ARS autoantibodies (other than anti-Jo-1/histidyl-tRNA synthetase) is not widely available, sometimes leading to delays in diagnosis and poor disease outcomes. PMID:24424190

  3. The caspase-cleaved form of LYN mediates a psoriasis-like inflammatory syndrome in mice

    PubMed Central

    Marchetti, Sandrine; Gamas, Parvati; Belhacène, Nathalie; Grosso, Sebastien; Pradelli, Ludivine A; Colosetti, Pascal; Johansen, Claus; Iversen, Lars; Deckert, Marcel; Luciano, Fréderic; Hofman, Paul; Ortonne, Nicolas; Khemis, Abdallah; Mari, Bernard; Ortonne, Jean-Paul; Ricci, Jean-Ehrland; Auberger, Patrick

    2009-01-01

    We showed previously that Lyn is a substrate for caspases, a family of cysteine proteases, involved in the regulation of apoptosis and inflammation. Here, we report that expression of the caspase-cleaved form of Lyn (LynΔN), in mice, mediates a chronic inflammatory syndrome resembling human psoriasis. Genetic ablation of TNF receptor 1 in a LynΔN background rescues a normal phenotype, indicating that LynΔN mice phenotype is TNF-α-dependent. The predominant role of T cells in the disease occurring in LynΔN mice was highlighted by the distinct improvement of LynΔN mice phenotype in a Rag1-deficient background. Using pan-genomic profiling, we also established that LynΔN mice show an increased expression of STAT-3 and inhibitory members of the NFκB pathway. Accordingly, LynΔN alters NFκB activity underlying a link between inhibition of NFκB and LynΔN mice phenotype. Finally, analysis of Lyn expression in human skin biopsies of psoriatic patients led to the detection of Lyn cleavage product whose expression correlates with the activation of caspase 1. Our data identify a new role for Lyn as a regulator of psoriasis through its cleavage by caspases. PMID:19590497

  4. Hyperperfusion in progressive multifocal leukoencephalopathy is associated with disease progression and absence of immune reconstitution inflammatory syndrome

    PubMed Central

    Khoury, Michael N.; Gheuens, Sarah; Ngo, Long; Wang, Xiaoen; Alsop, David C.

    2013-01-01

    We sought to characterize perfusion patterns of progressive multifocal leukoencephalopathy lesions by arterial spin labelling perfusion magnetic resonance imaging and to analyse their association with immune reconstitution inflammatory syndrome, and survival. A total of 22 patients with progressive multifocal leukoencephalopathy underwent a clinical evaluation and magnetic resonance imaging of the brain within 190 days of symptom onset. The presence of immune reconstitution inflammatory syndrome was determined based on clinical and laboratory criteria. Perfusion within progressive multifocal leukoencephalopathy lesions was determined by arterial spin labelling magnetic resonance imaging. We observed intense hyperperfusion within and at the edge of progressive multifocal leukoencephalopathy lesions in a subset of subjects. This hyperperfusion was quantified by measuring the fraction of lesion volume showing perfusion in excess of twice normal appearing grey matter. Hyperperfused lesion fraction was significantly greater in progressive multifocal leukoencephalopathy progressors than in survivors (12.8% versus 3.4% P = 0.02) corresponding to a relative risk of progression for individuals with a hyperperfused lesion fraction ≥ 4.0% of 9.1 (95% confidence interval of 1.4–59.5). The presence of hyperperfusion was inversely related to the occurrence of immune reconstitution inflammatory syndrome at the time of scan (P = 0.03). Indeed, within 3 months after symptom onset, hyperperfusion had a positive predictive value of 88% for absence of immune reconstitution inflammatory syndrome. Arterial spin labelling magnetic resonance imaging recognized regions of elevated perfusion within lesions of progressive multifocal leukoencephalopathy. These regions might represent virologically active areas operating in the absence of an effective adaptive immune response and correspond with a worse prognosis. PMID:24088807

  5. Red wine extract decreases pro-inflammatory markers, nuclear factor-?B and inducible NOS, in experimental metabolic syndrome.

    PubMed

    Janega, Pavol; Klimentov, Jana; Barta, Andrej; Kovcsov, Mria; Vrankov, Stanislava; Cebov, Martina; ?ierna, Zuzana; Matskov, Zuzana; Jakovljevic, Vladimir; Pechnov, Olga

    2014-09-01

    We aimed to analyse the effects of alcohol-free Alibernet red wine extract (AWE) on nitric oxide synthase (NOS) activity and pro-inflammatory markers such as nuclear factor-?B (NF?B) and inducible NOS (iNOS) protein expression in experimental metabolic syndrome. Young 6 week-old male Wistar Kyoto (WKY) and obese, spontaneously hypertensive rats (SHR/N-cp) were divided into control groups and groups treated with AWE (24.2 mg per kg per day) for 3 weeks (n = 6 in each group). Total NOS activity and endothelial NOS (eNOS), iNOS and NF?B (p65) protein expressions were determined in the heart left ventricle and aorta by Western blot and immunohistochemical analysis. All parameters investigated significantly increased in the aorta of SHR/N-cp rats. Pro-inflammatory markers such as NF?B and iNOS were increased in the left ventricle as well. AWE treatment did not affect total NOS activity and eNOS expression in the aorta; however, it was able to decrease NF?B and iNOS protein expression in both the left ventricle and aorta. In conclusion, in the cardiovascular system, Alibernet red wine extract decreased NF?B and iNOS protein expressions elevated as a consequence of developed metabolic syndrome. This effect may represent one of the protective, anti-inflammatory properties of Alibernet red wine polyphenols on cardiovascular risk factors related to metabolic syndrome. PMID:25051230

  6. [Difficulties in interpreting the monoclonal gammopathy of chance discovery: transitional gammopathy case in a significant inflammatory syndrome].

    PubMed

    Karfo, Raoul; Benchekroun, Laila; Zohoun, Alban; Chabraoui, Layachi

    2015-01-01

    The discovery of a monoclonal immunoglobulin is usually witnessed a malignant lymphoproliferative disease, but sometimes it is a transient event during viral, bacterial or fungal infections and during an inflammatory syndrome. Achieving electrophoresis performed in an elderly patient aged 55 with anemia to 63g/L hemoglobin showed a consistent profile with intense inflammatory syndrome and chronic atypical with elevated C-reactive protein (CRP) greater than 300mg/L (normal values: 0-8mg/L) associated with the presence of two thin appearance monoclonal migrating bands in gamma position. Achieving immunofixation showed IgM kappa monoclonal confirmed by using betamercaptoethanol (BME). Radiological findings, hematological, revealed nothing. The recovery of blood away from the inflammation on another sample report presented a CRP at 5mg/L and a subnormal profile electrophoresis and immunofixation revealed nothing. The comparison of the results of biochemical investigations, haematological and clinical and radiological control of the electrophoretic profile of a remote inflammatory syndrome to exclude cases of transient gammopathies. PMID:26411917

  7. Acute paretic syndrome in juvenile White Leghorn chickens resembles late stages of acute inflammatory demyelinating polyneuropathies in humans

    PubMed Central

    2010-01-01

    Background Sudden limb paresis is a common problem in White Leghorn flocks, affecting about 1% of the chicken population before achievement of sexual maturity. Previously, a similar clinical syndrome has been reported as being caused by inflammatory demyelination of peripheral nerve fibres. Here, we investigated in detail the immunopathology of this paretic syndrome and its possible resemblance to human neuropathies. Methods Neurologically affected chickens and control animals from one single flock underwent clinical and neuropathological examination. Peripheral nervous system (PNS) alterations were characterised using standard morphological techniques, including nerve fibre teasing and transmission electron microscopy. Infiltrating cells were phenotyped immunohistologically and quantified by flow cytometry. The cytokine expression pattern was assessed by quantitative real-time PCR (qRT-PCR). These investigations were accomplished by MHC genotyping and a PCR screen for Marek's disease virus (MDV). Results Spontaneous paresis of White Leghorns is caused by cell-mediated, inflammatory demyelination affecting multiple cranial and spinal nerves and nerve roots with a proximodistal tapering. Clinical manifestation coincides with the employment of humoral immune mechanisms, enrolling plasma cell recruitment, deposition of myelin-bound IgG and antibody-dependent macrophageal myelin-stripping. Disease development was significantly linked to a 539 bp microsatellite in MHC locus LEI0258. An aetiological role for MDV was excluded. Conclusions The paretic phase of avian inflammatory demyelinating polyradiculoneuritis immunobiologically resembles the late-acute disease stages of human acute inflammatory demyelinating polyneuropathy, and is characterised by a Th1-to-Th2 shift. PMID:20109187

  8. Soluble ST2 in the Fetal Inflammatory Response Syndrome: In-vivo Evidence of Activation of the Anti-inflammatory Limb of the Immune Response

    PubMed Central

    Stampalija, Tamara; Romero, Roberto; Korzeniewski, Steven J; Chaemsaithong, Piya; Miranda, Jezid; Yeo, Lami; Dong, Zhong; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn

    2014-01-01

    Objective Inflammation is a mechanism of host response to infection which can be harmful when inappropriately modulated. Soluble ST2 (sST2) is a decoy receptor of interleukin (IL)-33, and this complex modulates the balance in the Th1/Th2 immune response. Moreover, sST2 inhibits the production of pro-inflammatory cytokines in cooperation with an anti-inflammatory cytokine, IL-10. The objectives of this study were to: 1) determine whether umbilical cord plasma sST2 concentration differ between comparing preterm neonates with and without funisitis and between those with and without the fetal inflammatory response syndrome (FIRS); and 2) evaluate the relationship between sST2 and IL-10 among neonates with funisitis and/or FIRS. Methods Umbilical cord plasma was collected from neonates delivered prematurely due to preterm labor or preterm prelabor rupture of membranes with (n=36), and without funisitis (n=30). FIRS (umbilical cord IL-6 concentration ≥17.5 pg/mL) was identified in 29 neonates. Plasma sST2 and IL-10 concentrations were determined by ELISA. Results The median umbilical cord plasma sST2 concentration was 6.7-fold higher in neonates with FIRS than in those without FIRS (median 44.6 ng/mL, interquartile range [IQR] 13.8–80.3 ng/mL vs. median 6.7 ng/mL, IQR 5.6–20.1 ng/mL; p<0.0001). Similarly, the median umbilical cord plasma sST2 concentration was 2.6-fold higher in neonates with funisitis than in those without funisitis (median 19.1 ng/mL; IQR 7.1–75.0 ng/mL vs. median 7.2 ng/mL; IQR 5.9–23.1 ng/mL; p=0.008). There was a strong positive correlation between sST2 and IL-10 in neonates with funisitis and/or FIRS (Spearman’s Rho=0.7, p<0.0001). Conclusions FIRS and funisitis are associated with an elevation of umbilical cord plasma concentrations of soluble ST2. This protein represents an important mediator of the immune response in neonates diagnosed with fetal inflammatory response syndrome by promoting an anti-inflammatory effect in association with IL-10. PMID:23488731

  9. [Chronic inflammatory demyelinating polyneuropathy followed by systemic lupus erythematosus and Sjgren syndrome: a case report].

    PubMed

    Hatano, Taku; Fukuda, Momo; Shiotsuki, Hiromi; Miwa, Hideto; Urabe, Takao; Mizuno, Yoshikuni

    2006-03-01

    We report a 60-year-old man with chronic inflammatory demyelinating polyneuropathy (CIDP) accompanying systemic lupus erythematosus (SLE) and Sjgren syndrome (SS). He was admitted to our hospital because of progressive weakness and dysesthesia in the distal parts of the bilateral upper and lower extremities. We diagnosed the illness as CIDP and treated him with steroids, plasma filtration and high-dose intravenous immunoglobulin therapy (IvIg). Consequently, his symptoms improved gradually and he was discharged. However, 2 years after the first admission, he experienced dyspnea on effort and chest X-ray demonstrated right pleural effusion. Consequently, he gradually developed gait disturbance, loss of taste, and severe dysesthesia in his lower limbs. Therefore, he was admitted again. On neurological examination, mild weakness was detected in all limbs distally. Deep tendon reflexes were absent. The sensation of position and vibration was diminished in the fingers and toes. He could not walk by himself and demonstrated an ataxic gait with a wide base. Examination of cranial nerves demonstrated no abnormalities, except for loss of taste. Serological examination demonstrated positive auto-antibodies including antinuclear, anti-DNA, and anti-SS-A antibodies. Urinalyses showed albuminuria and microscopic hematuria. Cerebrospinal fluid (CSF) was clear and colorless, containing 3 mononuclear cells per cubic mm, with a protein of 275 mg/dl. Magnetic resonance images (MRIs) of the brain and entire spine were normal. Neurophysiological studies demonstrated an absence of sensory nerve action potentials in the right arm and markedly slow conduction velocities, conduction block in the ulnar forearm segment and absence of F waves in all limbs. The renal biopsy revealed lupus nephritis. The lip biopsy demonstrated chronic sialoadenitis consistent with SS, altough patient did not show symptoms of arthritis or vasculitis. It is well known that mononeuritis multiplex and acute demyelinating polyneuropathy accompany SLE. However there are few reports that describe the occurrence of CIDP in patients with SLE, and the association of "CIDP-like" neuropathy in patients with SS. Our case suggests that the autoimmune disease associated with SLE and SS may induce "CIDP-like" inflammatory demyelinating polyneuropathy. PMID:16642931

  10. [Inflammatory response and C?-reactive protein value in patient with acute coronary syndrome].

    PubMed

    Kubkov, L; Spinar, J; Pvkov Goldbergov, M; Jarkovsk, J; Pa?enica, J

    2013-11-01

    Inflammation plays an important role in the pathophysiology of acute coronary syndrome as well as in the process of atherosclerosis in general. At the moment of myocardial ischaemia, local and systemic inflammatory reaction is amplified; in ischaemic myocardium there is increased expression of proinflammatory cytokines, particularly interleukin-6, which mediates C?reactive protein (CRP) production by hepatocytes. CRP activates the complement cascade and thereby contributes to the lysis and removal of damaged cardiomyocytes. Whereas in a healthy population CRP levels range from 1.2 to 2.0 mg /?l, in patients with ACS the levels of CRP significantly increase with the peak of 2nd to 4th day from the onset of myocardial infarction. Peak CRP levels ranged from 20 to 250 mg /?l in patients with STEMI treated conservatively, the median of peak of CRP levels was 79 mg/?l in patients with anterior wall STEMI treated with primary PCI. There is a recommendation of CRP evaluation within the early risk stratification of patients with ACS according to the current ESC guidelines. In patients with NSTEMI, CRP levels > 10 mg/?l are associated with increased longterm mortality. In patients with STEMI treated with primary PCI, CRP levels > 79 mg/?l could predict negative left ventricle remodelation. The predictive value of GRACE risk score was improved using CRP, levels > 22 mg/?l predicted worse prognosis in patients with either STEMI or NSTEMI treated invasively. However, if also cardiac troponin and natriuretic peptides in addition to GRACE risk score were used, CRP levels were useless in further risk stratification improvement. In clinical practice, in terms of coinciding infection, problems with CRP levels interpretation can occur as well. Several patients either in cardiogenic shock or after cardiopulmonary resuscitation have signs of systemic inflammatory response, and sometimes it is very difficult to decide whether there is a necessity to iniciate the antibio-tic therapy because of infectious cause. In patients after cardiopulmonary resuscitation, CRP levels > 180 mg/?l indicate highly probable infection, but with the poor sensitivity. For patients in cardiogenic shock, procalcitonin appears to be more useful for the detection of infection; in this group of patients, procalcitonin levels > 2 ng/?ml are common, and levels > 10 ng/?ml indicate infection undoubtedly. PMID:24279442

  11. Are probiotics or prebiotics useful in pediatric irritable bowel syndrome or inflammatory bowel disease?

    PubMed

    Guandalini, Stefano

    2014-01-01

    Treatment options for irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) are notoriously either inadequate (IBS) or loaded with potentially serious side effects and risks (IBD). In recent years, a growing interest in effective and safer alternatives has focused on the potential role of probiotics and their metabolic substrates, prebiotics. It is in fact conceivable that the microbiome might be targeted by providing the metabolic fuel needed for the growth and expansion of beneficial microorganisms (prebiotics) or by administering to the host such microorganisms (probiotics). This review presents a concise update on currently available data, with a special emphasis on children. Data for prebiotics in IBS are scarce. Low doses have shown a beneficial effect, while high doses are counterproductive. On the contrary, several controlled trials of probiotics have yielded encouraging results. A meta-analysis including nine randomized clinical trials in children showed an improvement in abdominal pain for Lactobacillus GG, Lactobacillus reuteri DSM 17938, and the probiotic mixture VSL#3. The patients most benefiting from probiotics were those with predominant diarrhea or with a post-infectious IBS. In IBD, the use of prebiotics has been tested only rarely and in small scale clinical trials, with mixed results. As for probiotics, data in humans from about three dozens clinical trials offer mixed outcomes. So far, none of the tested probiotics has proven successful in Crohn's disease, while in ulcerative colitis a recent meta-analysis on 12 clinical trials (1 of them in children) showed efficacy for the probiotic mixture VSL#3 in contributing to induce and to maintain remission. It is evident that this is a rapidly evolving and promising field; more data are very likely to yield a better understanding on what strains should be used in different specific clinical settings and in what doses. PMID:25593899

  12. Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes

    PubMed Central

    2012-01-01

    Introduction Apolipoprotein M (apoM) is present in 5% of high-density lipoprotein (HDL) particles in plasma. It is a carrier of sphingosine-1-phosphate (S1P), which is important for vascular barrier protection. The aim was to determine the plasma concentrations of apoM during sepsis and systemic inflammatory response syndrome (SIRS) and correlate them to levels of apolipoprotein A-I (apoA1), apolipoprotein B (apoB), HDL-, and low-density lipoprotein (LDL)-cholesterol. Methods Plasma samples from patients with (1), severe sepsis with shock (n = 26); (2), severe sepsis without shock (n = 44); (3), sepsis (n = 100); (4), infections without SIRS (n = 43); and (5) SIRS without infection (n = 20) were analyzed. The concentrations of apoM, apoA1, and apoB were measured with enzyme-linked immunosorbent assays (ELISAs). Total, HDL-, and LDL-cholesterol concentrations were measured with a commercial HDL/LDL cholesterol test. Results ApoM concentrations correlated negatively to acute-phase markers. Thus, apoM behaved as a negative acute-phase protein. Decreased values were observed in all patient groups (P < 0.0001), with the most drastic decreases observed in the severely sick patients. ApoM levels correlated strongly to those of apoA1, apoB, HDL, and LDL cholesterol. The HDL and LDL cholesterol levels were low in all patient groups, as compared with controls (P < 0.0001), in particular, HDL cholesterol. ApoA1 and apoB concentrations were low only in the more severely affected patients. Conclusions During sepsis and SIRS, the plasma concentrations of apoM decrease dramatically, the degree of decrease reflecting the severity of the disease. As a carrier for barrier-protective S1P in HDL, the decrease in apoM could contribute to the increased vascular leakage observed in sepsis and SIRS. PMID:22512779

  13. Inflammatory role and prognostic value of platelet chemokines in acute coronary syndrome.

    PubMed

    Blanchet, X; Cesarek, K; Brandt, J; Herwald, H; Teupser, D; Kchenhoff, H; Karshovska, E; Mause, S F; Siess, W; Wasmuth, H; Soehnlein, O; Koenen, R R; Weber, C; von Hundelshausen, P

    2014-12-01

    Activated platelets and neutrophils exacerbate atherosclerosis. Platelets release the chemokines CXCL4, CXCL4L1 and CCL5, whereas myeloperoxidase (MPO) and azurocidin are neutrophil-derived. We investigated whether plasma levels of these platelet and neutrophil mediators are affected by the acute coronary syndrome (ACS), its medical treatment, concomitant clinical or laboratory parameters, and predictive for the progression of coronary artery disease (CAD). In an observational study, the association of various factors with plasma concentrations of platelet chemokines and neutrophil mediators in 204 patients, either upon admission with ACS and 6 hours later or without ACS or CAD, was determined by multiple linear regression. Mediator release was further analysed after activation of blood with ACS-associated triggers such as plaque material. CXCL4, CXCL4L1, CCL5, MPO and azurocidin levels were elevated in ACS. CXCL4 and CCL5 but not CXCL4L1 or MPO were associated with platelet counts and CRP. CXCL4 (in association with heparin treatment) and MPO declined over 6 hours during ACS. Elevated CCL5 was associated with a progression of CAD. Incubating blood with plaque material, PAR1 and PAR4 activation induced a marked release of CXCL4 and CCL5, whereas CXCL4L1 and MPO were hardly or not altered. Platelet chemokines and neutrophil products are concomitantly elevated in ACS and differentially modulated by heparin treatment. CCL5 levels during ACS predict a progression of preexisting CAD. Platelet-derived products appear to dominate the inflammatory response during ACS, adding to the emerging evidence that ACS per se may promote vascular inflammation. PMID:25183015

  14. Are Probiotics or Prebiotics Useful in Pediatric Irritable Bowel Syndrome or Inflammatory Bowel Disease?

    PubMed Central

    Guandalini, Stefano

    2014-01-01

    Treatment options for irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) are notoriously either inadequate (IBS) or loaded with potentially serious side effects and risks (IBD). In recent years, a growing interest in effective and safer alternatives has focused on the potential role of probiotics and their metabolic substrates, prebiotics. It is in fact conceivable that the microbiome might be targeted by providing the metabolic fuel needed for the growth and expansion of beneficial microorganisms (prebiotics) or by administering to the host such microorganisms (probiotics). This review presents a concise update on currently available data, with a special emphasis on children. Data for prebiotics in IBS are scarce. Low doses have shown a beneficial effect, while high doses are counterproductive. On the contrary, several controlled trials of probiotics have yielded encouraging results. A meta-analysis including nine randomized clinical trials in children showed an improvement in abdominal pain for Lactobacillus GG, Lactobacillus reuteri DSM 17938, and the probiotic mixture VSL#3. The patients most benefiting from probiotics were those with predominant diarrhea or with a post-infectious IBS. In IBD, the use of prebiotics has been tested only rarely and in small scale clinical trials, with mixed results. As for probiotics, data in humans from about three dozens clinical trials offer mixed outcomes. So far, none of the tested probiotics has proven successful in Crohn’s disease, while in ulcerative colitis a recent meta-analysis on 12 clinical trials (1 of them in children) showed efficacy for the probiotic mixture VSL#3 in contributing to induce and to maintain remission. It is evident that this is a rapidly evolving and promising field; more data are very likely to yield a better understanding on what strains should be used in different specific clinical settings and in what doses. PMID:25593899

  15. Incidence of Paradoxical Tuberculosis-Associated Immune Reconstitution Inflammatory Syndrome and Impact on Patient Outcome

    PubMed Central

    Bonnet, Maryline; Baudin, Elisabeth; Jani, Ilesh V.; Nunes, Elizabete; Verhoustraten, François; Calmy, Alexandra; Bastos, Rui; Bhatt, Nilesh B.; Michon, Christophe

    2013-01-01

    Objectives and Design We used data from a randomized trial of HIV-tuberculosis co-infected patients in Mozambique to determine the incidence and predictors of paradoxical tuberculosis-associated immune reconstitution inflammatory syndrome (IRIS) occurring within 12 weeks of starting antiretroviral therapy, and to evaluate its association with patient outcome at 48 weeks. Methods HIV-tuberculosis co-infected and antiretroviral therapy-naïve adults with less than 250 CD4/mm3 were randomized to a nevirapine or efavirenz-based antiretroviral therapy initiated 4 to 6 weeks after starting tuberculosis treatment, and were then followed for 48 weeks. Tuberculosis cases were diagnosed using WHO guidelines, and tuberculosis-IRIS by case definitions of the International Network for the Study of HIV-associated IRIS. Results The 573 HIV-tuberculosis co-infected patients who initiated antiretroviral therapy had a median CD4 count of 92 cells/mm3 and HIV-1 RNA of 5.6 log10 copies/mL. Mortality at week 48 was 6.1% (35/573). Fifty-three (9.2%) patients presented a tuberculosis-IRIS within 12 weeks of starting antiretroviral therapy. Being female and having a low CD4 count, high HIV-1 RNA load, low body mass index and smear-positive pulmonary tuberculosis were independently associated with tuberculosis-IRIS. After adjustment for baseline body mass index, CD4 count and hemoglobin, occurrence of tuberculosis-IRIS was independently associated with 48-week mortality (aOR 2.72 95%CI 1.14-6.54). Immunological and HIV-1 virological responses and tuberculosis treatment outcomes were not different between patients with and without tuberculosis-IRIS. Conclusion In this large prospective cohort, tuberculosis-IRIS occurrence within 12 weeks of starting antiretroviral therapy was independently associated with the mortality of HIV-tuberculosis co-infected patients at 48 weeks post antiretroviral therapy initiation. PMID:24367678

  16. Association between inflammatory biomarkers and adiposity in obese patients with heart failure and metabolic syndrome

    PubMed Central

    MOTIE, MARJAN; EVANGELISTA, LORRAINE S.; HORWICH, TAMARA; LOMBARDO, DAWN; ZALDIVAR, FRANK; HAMILTON, MICHELE; FONAROW, GREGG C.

    2014-01-01

    Obesity, type 2 diabetes mellitus (DM) and metabolic syndrome (MS) are common in patients with heart failure (HF). Studies investigating the association between known biomarkers and adiposity in patient populations are limited. The aim of the present study was to investigate the association between C-reactive protein (CRP) and leptin with adiposity in a sub-group of overweight/obese patients with HF, DM and/or MS. A total of 36 patients (mean age, 56.729.78 years; ranging between 27 and 76 years of age; 80.6% male; 52.8% Caucasian) were enrolled and their height, weight, waist circumference and body composition (e.g. percentage body fat and lean mass), as well as the levels of CRP and leptin, were assessed. The results demonstrated that there was a significant association between CRP and leptin, CRP and body mass index (BMI) and gender and percentage body fat (P<0.05, for all associations). Analysis of leptin and CRP levels revealed that patients in the highest BMI quartile (BMI, 40.361.2) had higher CRP levels (4.83 ?g/ml vs. 3.03 ?g/ml; P=0.033) and higher leptin levels (44.97 ng/ml vs. 24.64 ng/ml; P=0.042) compared with patients in the lower BMI quartile (BMI, 28.632.4). In conclusion, among obese patients with HF, DM and/or MS, an association between CRP and leptin was identified, providing further evidence that metabolic and inflammatory mechanisms are involved in these diseases. Future investigation to assess the potential impact of inflammation and adiposity, and the role of dietary interventions and weight loss on clinical outcomes in this population of chronically ill patients is warranted. PMID:24944619

  17. Association between inflammatory biomarkers and adiposity in obese patients with heart failure and metabolic syndrome.

    PubMed

    Motie, Marjan; Evangelista, Lorraine S; Horwich, Tamara; Lombardo, Dawn; Zaldivar, Frank; Hamilton, Michele; Fonarow, Gregg C

    2014-07-01

    Obesity, type 2 diabetes mellitus (DM) and metabolic syndrome (MS) are common in patients with heart failure (HF). Studies investigating the association between known biomarkers and adiposity in patient populations are limited. The aim of the present study was to investigate the association between C-reactive protein (CRP) and leptin with adiposity in a sub-group of overweight/obese patients with HF, DM and/or MS. A total of 36 patients (mean age, 56.729.78 years; ranging between 27 and 76 years of age; 80.6% male; 52.8% Caucasian) were enrolled and their height, weight, waist circumference and body composition (e.g. percentage body fat and lean mass), as well as the levels of CRP and leptin, were assessed. The results demonstrated that there was a significant association between CRP and leptin, CRP and body mass index (BMI) and gender and percentage body fat (P<0.05, for all associations). Analysis of leptin and CRP levels revealed that patients in the highest BMI quartile (BMI, 40.3-61.2) had higher CRP levels (4.83 ?g/ml vs. 3.03 ?g/ml; P=0.033) and higher leptin levels (44.97 ng/ml vs. 24.64 ng/ml; P=0.042) compared with patients in the lower BMI quartile (BMI, 28.6-32.4). In conclusion, among obese patients with HF, DM and/or MS, an association between CRP and leptin was identified, providing further evidence that metabolic and inflammatory mechanisms are involved in these diseases. Future investigation to assess the potential impact of inflammation and adiposity, and the role of dietary interventions and weight loss on clinical outcomes in this population of chronically ill patients is warranted. PMID:24944619

  18. Overlapping irritable bowel syndrome and inflammatory bowel disease: less to this than meets the eye?

    PubMed Central

    Quigley, Eamonn M. M.

    2016-01-01

    Though distinct in terms of pathology, natural history and therapeutic approach, irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) have some features in common. These include shared symptomatology and largely similar demographics. However, in most instances, clinical presentation, together with laboratory, imaging and endoscopic findings will readily permit the differentiation of active IBD from IBS. More problematic is the situation where a subject with IBD, in apparent remission, continues to complain of symptoms which, in aggregate, satisfy commonly employed criteria for the diagnosis of IBS. Access to methodologies, such the assay for levels of calprotectin in feces, now allows identification of ongoing inflammation in some such individuals and prompts appropriate therapy. More challenging is the IBD patient with persisting symptoms and no detectable evidence of inflammation; is this coincident IBS, IBS triggered by IBD or an even more subtle level of IBD activity unrecognized by available laboratory or imaging methods? Arguments can be advanced for each of these proposals; lacking definitive data, this issue remains unresolved. The occurrence of IBS-type symptoms in the IBD patient, together with some data suggesting a very subtle level of ‘inflammation‘ or ‘immune activation‘ in IBS, raises other questions: is IBS a prodromal form of IBD; and are IBS and IBD part of the spectrum of the same disease? All of the available evidence indicates that the answer to both these questions should be a resounding ‘no’. Indeed, the whole issue of overlap between IBS and IBD should be declared moot given their differing pathophysiologies, contrasting natural histories and divergent treatment paths. The limited symptom repertoire of the gastrointestinal tract may well be fundamental to the apparent confusion that has, of late, bedeviled this area. PMID:26929782

  19. Neither classical nor alternative macrophage activation is required for Pneumocystis clearance during immune reconstitution inflammatory syndrome.

    PubMed

    Zhang, Zhuo-Qian; Wang, Jing; Hoy, Zachary; Keegan, Achsah; Bhagwat, Samir; Gigliotti, Francis; Wright, Terry W

    2015-12-01

    Pneumocystis is a respiratory fungal pathogen that causes pneumonia (Pneumocystis pneumonia [PcP]) in immunocompromised patients. Alveolar macrophages are critical effectors for CD4(+) T cell-dependent clearance of Pneumocystis, and previous studies found that alternative macrophage activation accelerates fungal clearance during PcP-related immune reconstitution inflammatory syndrome (IRIS). However, the requirement for either classically or alternatively activated macrophages for Pneumocystis clearance has not been determined. Therefore, RAG2(-/-) mice lacking either the interferon gamma (IFN-γ) receptor (IFN-γR) or interleukin 4 receptor alpha (IL-4Rα) were infected with Pneumocystis. These mice were then immune reconstituted with wild-type lymphocytes to preserve the normal T helper response while preventing downstream effects of Th1 or Th2 effector cytokines on macrophage polarization. As expected, RAG2(-/-) mice developed severe disease but effectively cleared Pneumocystis and resolved IRIS. Neither RAG/IFN-γR(-/-) nor RAG/IL-4Rα(-/-) mice displayed impaired Pneumocystis clearance. However, RAG/IFN-γR(-/-) mice developed a dysregulated immune response, with exacerbated IRIS and greater pulmonary function deficits than those in RAG2 and RAG/IL-4Rα(-/-) mice. RAG/IFN-γR(-/-) mice had elevated numbers of lung CD4(+) T cells, neutrophils, eosinophils, and NK cells but severely depressed numbers of lung CD8(+) T suppressor cells. Impaired lung CD8(+) T cell responses in RAG/IFN-γR(-/-) mice were associated with elevated lung IFN-γ levels, and neutralization of IFN-γ restored the CD8 response. These data demonstrate that restricting the ability of macrophages to polarize in response to Th1 or Th2 cytokines does not impair Pneumocystis clearance. However, a cell type-specific IFN-γ/IFN-γR-dependent mechanism regulates CD8(+) T suppressor cell recruitment, limits immunopathogenesis, preserves lung function, and enhances the resolution of PcP-related IRIS. PMID:26371121

  20. Overlapping irritable bowel syndrome and inflammatory bowel disease: less to this than meets the eye?

    PubMed

    Quigley, Eamonn M M

    2016-03-01

    Though distinct in terms of pathology, natural history and therapeutic approach, irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) have some features in common. These include shared symptomatology and largely similar demographics. However, in most instances, clinical presentation, together with laboratory, imaging and endoscopic findings will readily permit the differentiation of active IBD from IBS. More problematic is the situation where a subject with IBD, in apparent remission, continues to complain of symptoms which, in aggregate, satisfy commonly employed criteria for the diagnosis of IBS. Access to methodologies, such the assay for levels of calprotectin in feces, now allows identification of ongoing inflammation in some such individuals and prompts appropriate therapy. More challenging is the IBD patient with persisting symptoms and no detectable evidence of inflammation; is this coincident IBS, IBS triggered by IBD or an even more subtle level of IBD activity unrecognized by available laboratory or imaging methods? Arguments can be advanced for each of these proposals; lacking definitive data, this issue remains unresolved. The occurrence of IBS-type symptoms in the IBD patient, together with some data suggesting a very subtle level of 'inflammation' or 'immune activation' in IBS, raises other questions: is IBS a prodromal form of IBD; and are IBS and IBD part of the spectrum of the same disease? All of the available evidence indicates that the answer to both these questions should be a resounding 'no'. Indeed, the whole issue of overlap between IBS and IBD should be declared moot given their differing pathophysiologies, contrasting natural histories and divergent treatment paths. The limited symptom repertoire of the gastrointestinal tract may well be fundamental to the apparent confusion that has, of late, bedeviled this area. PMID:26929782

  1. Pathology of immune reconstitution inflammatory syndrome in multiple sclerosis with natalizumab-associated progressive multifocal leukoencephalopathy.

    PubMed

    Metz, Imke; Radue, Ernst-Wilhelm; Oterino, Agustin; Kmpfel, Tania; Wiendl, Heinz; Schippling, Sven; Kuhle, Jens; Sahraian, Mohammad Ali; Gray, Francoise; Jakl, Veronika; Husler, Darius; Brck, Wolfgang

    2012-02-01

    Natalizumab is an approved medication for highly active multiple sclerosis (MS). Progressive multifocal leukoencephalopathy (PML) may occur as a severe side effect of this drug. Here, we describe pathological and radiological characteristics of immune reconstitution inflammatory syndrome (IRIS), which occurs in natalizumab-associated PML after the cessation of therapy, and we differentiate it from ongoing PML. Brain biopsy tissue and MRI scans from five MS patients with natalizumab-associated PML were analyzed and their histology compared with non-MS PML. Histology showed an extensive CD8-dominated T cell infiltrate and numerous macrophages within lesions, and in nondemyelinated white and grey matter, in four out of five cases. Few or no virally infected cells were found. This was indicative of IRIS as known from HIV patients with PML. Outstandingly high numbers of plasma cells were present as compared to non-MS PML and typical MS lesions. MRI was compatible with IRIS, revealing enlarging lesions with a band-like or speckled contrast enhancement either at the lesion edge or within lesions. Only the fifth patient showed typical PML pathology, with low inflammation and high numbers of virally infected cells. This patient showed a similar interval between drug withdrawal and biopsy (3.5 months) to the rest of the cohort (range 2.5-4 months). MRI could not differentiate between PML-associated IRIS and ongoing PML. We describe in detail the histopathology of IRIS in natalizumab-associated PML. PML-IRIS, ongoing PML infection, and MS exacerbation may be impossible to discern clinically alone. MRI may provide some clues for distinguishing different pathologies that can be differentiated histologically. In our individual cases, biopsy helped to clarify diagnoses in natalizumab-associated PML. PMID:22057786

  2. Rosuvastatin improves hepatopulmonary syndrome through inhibition of inflammatory angiogenesis of lung.

    PubMed

    Chang, Ching-Chih; Wang, Sun-Sang; Hsieh, Hsian-Guey; Lee, Wen-Shin; Chuang, Chiao-Lin; Lin, Han-Chieh; Lee, Fa-Yauh; Lee, Shou-Dong; Huang, Hui-Chun

    2015-09-01

    The hepatopulmonary syndrome (HPS) is characterized by hypoxia and increased intrapulmonary shunts in cirrhotic patients. Emerging evidence showed promising results of treating HPS by abolishment of intrapulmonary inflammation and angiogenesis. Rosuvastatin is a kind of 3-hydroxy-methyl-3-glutamyl coenzyme A reductase inhibitor. In addition to lipid-lowering effects, it has anti-inflammation and anti-angiogenesis properties. We postulated that rosuvastatin treatment can ameliorate HPS. Common bile duct ligation (CBDL) was applied in an experimental HPS animal model. CBDL rats received 2-week rosuvastatin (20 mg/kg/day) treatments from the fifteenth day after operation. The haemodynamic data, blood gas analysis, liver biochemistries, tumour necrosis factor-? (TNF-?) and vascular endothelial growth factor (VEGF) were examined after rosuvastatin treatment. The liver and lung tissues were dissected for histopathological studies and protein analyses. In the parallel groups, intrapulmonary shunts were determined. The haemodynamic and liver biochemistries were not changed after rosuvastatin treatment in CBDL rats, but the alveolar-arterial oxygen pressure gradient was significantly decreased, implying that HPS-induced hypoxia was reversed after rosuvastatin treatment. In addition, rosuvastatin treatment reduced intrapulmonary shunts and plasma levels of VEGF and TNF-?. Besides, the intrapulmonary protein expression of nuclear factor kappa B (NF-?B), VEGF receptor (VEGFR)-1,2 and Rho-associated A kinase were significantly down-regulated and the intrapulmonary angiogenesis was ameliorated. We concluded that rosuvastatin alleviates experimental HPS through blockade of pulmonary inflammatory angiogenesis via TNF-?/NF-?B and VEGF/Rho-associated A kinase pathways down-regulation. PMID:25940601

  3. Idiopathic Pyoderma Gangrenosum as a Novel Manifestation of the HIV Immune Reconstitution Inflammatory Syndrome: A Report of Three Cases.

    PubMed

    Nambudiri, Vinod E; Kersellius, Romona; Harp, Joanna; Maniar, J K; Maurer, Toby A

    2015-07-01

    The initiation of antiretroviral treatment for individuals with HIV may be accompanied by a paradoxical flare of underlying inflammatory diseases, the recurrence of dormant infections, or worsening of prior treated opportunistic infections, termed the immune reconstitution inflammatory syndrome (IRIS). Cutaneous manifestations of IRIS are common. Pyoderma gangrenosum is a neutrophilic dermatosis postulated to reflect disrupted innate immune regulation causing altered neutrophil chemotaxis. It is uncommonly reported in association with HIV. In this case series, we present three cases of IRIS manifesting with pyoderma gangrenosum in individuals with HIV from India and the United States to raise awareness of this previously undescribed presentation and discuss the treatment challenges in the management of these patients. PMID:26731836

  4. Inflammatory cytokines regulate secretion of VEGF and chemokines by human conjunctival fibroblasts: Role in dysfunctional tear syndrome.

    PubMed

    Nagineni, Chandrasekharam N; William, Abitha; Cherukuri, Aswini; Samuel, William; Hooks, John J; Detrick, Barbara

    2016-02-01

    Ocular surface inflammation is one of the primary mechanisms associated with dysfunctional tear syndrome (DTS), also known as dry eye disease. DTS, more prevalent in older populations, causes ocular discomfort and visual disturbance due to dryness on the surface layer in the eye. We used human conjunctival fibroblast cultures (HCJVF) to investigate the effects of inflammatory cytokines IFN-?, TNF-? and IL-1? (ITI) on the secretions of VEGF and chemokines. Our results demonstrate the elevated secretion of angiogenic VEGF molecules by ITI without affecting anti-angiogenic molecules, PEDF, endostatin, thrombospondin and sVEGF-R1. The secretion of interferon-? inducible chemokines, CXCL9, -10, -11 by HCJVF were significantly enhanced by ITI. Our in vitro study supports previously reported observations of elevated VEGF and chemokines in tear fluids of DTS patients, reiterating the role of inflammatory reactions in DTS. PMID:26615568

  5. The metalloproteinase ADAM17 and the epidermal growth factor receptor (EGFR) signaling drive the inflammatory epithelial response in Sjgren's syndrome.

    PubMed

    Sisto, Margherita; Lisi, Sabrina; D'Amore, Massimo; Lofrumento, Dario Domenico

    2015-05-01

    Primary Sjgren's syndrome (pSS) is a chronic autoimmune disorder that particularly compromises the function of exocrine glands. The pathogenetic mechanisms of this autoimmune exocrinopathy have not been fully elucidated. Since increasing evidence actually suggests that the epidermal growth factor receptor (EGFR) pathway has a major impact on the inflammatory/immune reactions of the epithelial cells, in the apparent effort of enhancing innate immune defense while opposing overactivation of pro-inflammatory functions, the focus of the work presented here is clarify whether the EGFR-extracellular-signal-regulated kinase (ERK) pathway plays a role in the pro-inflammatory responses mounted by pSS salivary gland epithelial cells (SGEC). Investigations revealed that the EGFR-mediated activation of the downstream effectors ERK1/2 in pSS SGEC appeared to require ADAM17-dependent release of the endogenous EGFR ligand amphiregulin and transactivation of the EGFR. Moreover, blockade of amphiregulin bioactivity using a neutralizing Ab significantly reduced EGFR transactivation and ERK1/2 phosphorylation. In addition, pSS SGEC treated with the specific ADAM17 inhibitor TAPI-1 and with the EGFR inhibitor AG1478 exhibited deactivated AREG/EGFR/ERK signaling pathway and reduced pro-inflammatory cytokines released. PMID:24664458

  6. Oxidative and Nitrosative Stress and Immune-Inflammatory Pathways in Patients with Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS)

    PubMed Central

    Morris, Gerwyn; Maes, Michael

    2014-01-01

    Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS) has been classified as a disease of the central nervous system by the WHO since 1969. Many patients carrying this diagnosis do demonstrate an almost bewildering array of biological abnormalities particularly the presence of oxidative and nitrosative stress (O&NS) and a chronically activated innate immune system. The proposal made herein is that once generated chronically activated O&NS and immune-inflammatory pathways conspire to generate a multitude of self-sustaining and self-amplifying pathological processes which are associated with the onset of ME/CFS. Sources of continuous activation of O&NS and immune-inflammatory pathways in ME/CFS are chronic, intermittent and opportunistic infections, bacterial translocation, autoimmune responses, mitochondrial dysfunctions, activation of the Toll-Like Receptor Radical Cycle, and decreased antioxidant levels. Consequences of chronically activated O&NS and immune-inflammatory pathways in ME/CFS are brain disorders, including neuroinflammation and brain hypometabolism / hypoperfusion, toxic effects of nitric oxide and peroxynitrite, lipid peroxidation and oxidative damage to DNA, secondary autoimmune responses directed against disrupted lipid membrane components and proteins, mitochondrial dysfunctions with a disruption of energy metabolism (e.g. compromised ATP production) and dysfunctional intracellular signaling pathways. The interplay between all of these factors leads to self-amplifying feed forward loops causing a chronic state of activated O&NS, immune-inflammatory and autoimmune pathways which may sustain the disease. PMID:24669210

  7. Prolonged REM sleep restriction induces metabolic syndrome-related changes: Mediation by pro-inflammatory cytokines.

    PubMed

    Venancio, Daniel Paulino; Suchecki, Deborah

    2015-07-01

    Chronic sleep restriction in human beings results in metabolic abnormalities, including changes in the control of glucose homeostasis, increased body mass and risk of cardiovascular disease. In rats, 96h of REM sleep deprivation increases caloric intake, but retards body weight gain. Moreover, this procedure increases the expression of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-?) and interleukin-6 (IL-6), which may be involved with the molecular mechanism proposed to mediate insulin resistance. The goal of the present study was to assess the effects of a chronic protocol of sleep restriction on parameters of energy balance (food intake and body weight), leptin plasma levels and its hypothalamic receptors and mediators of the immune system in the retroperitoneal adipose tissue (RPAT). Thirty-four Wistar rats were distributed in control (CTL) and sleep restriction groups; the latter was kept onto individual narrow platforms immersed in water for 18h/day (from 16:00h to 10:00h), for 21days (SR21). Food intake was assessed daily, after each sleep restriction period and body weight was measured daily, after the animals were taken from the sleep deprivation chambers. At the end of the 21day of sleep restriction, rats were decapitated and RPAT was obtained for morphological and immune functional assays and expression of insulin receptor substrate 1 (IRS-1) was assessed in skeletal muscle. Another subset of animals was used to evaluate blood glucose clearance. The results replicated previous findings on energy balance, e.g., increased food intake and reduced body weight gain. There was a significant reduction of RPAT mass (p<0.001), of leptin plasma levels and hypothalamic leptin receptors. Conversely, increased levels of TNF-? and IL-6 and expression of phosphorylated NF?-? in the RPAT of SR21 compared to CTL rats (p<0.01, for all parameters). SR21 rats also displayed reduced glucose clearance and IRS-1 expression than CTL rats (p<0.01). The present results indicated that 21days of sleep restriction by the platform method induced metabolic syndrome-related alterations that may be mediated by inflammation of the RPAT. PMID:25532784

  8. Genomic expression profiling across the pediatric systemic inflammatory response syndrome, sepsis, and septic shock spectrum

    PubMed Central

    Wong, Hector R.; Cvijanovich, Natalie; Allen, Geoffrey L.; Lin, Richard; Anas, Nick; Meyer, Keith; Freishtat, Robert J.; Monaco, Marie; Odoms, Kelli; Sakthivel, Bhuvaneswari; Shanley, Thomas P.

    2009-01-01

    Objectives To advance our biological understanding of pediatric septic shock, we measured the genome-level expression profiles of critically ill children representing the systemic inflammatory response syndrome (SIRS), sepsis, and septic shock spectrum. Design Prospective observational study involving microarray-based bioinformatics. Setting Multiple pediatric intensive care units in the United States. Patients Children ?10 years of age: 18 normal controls, 22 meeting criteria for SIRS, 32 meeting criteria for sepsis, and 67 meeting criteria for septic shock on day 1. The available day 3 samples included 20 patients still meeting sepsis criteria, 39 patients still meeting septic shock criteria, and 24 patients meeting the exclusive day 3 category, SIRS resolved. Interventions None other than standard care. Measurements and Main Results Longitudinal analyses were focused on gene expression relative to control samples and patients having paired day 1 and day 3 samples. The longitudinal analysis focused on up-regulated genes revealed common patterns of up-regulated gene expression, primarily corresponding to inflammation and innate immunity, across all patient groups on day 1. These patterns of up-regulated gene expression persisted on day 3 in patients with septic shock, but not to the same degree in the other patient classes. The longitudinal analysis focused on down-regulated genes demonstrated gene repression corresponding to adaptive immunity-specific signaling pathways and was most prominent in patients with septic shock on days 1 and 3. Gene network analyses based on direct comparisons across the SIRS, sepsis, and septic shock spectrum, and all available patients in the database, demonstrated unique repression of gene networks in patients with septic shock corresponding to major histocompatibility complex antigen presentation. Finally, analyses focused on repression of genes corresponding to zinc-related biology demonstrated that this pattern of gene repression is unique to patients with septic shock. Conclusions Although some common patterns of gene expression exist across the pediatric SIRS, sepsis, and septic shock spectrum, septic shock is particularly characterized by repression of genes corresponding to adaptive immunity and zinc-related biology. (Crit Care Med 2009; 37:15581566) PMID:19325468

  9. Epidemiology of the Systemic Inflammatory Response Syndrome (SIRS) in the Emergency Department

    PubMed Central

    Horeczko, Timothy; Green, Jeffrey P.; Panacek, Edward A.

    2014-01-01

    Introduction: Consensus guidelines recommend sepsis screening for adults with systemic inflammatory response syndrome (SIRS), but the epidemiology of SIRS among adult emergency department (ED) patients is poorly understood. Recent emphasis on cost-effective, outcomes-based healthcare prompts the evaluation of the performance of large-scale efforts such as sepsis screening. We studied a nationally representative sample to clarify the epidemiology of SIRS in the ED and subsequent category of illness. Methods: This was a retrospective analysis of ED visits by adults from 2007 to 2010 in the National Hospital Ambulatory Medical Care Survey (NHAMCS). We estimated the incidence of SIRS using initial ED vital signs and a Bayesian construct to estimate white blood cell count based on test ordering. We report estimates with Bayesian modified credible intervals (mCIs). Results: We used 103,701 raw patient encounters in NHAMCS to estimate 372,844,465 ED visits over the 4-year period. The moderate estimate of SIRS in the ED was 17.8% (95% mCI: 9.7 to 26%). This yields a national moderate estimate of approximately 16.6 million adult ED visits with SIRS per year. Adults with and without SIRS had similar demographic characteristics, but those with SIRS were more likely to be categorized as emergent in triage (17.7% versus 9.9%, p<0.001), stay longer in the ED (210 minutes versus 153 minutes, p<0.0001), and were more likely to be admitted (31.5% versus 12.5%, p<0.0001). Infection accounted for only 26% of SIRS patients. Traumatic causes of SIRS comprised 10% of presentations; other traditional categories of SIRS were rare. Conclusion: SIRS is very common in the ED. Infectious etiologies make up only a quarter of adult SIRS cases. SIRS may be more useful if modified by clinician judgment when used as a screening test in the rapid identification and assessment of patients with the potential for sepsis. [West J Emerg Med. 2014;15(3):329336.] PMID:24868313

  10. Serum Osteocalcin Is Associated with Inflammatory Factors in Metabolic Syndrome: A Population-Based Study in Chinese Males

    PubMed Central

    Liao, Ming; Huang, Lirong; Mao, Yan; Jiang, Yonghua; Yao, Ziting; Lin, Xinggu; Lu, Zheng; Wu, Chunlei; Qin, Xue; Zhang, Haiying; Mo, Zengnan

    2015-01-01

    Osteocalcin (OCN) was potentially associated with inflammatory factors, so we explored the metabolic role in this association in general population. Our findings suggest that OCN was positively associated with IgG while inversely associated with C3, both of which were probably mediated by obesity. Moreover, serum OCN was inversely associated with hsCRP in men with impaired fasting glucose, hyperglycemia, or metabolic syndrome, while its association with IgE was significantly observed in men with a normal metabolic profile. PMID:26578821

  11. Elevated plasma inflammatory mediators in post-polio syndrome: No association with long-term functional decline.

    PubMed

    Bickerstaffe, A; Beelen, A; Lutter, R; Nollet, F

    2015-12-15

    A key feature of post-polio syndrome (PPS) is progressive loss of muscle strength. In other chronic diseases systemic inflammation has been linked to muscle wasting. In this study plasma TNF-?, IL-6, IL-8, and leptin levels were significantly increased in PPS-patients compared to healthy controls. There was however no association between these raised systemic levels of inflammatory mediators and long-term decline in quadriceps strength or other clinical parameters. In conclusion, there is evidence for systemic inflammation in PPS, yet the relationship with clinical deterioration remains tenuous. PMID:26616886

  12. Serum Osteocalcin Is Associated with Inflammatory Factors in Metabolic Syndrome: A Population-Based Study in Chinese Males.

    PubMed

    Liao, Ming; Huang, Lirong; Mao, Yan; Jiang, Yonghua; Yao, Ziting; Lin, Xinggu; Lu, Zheng; Wu, Chunlei; Qin, Xue; Zhang, Haiying; Mo, Zengnan

    2015-01-01

    Osteocalcin (OCN) was potentially associated with inflammatory factors, so we explored the metabolic role in this association in general population. Our findings suggest that OCN was positively associated with IgG while inversely associated with C3, both of which were probably mediated by obesity. Moreover, serum OCN was inversely associated with hsCRP in men with impaired fasting glucose, hyperglycemia, or metabolic syndrome, while its association with IgE was significantly observed in men with a normal metabolic profile. PMID:26578821

  13. Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy: immune mechanisms and update on current therapies.

    PubMed

    van der Meché, F G; van Doorn, P A

    1995-05-01

    The relation between Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy is discussed. Most likely they represent parts of a continuum, arbitrarily separated by their time course. Within the concept of chronic inflammatory demyelinating polyneuropathy the presence of a monoclonal gammopathy of undetermined significance is discussed. The pathogenesis of inflammatory demyelinating polyneuropathies has not been elucidated yet, but involvement of the immune system has been firmly established. Preceding infections, especially with Campylobacter jejuni, and the analysis of antiganglioside antibodies lend new support to the hypothesis of molecular mimicry between epitopes on infectious agents and peripheral nerve constituents as one of the mechanisms in Guillain-Barré syndrome. In the future, a further classification of individual patients based on clinical, epidemiological, electrophysiological, pathological, microbiological, and immunological criteria may give a basis for more individualized treatment strategies. In Guillain-Barré syndrome the efficacy of high-dose intravenous immune globulin treatment was established after earlier positive findings with plasma exchange; immune globulins are easier to administer and may be superior. Even with these treatments it should be anticipated that one fourth of patients after immune globulin treatment and one third of patients after plasma exchange will show further deterioration in the first 2 weeks after onset of treatment. Despite this, just one treatment course usually is indicated in the individual patient, and no valid arguments were found to switch to the other treatment modality. In chronic inflammatory demyelinating polyneuropathy, prednisone, plasma exchange, and immune globulins are effective in a proportion of patients. The last two are equally effective. Patients may respond to one of these if a previous treatment failed, and here switching therapy may be effective due to the chronic course of the disease. Complexity and costs make plasma exchange the last choice. Whether prednisone or immune globulin is the first choice depends on the speed of recovery and the estimation of long-term loss of quality of life due to side effects of prednisone versus the costs of immune globulins. The mechanism of immune globulins in inflammatory polyneuropathies is discussed. There is evidence that idiotypic-antiidiotypic interaction may play a role, but several other mechanisms also may be involved. PMID:8968214

  14. Polyphenols rich fraction from Geoffroea decorticans fruits flour affects key enzymes involved in metabolic syndrome, oxidative stress and inflammatory process.

    PubMed

    Costamagna, M S; Zampini, I C; Alberto, M R; Cuello, S; Torres, S; Pérez, J; Quispe, C; Schmeda-Hirschmann, G; Isla, M I

    2016-01-01

    Geoffroea decorticans (chañar), is widely distributed throughout Northwestern Argentina. Its fruit is consumed as flour, arrope or hydroalcoholic beverage. The chañar fruits flour was obtained and 39 phenolic compounds were tentatively identified by HPLC-MS/MS(n). The compounds comprised caffeic acid glycosides, simple phenolics (protocatechuic acid and vanillic acid), a glycoside of vanillic acid, p-coumaric acid and its phenethyl ester as well as free and glycosylated flavonoids. The polyphenols enriched extract with and without gastroduodenal digestion inhibited enzymes associated with metabolic syndrome, including α-amylase, α-glucosidase, lipase and hydroxyl methyl glutaryl CoA reductase. The polyphenolic extract exhibited antioxidant activity by different mechanisms and inhibited the pro-inflammatory enzymes (ciclooxygenase, lipoxygenase and phospholipase A2). The polyphenolic extract did not showed mutagenic effect by Ames test against Salmonella typhimurium TA98 and TA100 strains. These findings add evidence that chañar fruit flour may be considered a functional food with preventive properties against diseases associated with oxidative stress, inflammatory mediators and metabolic syndrome. PMID:26212988

  15. Severe Pulmonary Suppuration with Infection-Induced Systemic Inflammatory Response Syndrome following Tongue Cancer Surgery in a Patient Undergoing Tocilizumab Therapy for Rheumatoid Arthritis

    PubMed Central

    Yamagata, Kenji; Shimojo, Nobutake; Ito, Hiroyuki; Ijima, Junya; Hasegawa, Shogo; Yanagawa, Toru; Mizutani, Taro; Bukawa, Hiroki

    2014-01-01

    A 65-year-old woman with rheumatoid arthritis treated by tocilizumab (TCZ) presented with tongue squamous cell carcinoma. While surgery was performed without any complications the aspiration pneumonia rapidly worsened by postoperative day 2 and severe pulmonary suppuration in the right lung field with infection-induced systemic inflammatory response syndrome (SIRS) was diagnosed. Antibiotic and respirator treatment improved her condition. The anti-inflammatory effect of TCZ may mask the symptoms and signs of severe infection with SIRS. PMID:24872899

  16. Severe Pulmonary Suppuration with Infection-Induced Systemic Inflammatory Response Syndrome following Tongue Cancer Surgery in a Patient Undergoing Tocilizumab Therapy for Rheumatoid Arthritis.

    PubMed

    Yamagata, Kenji; Shimojo, Nobutake; Ito, Hiroyuki; Ijima, Junya; Hasegawa, Shogo; Yanagawa, Toru; Mizutani, Taro; Bukawa, Hiroki

    2014-01-01

    A 65-year-old woman with rheumatoid arthritis treated by tocilizumab (TCZ) presented with tongue squamous cell carcinoma. While surgery was performed without any complications the aspiration pneumonia rapidly worsened by postoperative day 2 and severe pulmonary suppuration in the right lung field with infection-induced systemic inflammatory response syndrome (SIRS) was diagnosed. Antibiotic and respirator treatment improved her condition. The anti-inflammatory effect of TCZ may mask the symptoms and signs of severe infection with SIRS. PMID:24872899

  17. An Intense and Short-Lasting Burst of Neutrophil Activation Differentiates Early Acute Myocardial Infarction from Systemic Inflammatory Syndromes

    PubMed Central

    Maugeri, Norma; Rovere-Querini, Patrizia; Evangelista, Virgilio; Godino, Cosmo; Demetrio, Monica; Baldini, Mattia; Figini, Filippo; Coppi, Giovanni; Slavich, Massimo; Camera, Marina; Bartorelli, Antonio; Marenzi, Giancarlo; Campana, Lara; Baldissera, Elena; Sabbadini, Maria Grazia; Cianflone, Domenico; Tremoli, Elena; DAngelo, Armando; Manfredi, Angelo A.; Maseri, Attilio

    2012-01-01

    Background Neutrophils are involved in thrombus formation. We investigated whether specific features of neutrophil activation characterize patients with acute coronary syndromes (ACS) compared to stable angina and to systemic inflammatory diseases. Methods and Findings The myeloperoxidase (MPO) content of circulating neutrophils was determined by flow cytometry in 330 subjects: 69 consecutive patients with acute coronary syndromes (ACS), 69 with chronic stable angina (CSA), 50 with inflammation due to either non-infectious (acute bone fracture), infectious (sepsis) or autoimmune diseases (small and large vessel systemic vasculitis, rheumatoid arthritis). Four patients have also been studied before and after sterile acute injury of the myocardium (septal alcoholization). One hundred thirty-eight healthy donors were studied in parallel. Neutrophils with normal MPO content were 96% in controls, >92% in patients undergoing septal alcoholization, 91% in CSA patients, but only 35 and 30% in unstable angina and AMI (STEMI and NSTEMI) patients, compared to 80%, 75% and 2% of patients with giant cell arteritis, acute bone fracture and severe sepsis. In addition, in 32/33 STEMI and 9/21 NSTEMI patients respectively, 20% and 12% of neutrophils had complete MPO depletion during the first 4 hours after the onset of symptoms, a feature not observed in any other group of patients. MPO depletion was associated with platelet activation, indicated by P-selectin expression, activation and transactivation of leukocyte ?2-integrins and formation of platelet neutrophil and -monocyte aggregates. The injection of activated platelets in mice produced transient, P-selectin dependent, complete MPO depletion in about 50% of neutrophils. Conclusions ACS are characterized by intense neutrophil activation, like other systemic inflammatory syndromes. In the very early phase of acute myocardial infarction only a subpopulation of neutrophils is massively activated, possibly via platelet-P selectin interactions. This paroxysmal activation could contribute to occlusive thrombosis. PMID:22761804

  18. Chylous Ascites in a Patient with HIV/AIDS: A Late Complication of Mycobacterium avium Complex-Immune Reconstitution Inflammatory Syndrome

    PubMed Central

    Shaik, Imam H.; Khan, Rumana; Shah, Saira; Syed, Amer K.; Lintz, David

    2014-01-01

    Chylous ascites is very rare in HIV/AIDS and its association with Mycobacterium avium complex-immune reconstitution inflammatory syndrome (MAC-IRIS) has been rarely reported. Here, we report a case of a young African-American male who developed chylous ascites as a late sequela to immune reconstitution inflammatory syndrome while on treatment for MAC. Antiretroviral drug-naive patients who start HAART in close proximity to the diagnosis of an opportunistic infection and have a rapid decline in HIV RNA level should be monitored for development of IRIS. Although the long term prognosis is poor, early diagnosis and treatment help to improve quality of life. PMID:25478257

  19. Ulcerating type 1 lepra reaction mimicking lazarine leprosy: an unusual presentation of immune reconstitution inflammatory syndrome in an HIV-infected patient.

    PubMed

    Bhat, Ramesh; Pinto, Malcolm; Dandakeri, Sukumar; Kambil, Srinath

    2013-12-01

    Leprosy maybe "unmasked" in the context of immune reconstitution inflammatory syndrome and treating dermatologists, particularly in highly endemic areas for Hansen's disease, need to be cognizant to this possibility. It may also reflect emergence of a previously clinically silent infection in the course of immunologic restoration. PMID:24216029

  20. Inflammatory Cytokine Profile Associated with Metabolic Syndrome in Adult Patients with Type 1 Diabetes

    PubMed Central

    Ferreira-Hermosillo, Aldo; Molina-Ayala, Mario; Ramrez-Rentera, Claudia; Vargas, Guadalupe; Gonzalez, Baldomero; Isibasi, Armando; Archundia-Riveros, Irma; Mendoza, Victoria

    2015-01-01

    Objective. To compare the serum concentration of IL-6, IL-10, TNF, IL-8, resistin, and adiponectin in type 1 diabetic patients with and without metabolic syndrome and to determine the cut-off point of the estimated glucose disposal rate that accurately differentiated these groups. Design. We conducted a cross-sectional evaluation of all patients in our type 1 diabetes clinic from January 2012 to January 2013. Patients were considered to have metabolic syndrome when they fulfilled the joint statement criteria and were evaluated for clinical, biochemical, and immunological features. Methods. We determined serum IL-6, IL-8, IL-10, and TNF with flow cytometry and adiponectin and resistin concentrations with enzyme linked immunosorbent assay in patients with and without metabolic syndrome. We also compared estimated glucose disposal rate between groups. Results. We tested 140 patients. Forty-four percent fulfilled the metabolic syndrome criteria (n = 61), 54% had central obesity, 30% had hypertriglyceridemia, 29% had hypoalphalipoproteinemia, and 19% had hypertension. We observed that resistin concentrations were higher in patients with MS. Conclusion. We found a high prevalence of MS in Mexican patients with T1D. The increased level of resistin may be related to the increased fat mass and could be involved in the development of insulin resistance. PMID:26273680

  1. Anti-inflammatory effect of exercise, via reduced leptin levels, in obese women with Down syndrome.

    PubMed

    Ordoez, Francisco J; Fornieles-Gonzalez, Gabriel; Camacho, Alejandra; Rosety, Miguel A; Rosety, Ignacio; Diaz, Antonio J; Rosety-Rodriguez, Manuel

    2013-06-01

    Recent studies have reported that obese young people with Down syndrome suffer from low-grade systemic inflammation. Whereas this condition may be improved in the general population by regular exercise, the problem has received no attention in the case of people with intellectual disability. Therefore, the authors' aim was to assess the influence of aerobic training on plasma adipokines in obese women with Down syndrome. Twenty obese young women with Down syndrome volunteered for this study, 11 of whom were randomly assigned to a 10-wk aerobic-training program. They attended 3 sessions/wk, which consisted of warm-up exercises followed by the main activity on a treadmill (30-40 min) at a work intensity of 55-65% of peak heart rate and ended with a cooling-down period. The control group included 9 women with Down syndrome matched for age, sex, and body-mass index. Fat-mass percentage and distribution were measured, and plasma adipokine levels (leptin and adiponectin) were assessed. In addition, each participant performed a maximal graded continuous treadmill exercise test. These parameters were assessed pre- and postintervention. Aerobic training produced a significant increase in participants' maximal oxygen uptake (20.2 5.8 vs.23.7 6.3 ml kg-1 min-1; p < .001), and plasma leptin levels were significantly reduced in the intervention group (54.2 6.7 vs.45.7 6.1 ng/ml; p = .026). Further significant correlations between plasma leptin and indices of obesity were found. In contrast, no significant changes were found in adiponectin levels (p > .05). None of the tested parameters changed in the control group. In conclusion, a 10-week training program reduced leptin levels in obese young women with Down syndrome. PMID:23307488

  2. A novel experimental model of Cryptococcus neoformans-related immune reconstitution inflammatory syndrome (IRIS) provides insights into pathogenesis.

    PubMed

    Eschke, Maria; Piehler, Daniel; Schulze, Bianca; Richter, Tina; Grahnert, Andreas; Protschka, Martina; Mller, Uwe; Khler, Gabriele; Hfling, Corinna; Rossner, Steffen; Alber, Gottfried

    2015-12-01

    Antiretroviral therapy (ART) has yielded major advances in fighting the HIV pandemic by restoring protective immunity. However, a significant proportion of HIV patients co-infected with the opportunistic fungal pathogen Cryptococcus neoformans paradoxically develops a life-threatening immune reconstitution inflammatory syndrome (IRIS) during antiretroviral therapy. Despite several clinical studies, the underlying pathomecha-nisms are poorly understood. Here, we present the first mouse model of cryptococcal IRIS that allows for a detailed analysis of disease development. Lymphocyte-deficient RAG-1(-/-) mice are infected with C. neoformans and 4 weeks later adoptively transferred with purified CD4(+) T cells. Reconstitution of CD4(+) T cells is sufficient to induce a severe inflammatory disease similar to clinical IRIS in C. neoformans-infected RAG-1(-/-) mice of different genetic backgrounds and immunological phenotypes (i.e. C57BL/6 and BALB/c). Multiorgan inflammation is accompanied by a systemic release of distinct proinflammatory cytokines, i.e. IFN-?, IL-6, and TNF-?. IRIS development is characterized by infection-dependent activation of donor CD4(+) T cells, which are the source of IFN-?. Interestingly, IFN-?-mediated effects are not required for disease induction. Taken together, this novel mouse model of cryptococcal IRIS provides a useful tool to verify potential mechanisms of pathogenesis, revealing targets for diagnosis and therapeutic interventions. PMID:26381487

  3. Immunohistochemical expression of MPO, CD163 and VEGF in inflammatory cells in acute respiratory distress syndrome: a case report

    PubMed Central

    Maretta, Milan; Toth, Stefan; Jonecova, Zuzana; Kruzliak, Peter; Kubatka, Peter; Pingorova, Stanislava; Vesela, Jarmila

    2014-01-01

    Acute respiratory distress syndrome (ARDS) is a serious medical condition occurring in patients with polytrauma, pulmonary or non-pulmonary sepsis, pneumonia and many other circumstances. It causes inflammation of the lung parenchyma leading to impaired gas exchange with a systemic release of inflammatory mediators, causing consequential lung tissue injury, hypoxemia and frequently multiple organ failure. The aim of current study was to describe expression of inflammatory markers (myeloperoxidase, CD163 and vascular endothelial growth factor) by the cells in acute phase of ARDS. The lung samples of a 20-year-old man who had suffered a serious motorbike accident were obtained for histological examination. He died on the seventh day as a consequence of respiratory failure. Our results imply that expression of CD163 was restricted to activated alveolar macrophages and monocytes. Immunopositivityof MPO was observed in neutrophil granulocytes within lung alveoli and lung blood vessels. Myeloperoxidase positivity was observed in alveolar macrophages, too. Vascular endothelial growth factor was expressed in cytoplasm of neutrophil granulocytes, monocytes, small-sized alveolar macrophages and type II pneumocytes localized mostly inside lung alveoli. On the contrary, no positivity was observed in lung endothelial cells of blood vessels. PMID:25120850

  4. Latest Study on the Relationship between Pathological Process of Inflammatory Injury and the Syndrome of Spleen Deficiency and Fluid Retention in Alzheimer's Disease

    PubMed Central

    Yu, Beibei; Zhou, Chunxiang; Zhang, Jiangyuan; Ling, Yun; Hu, Qianfeng; Wang, Yi; Bai, Kangkang

    2014-01-01

    Inflammation exists throughout the incidence and progression of Alzheimer's disease (AD). Traditional Chinese medicine (TCM) differentiates the pathogenesis of AD as kidney essence deficiency and qi and blood deficiency as well as blood stasis in syndromes, whose action mechanisms are all associated with the intervention in its inflammatory process. Our preliminary studies both in clinic and in vitro have demonstrated that the syndrome of spleen deficiency and fluid retention has also been an important pathogenesis for the incidence and development of AD. Hence, the paper aims to further illustrate the correlation between inflammatory process in AD and the syndrome of spleen deficiency and fluid retention, laying solid foundation for the application of invigorating the spleen and eliminating the dampness in clinic, and enriching the theoretical connotation for AD prevention and treatment in TCM. PMID:24799943

  5. Functional Outcomes and Efficiency of Rehabilitation in a National Cohort of Patients with Guillain - Barr Syndrome and Other Inflammatory Polyneuropathies

    PubMed Central

    Alexandrescu, Roxana; Siegert, Richard John; Turner-Stokes, Lynne

    2014-01-01

    Objectives To describe functional outcomes, care needs and cost-efficiency of hospital rehabilitation for a UK cohort of inpatients with complex rehabilitation needs arising from inflammatory polyneuropathies. Subjects and Setting 186 patients consecutively admitted to specialist neurorehabilitation centres in England with Guillain-Barr Syndrome (n?=?118 (63.4%)) or other inflammatory polyneuropathies, including chronic inflammatory demyelinating polyneuropathy (n?=?15 (8.1%) or critical illness neuropathy (n?=?32 (17.2%)). Methods Cohort analysis of data from the UK Rehabilitation Outcomes Collaborative national clinical dataset. Outcome measures include the UK Functional Assessment Measure, Northwick Park Dependency Score (NPDS) and Care Needs Assessment (NPCNA). Patients were analysed in three groups of dependency based on their admission NPDS score: low (NPDS<10), medium (NPDS 1024) and high (NPDS ?25). Cost-efficiency was measured as the time taken to offset the cost of rehabilitation by savings in NPCNA-estimated costs of on-going care in the community. Results The mean rehabilitation length of stay was 72.2 (sd?=?66.6) days. Significant differences were seen between the diagnostic groups on admission, but all showed significant improvements between admission and discharge, in both motor and cognitive function (p<0.0001). Patients who were highly dependent on admission had the longest lengths of stay (mean 97.0 (SD 79.0) days), but also showed the greatest reduction in on-going care costs (1049 per week (SD 994)), so that overall they were the most cost-efficient to treat. Conclusions Patients with polyneuropathies have both physical and cognitive disabilities that are amenable to change with rehabilitation, resulting in significant reduction in on-going care-costs, especially for highly dependent patients. PMID:25402491

  6. Mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways.

    PubMed

    Morris, Gerwyn; Maes, Michael

    2014-03-01

    Myalgic encephalomyelitis/chronic fatigue syndrome (ME/cfs) is classified by the World Health Organization as a disorder of the central nervous system. ME/cfs is an neuro-immune disorder accompanied by chronic low-grade inflammation, increased levels of oxidative and nitrosative stress (O&NS), O&NS-mediated damage to fatty acids, DNA and proteins, autoimmune reactions directed against neoantigens and brain disorders. Mitochondrial dysfunctions have been found in ME/cfs, e.g. lowered ATP production, impaired oxidative phosphorylation and mitochondrial damage. This paper reviews the pathways that may explain mitochondrial dysfunctions in ME/cfs. Increased levels of pro-inflammatory cytokines, such as interleukin-1 and tumor necrosis factor-?, and elastase, and increased O&NS may inhibit mitochondrial respiration, decrease the activities of the electron transport chain and mitochondrial membrane potential, increase mitochondrial membrane permeability, interfere with ATP production and cause mitochondrial shutdown. The activated O&NS pathways may additionally lead to damage of mitochondrial DNA and membranes thus decreasing membrane fluidity. Lowered levels of antioxidants, zinc and coenzyme Q10, and ?3 polyunsaturated fatty acids in ME/cfs may further aggravate the activated immuno-inflammatory and O&NS pathways. Therefore, it may be concluded that immuno-inflammatory and O&NS pathways may play a role in the mitochondrial dysfunctions and consequently the bioenergetic abnormalities seen in patients with ME/cfs. Defects in ATP production and the electron transport complex, in turn, are associated with an elevated production of superoxide and hydrogen peroxide in mitochondria creating adaptive and synergistic damage. It is argued that mitochondrial dysfunctions, e.g. lowered ATP production, may play a role in the onset of ME/cfs symptoms, e.g. fatigue and post exertional malaise, and may explain in part the central metabolic abnormalities observed in ME/cfs, e.g. glucose hypometabolism and cerebral hypoperfusion. PMID:24557875

  7. Inflammatory myofibroblastic bladder tumor in a patient with wolf-hirschhorn syndrome.

    PubMed

    Marte, Antonio; Indolfi, Paolo; Ficociello, Carmine; Russo, Daniela; Oreste, Matilde; Bottigliero, Gaetano; Gualdiero, Giovanna; Barone, Ciro; Vigliar, Elena; Indolfi, Cristiana; Casale, Fiorina

    2013-01-01

    Inflammatory myofibroblastic tumor (IMT) is a rare neoplasm described in several tissues and organs including genitourinary system, lung, head, and neck. The etiology of IMT is contentious, and whether it is a postinflammatory process or a true neoplasm remains controversial. To our knowledge, we report the first reported case of IMT of urinary bladder in a pediatric patient with Wolf-Hirschhorn (WHS). We also review the literature about patients with associated neoplasia. PMID:24024066

  8. Effects of Acupuncture Knife on Inflammatory Factors and Pain in Third Lumbar Vertebrae Transverse Process Syndrome Model Rats

    PubMed Central

    Yu, Jia Ni; Guo, Chang Qing; Hu, Bo; Liu, Nai Gang; Sun, Hong Mei; Xu, Hong; Wu, Hai Xia; Guo, Yan; Liang, Chu Xi; Chen, Zhan Xia; Li, Xiao Hong

    2014-01-01

    The aim of this paper was to explore the long-term effects and pain relief mechanism of acupuncture knife on third lumbar vertebrae (L3) transverse process syndrome. Forty SD rats were randomized into control, model, electroacupuncture (EA), and acupuncture knife (AK) group. Except control rats, other rats were subjected to an operation to emulate L3 transverse process syndrome. Fourteen days after the operation, EA and AK rats were given electroacupuncture and acupuncture knife treatments, respectively. Fifty-six days after the operation, enzyme-linked immunosorbent assay was used to measure substance P (SP), 5-hydroxytryptamine (5-HT), interleukin-1? (IL-1?), interleukin-10 (IL-10), tumor necrosis factor-? (TNF-?), and transforming growth factor-? (TGF-?) in peripheral blood. The tail flick test was used to observe pain threshold. We found that rats with the simulation operation had significantly higher levels of SP, 5-HT, IL-1, IL-10, TNF-?, and TGF-?, while the AK rats had lower levels. In addition, the pain threshold of AK rats was similar to that of control rats. AK pretreatment could alleviate pain through modulating inflammatory response. PMID:25544854

  9. Lung inflammatory response syndrome after cardiac-operations and treatment of lornoxicam

    PubMed Central

    Tsakiridis, Kosmas; Mpakas, Andreas; Kesisis, George; Arikas, Stamatis; Argyriou, Michael; Siminelakis, Stavros; Katsikogiannis, Nikolaos; Kougioumtzi, Ioanna; Tsiouda, Theodora; Sarika, Eirini; Katamoutou, Ioanna; Zarogoulidis, Konstantinos

    2014-01-01

    The majority of patients survive after extracorporeal circulation without any clinically apparent deleterious effects. However, disturbances exist in various degrees sometimes, which indicate the harmful effects of cardiopulmonary bypass (CPB) in the body. Several factors during extracorporeal circulation either mechanical dependent (exposure of blood to non-biological area) or mechanical independent (surgical wounds, ischemia and reperfusion, alteration in body temperature, release of endotoxins) have been shown to trigger the inflammatory reaction of the body. The complement activation, the release of cytokines, the leukocyte activation and accumulation as well as the production of several “mediators” such as oxygen free radicals, metabolites of arachidonic acid, platelet activating factors (PAF), nitric acid, and endothelin. The investigation continues today on the three metabolites of lornoxicam (the hydroxylated metabolite and two other metabolites of unknown chemical composition) to search for potential new pharmacological properties and activities. PMID:24672703

  10. Sjgren's syndrome autoantibodies provoke changes in gene expression profiles of inflammatory cytokines triggering a pathway involving TACE/NF-?B.

    PubMed

    Lisi, Sabrina; Sisto, Margherita; Lofrumento, Dario Domenico; D'Amore, Massimo

    2012-04-01

    We explore the association of the inflammatory gene expression profile observed in the chronic inflammatory autoimmune disorder Sjgren's syndrome (SS) with changes in TNF-? converting enzyme (TACE), tumor necrosis factor (TNF)-? and nuclear factor (NF)-?B levels showing that pathways that include TNF-? signaling converge on NF-?B contributing to exacerbate the diseases. The treatment of human salivary gland epithelial cells (SGECs) with SS anti-Ro/SSA autoantibodies (Abs) result in a progressive increase in NF-?B-DNA binding, that includes a marked enhancement in NF-?B subunit p65 protein-DNA binding. A human cytokine multi-analyte array demonstrated that the NF-?B proinflammatory target genes, increased by anti-Ro/SSA Abs treatment, includes CXC chemokines (CXCL1, CXCL6 and CXCL9), CC chemokines (CCL2, CCL13 and CCL20), interleukins (IL-1?, IL-1?, IL-1F8, IL-6, IL-8, IL-9, IL-13, IL-17 and IL-22) and their receptors (IL-1RN, IL-10R?, IL-13R?, CCR1, CCR2, CCR3, CCR4 and CXCR1). Blockade of TACE through the use of the specific inhibitor TAPI-1 regulates proinflammatory cytokines production in SGEC treated with anti-Ro/SSA Abs inhibiting NF-?B nuclear translocation and activation. To further investigate the role of NF-?B on anti-Ro/SSA Abs-determined proinflammatory gene expression, we used the inhibitory protein I?B-? dominant negative super-repressor as inhibitor of NF-?B-DNA binding, demonstrating that transfection with dominant-negative I?B-? in anti-Ro/SSA-treated SGEC determined a marked reduction of proinflammatory cytokines gene expression. Although further studies are needed to clarify the mechanisms underlying SS, our results demonstrate that SS Abs exert their pathogenic effects via triggering the TACE/TNF-?/NF-?B axis. PMID:22157716

  11. Daily cytokine fluctuations, driven by leptin, are associated with fatigue severity in chronic fatigue syndrome: evidence of inflammatory pathology

    PubMed Central

    2013-01-01

    Background Chronic fatigue syndrome (CFS) is a debilitating disorder characterized by persistent fatigue that is not alleviated by rest. The lack of a clearly identified underlying mechanism has hindered the development of effective treatments. Studies have demonstrated elevated levels of inflammatory factors in patients with CFS, but findings are contradictory across studies and no biomarkers have been consistently supported. Single time-point approaches potentially overlook important features of CFS, such as fluctuations in fatigue severity. We have observed that individuals with CFS demonstrate significant day-to-day variability in their fatigue severity. Methods Therefore, to complement previous studies, we implemented a novel longitudinal study design to investigate the role of cytokines in CFS pathophysiology. Ten women meeting the Fukuda diagnostic criteria for CFS and ten healthy age- and body mass index (BMI)-matched women underwent 25 consecutive days of blood draws and self-reporting of symptom severity. A 51-plex cytokine panel via Luminex was performed for each of the 500 serum samples collected. Our primary hypothesis was that daily fatigue severity would be significantly correlated with the inflammatory adipokine leptin, in the women with CFS and not in the healthy control women. As a post-hoc analysis, a machine learning algorithm using all 51 cytokines was implemented to determine whether immune factors could distinguish high from low fatigue days. Results Self-reported fatigue severity was significantly correlated with leptin levels in six of the participants with CFS and one healthy control, supporting our primary hypothesis. The machine learning algorithm distinguished high from low fatigue days in the CFS group with 78.3% accuracy. Conclusions Our results support the role of cytokines in the pathophysiology of CFS. PMID:23570606

  12. Levels of Neopterin and other Inflammatory Markers in Obese and Non-Obese Patients with Polycystic Ovary Syndrome

    PubMed Central

    Agacayak, Elif; Tunc, Senem Yaman; Sak, Sibel; Basaranoglu, Serdar; Yksel, Hatice; Turgut, Abdulkadir; Gul, Talip

    2015-01-01

    Background We aimed to measure the levels of inflammatory markers and neopterin in obese and non-obese patients with PCOS by using 2 separate control groups with matching body mass index (BMI). Material/Methods A total of 60 women of reproductive age with (n=30) and without (n=30) PCOS were included in this study. Based on their BMI, patients with PCOS were divided into 2 groups as obese (n=15) and non-obese (n=15) PCOS groups. In addition, 2 BMI-matched control groups were formed. Neopterin, tumor necrosis factor-? (TNF-?), interleukin-6 (IL-6), C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (N/L ratio), and vitamin B12 were assessed by complete blood count. Results No significant difference was found between patients with PCOS and control subjects in neopterin, IL-6, TNF-?, and CRP levels. However, N/L ratio levels were significantly higher (p 0.045) and vitamin B12 levels were significantly lower (p 0.033) in patients with PCOS compared to control subjects. No statistically significant difference was found between obese and non-obese patients with PCOS and control subjects in neopterin, IL-6, TNF-?, and N/L ratio levels. However, CRP levels were significantly higher in obese patients with PCOS compared to obese control subjects (p 0.007). Conclusions It can be concluded that inflammatory activity is increased in patients with PCOS, can lead to an increased risk for atherosclerosis, and this increase is not caused by obesity but rather by the polycystic ovary syndrome itself. However, studies with larger sample sizes are needed in this area. PMID:26292090

  13. [Multifocal inflammatory syndrome after invasive infection due to an M1 strain of Streptococcus pyogenes].

    PubMed

    Filleron, A; Marchandin, H; Rodière, M; Jeziorski, E

    2010-09-01

    We report on a case of Streptococcus pyogenes invasive disease with toxic shock syndrome due to an M1 strain producing SpeA and SmeZ superantigenic toxins. Post-streptococcal sequelae included several episodes of reactive arthritis and orchitis whose outcome was favorable with corticosteroid therapy. Invasive streptococcal infections are increasingly reported and may associate septic, toxinic, and immunological diseases. High-grade systemic inflammation may induce nonsuppurative complications and autoimmune diseases by molecular mimicry. Among them, reactive arthritis has been recognized as a separate entity from acute rheumatic fever and post-streptococcal orchitis has not been described before. Treatment should be quickly started and should be effective on the etiologic agent but also on its toxins due to the severity of the invasive infections associated with the spread of highly virulent bacterial clones and the potential development of multifocal nonsuppurative sequelae. PMID:20709506

  14. Clinical Manifestations of Kaposi Sarcoma Herpesvirus Lytic Activation: Multicentric Castleman Disease (KSHVMCD) and the KSHV Inflammatory Cytokine Syndrome

    PubMed Central

    Polizzotto, Mark N.; Uldrick, Thomas S.; Hu, Duosha; Yarchoan, Robert

    2012-01-01

    Soon after the discovery of Kaposi sarcoma (KS)-associated herpesvirus (KSHV), it was appreciated that this virus was associated with most cases of multicentric Castleman disease (MCD) arising in patients infected with human immunodeficiency virus. It has subsequently been recognized that KSHVMCD is a distinct entity from other forms of MCD. Like MCD that is unrelated to KSHV, the clinical presentation of KSHVMCD is dominated by systemic inflammatory symptoms including fevers, cachexia, and laboratory abnormalities including cytopenias, hypoalbuminemia, hyponatremia, and elevated C-reactive protein. Pathologically KSHVMCD is characterized by polyclonal, IgM-lambda restricted plasmacytoid cells in the intrafollicular areas of affected lymph nodes. A portion of these cells are infected with KSHV and a sizable subset of these cells express KSHV lytic genes including a viral homolog of interleukin-6 (vIL-6). Patients with KSHVMCD generally have elevated KSHV viral loads in their peripheral blood. Production of vIL-6 and induction of human (h) IL-6 both contribute to symptoms, perhaps in combination with overproduction of IL-10 and other cytokines. Until recently, the prognosis of patients with KSHVMCD was poor. Recent therapeutic advances targeting KSHV-infected B cells with the anti-CD20 monoclonal antibody rituximab and utilizing KSHV enzymes to target KSHV-infected cells have substantially improved patient outcomes. Recently another KSHV-associated condition, the KSHV inflammatory cytokine syndrome (KICS) has been described. Its clinical manifestations resemble those of KSHVMCD but lymphadenopathy is not prominent and the pathologic nodal changes of KSHVMCD are absent. Patients with KICS exhibit elevated KSHV viral loads and elevation of vIL-6, homolog of human interleukin-6 and IL-10 comparable to those seen in KSHVMCD; the cellular origin of these is a matter of investigation. KICS may contribute to the inflammatory symptoms seen in some patients with severe KS or primary effusion lymphoma. Additional research is needed to better define the clinical spectrum of KICS and its relationship to KSHVMCD. In additional, research is needed to better understand the pathogenesis and epidemiology of both KICS and KSHVMCD, as well as the optimal therapy for both of these disorders. PMID:22403576

  15. Opportunistic infections and immune reconstitution inflammatory syndrome in HIV-1-infected adults in the combined antiretroviral therapy era: a comprehensive review.

    PubMed

    Manzardo, Christian; Guardo, Alberto C; Letang, Emilio; Plana, Montserrat; Gatell, Jose M; Miro, Jose M

    2015-06-01

    Despite the availability of effective combined antiretroviral treatment, many patients still present with advanced HIV infection, often accompanied by an AIDS-defining disease. A subgroup of patients starting antiretroviral treatment under these clinical conditions may experience paradoxical worsening of their disease as a result of an exaggerated immune response towards an active (but also subclinical) infectious agent, despite an appropriate virological and immunological response to the treatment. This clinical condition, known as immune reconstitution inflammatory syndrome, may cause significant morbidity and even mortality if it is not promptly recognized and treated. This review updates current knowledge about the incidence, diagnostic criteria, risk factors, clinical manifestations, and management of opportunistic infections and immune reconstitution inflammatory syndrome in the combined antiretroviral treatment era. PMID:25860288

  16. Inherited STING-activating mutation underlies a familial inflammatory syndrome with lupus-like manifestations

    PubMed Central

    Jeremiah, Nadia; Neven, Bndicte; Gentili, Matteo; Callebaut, Isabelle; Maschalidi, Sophia; Stolzenberg, Marie-Claude; Goudin, Nicolas; Frmond, Marie-Louis; Nitschke, Patrick; Molina, Thierry J.; Blanche, Stphane; Picard, Capucine; Rice, Gillian I.; Crow, Yanick J.; Manel, Nicolas; Fischer, Alain; Bader-Meunier, Brigitte; Rieux-Laucat, Frdric

    2014-01-01

    Innate immunity to viral infection involves induction of the type I IFN response; however, dysfunctional regulation of this pathway leads to inappropriate inflammation. Here, we evaluated a nonconsanguineous family of mixed European descent, with 4 members affected by systemic inflammatory and autoimmune conditions, including lupus, with variable clinical expression. We identified a germline dominant gain-of-function mutation in TMEM173, which encodes stimulator of type I IFN gene (STING), in the affected individuals. STING is a key signaling molecule in cytosolic DNA-sensing pathways, and STING activation normally requires dimerization, which is induced by 2?3? cyclic GMP-AMP (cGAMP) produced by the cGAMP synthase in response to cytosolic DNA. Structural modeling supported constitutive activation of the mutant STING protein based on stabilized dimerization. In agreement with the model predictions, we found that the STING mutant spontaneously localizes in the Golgi of patient fibroblasts and is constitutively active in the absence of exogenous 2?3?-cGAMP in vitro. Accordingly, we observed elevated serum IFN activity and a type I IFN signature in peripheral blood from affected family members. These findings highlight the key role of STING in activating both the innate and adaptive immune responses and implicate aberrant STING activation in features of human lupus. PMID:25401470

  17. Partial recovery after severe immune reconstitution inflammatory syndrome in a multiple sclerosis patient with progressive multifocal leukoencephalopathy.

    PubMed

    Calvi, Alberto; De Riz, Milena; Pietroboni, Anna M; Ghezzi, Laura; Maltese, Virginia; Arighi, Andrea; Fumagalli, Giorgio G; Jacini, Francesca; Donelli, Carlotta; Comi, Giancarlo; Galimberti, Daniela; Scarpini, Elio

    2014-01-01

    Progressive multifocal leukoencephalopathy (PML) is a rare and severe complication of natalizumab therapy in patients with multiple sclerosis and it may be accompanied by immune reconstitution inflammatory syndrome (IRIS). Here, we describe a case of abnormally severe IRIS, which occurred 2 months after natalizumab-associated PML in a 38-year-old woman affected by multiple sclerosis. The patient was John Cunningham virus-positive and was treated for 21 months when she developed PML. The subsequent IRIS diffusely afflicted the brain, producing edema and signs of intracranial hypertension, with a clinically severe form compromising the state of consciousness, requiring intensive care and high-dosage steroid treatment. Nevertheless, she survived and partially recovered. There is still difficulty in differentiating PML progression from IRIS onset and there is not a clear description in the literature about different clinical forms of IRIS, prognostic factors and guidelines to properly treat this complication in order to reduce the residual disability of the patient surviving this treatment complication. PMID:24341880

  18. Acute Kidney Injury Induced by Systemic Inflammatory Response Syndrome is an Avid and Persistent Sodium-Retaining State

    PubMed Central

    Vitorio, Daniel; Maciel, Alexandre Toledo

    2014-01-01

    Acute kidney injury (AKI) is a frequent complication of the systemic inflammatory response syndrome (SIRS), which is triggered by many conditions in the intensive care unit, including different types of circulatory shock. One under-recognized characteristic of the SIRS-induced AKI is its avidity for sodium retention, with progressive decreases in urinary sodium concentration (NaU) and its fractional excretion (FENa). This phenomenon occurs in parallel with increases in serum creatinine, being only transitorily mitigated by diuretic use. In the present case, we report a situation of two consecutive shocks: the first shock is hemorrhagic in origin and then the second shock is a septic one in the same patient. The SIRS and AKI triggered by the first shock were not completely solved when the second shock occurred. This could be viewed as a persistent avid sodium-retaining state, which may be appreciated even during renal replacement therapy (in the absence of complete anuria) and that usually solves only after complete AKI and SIRS resolution. We suggest that decreases in NaU and FENa are major characteristics of SIRS-induced AKI, irrespective of the primary cause, and may serve as additional monitoring tools in its development and resolution. PMID:25309760

  19. Porcine reproductive and respiratory syndrome virus-induced immunosuppression exacerbates the inflammatory response to porcine respiratory coronavirus in pigs.

    PubMed

    Renukaradhya, Gourapura J; Alekseev, Konstantin; Jung, Kwonil; Fang, Ying; Saif, Linda J

    2010-10-01

    We performed a comprehensive analysis of innate and adaptive immune responses in dual-virus infected pigs to understand whether a pre-existing immunomodulatory respiratory viral infection affects the overall immunity to a subsequent porcine respiratory coronavirus (PRCV) infection in pigs. Pigs were either mock-infected or infected with porcine reproductive and respiratory syndrome virus (PRRSV), a virus known to cause immunosuppressive respiratory disease, and then pigs were co-infected with PRCV, which normally causes subclinical respiratory infection. We collected samples for six independent experiments from 178 pigs that were also used for pathological studies. We detected a significant reduction in innate NK-cell-mediated cytotoxic function in PRRSV-infected pigs, which was synergistically further decreased in pigs co-infected with PRCV. Subsequently, in association with clinical signs we observed elevated levels of proinflammatory (IL-6), Th-1 (IL-12), and regulatory (IL-10 and TGF-?) cytokines. Increased frequencies of CD4CD8 double-positive T lymphocytes and myeloid cells, in addition to the elevated Th-1 and proinflammatory cytokines in dual-infected pigs, contributed to the severity of lung disease in pigs. The results of our study clarify how each virus modulates the host innate and adaptive immune responses, leading to inflammatory reactions and lung pathology. Thus measurements of cytokines and frequencies of immune cells may serve as indicators of the progression of respiratory viral co-infections, and provide more definitive approaches for treatment. PMID:20883160

  20. Porcine Reproductive and Respiratory Syndrome VirusInduced Immunosuppression Exacerbates the Inflammatory Response to Porcine Respiratory Coronavirus in Pigs

    PubMed Central

    Alekseev, Konstantin; Jung, Kwonil; Fang, Ying; Saif, Linda J.

    2010-01-01

    Abstract We performed a comprehensive analysis of innate and adaptive immune responses in dual-virus infected pigs to understand whether a pre-existing immunomodulatory respiratory viral infection affects the overall immunity to a subsequent porcine respiratory coronavirus (PRCV) infection in pigs. Pigs were either mock-infected or infected with porcine reproductive and respiratory syndrome virus (PRRSV), a virus known to cause immunosuppressive respiratory disease, and then pigs were co-infected with PRCV, which normally causes subclinical respiratory infection. We collected samples for six independent experiments from 178 pigs that were also used for pathological studies. We detected a significant reduction in innate NK-cell-mediated cytotoxic function in PRRSV-infected pigs, which was synergistically further decreased in pigs co-infected with PRCV. Subsequently, in association with clinical signs we observed elevated levels of proinflammatory (IL-6), Th-1 (IL-12), and regulatory (IL-10 and TGF-?) cytokines. Increased frequencies of CD4CD8 double-positive T lymphocytes and myeloid cells, in addition to the elevated Th-1 and proinflammatory cytokines in dual-infected pigs, contributed to the severity of lung disease in pigs. The results of our study clarify how each virus modulates the host innate and adaptive immune responses, leading to inflammatory reactions and lung pathology. Thus measurements of cytokines and frequencies of immune cells may serve as indicators of the progression of respiratory viral co-infections, and provide more definitive approaches for treatment. PMID:20883160

  1. Integrated Haematological Profiles of Redox Status, Lipid, and Inflammatory Protein Biomarkers in Benign Obesity and Unhealthy Obesity with Metabolic Syndrome

    PubMed Central

    Lubrano, Carla; Valacchi, Giuseppe; Specchia, Palma; Gnessi, Lucio; Rubanenko, Elizaveta P.; Shuginina, Elena A.; Trukhanov, Arseny I.; Korkina, Liudmila G.; De Luca, Chiara

    2015-01-01

    The pathogenesis of obesity (OB) and metabolic syndrome (MetS) implies free radical-, oxidized lipid- (LOOH-), and inflammatory cytokine-mediated altered pathways in target organs. Key elements of the transition from benign OB to unhealthy OB+MetS remain unclear. Here, we measured a panel of redox, antioxidant, and inflammation markers in the groups of OB patients (67 with, 45 without MetS) and 90 controls. Both OB groups displayed elevated levels of adipokines and heavy oxidative stress (OS) evidenced by reduced levels of glutathione, downregulated glutathione-S-transferase, increased 4-hydroxynonenal-protein adducts, reactive oxygen species, and membrane-bound monounsaturated fatty acids (MUFA). Exclusively in OB+MetS, higher-than-normal glutathione peroxidase activity, tumor necrosis factor-α, and other proinflammatory cytokines/chemokines/growth factors were observed; a combination of high adipokine plasminogen activator inhibitor-1 and MUFA was consistent with increased cardiovascular risk. The uncomplicated OB group showed features of adaptation to OS such as decreased levels of vitamin E, activated superoxide dismutase, and inhibited catalase, suggesting H2O2 hyperproduction. Proinflammatory cytokine pattern was normal, except few markers like RANTES, a suitable candidate for therapeutic approaches to prevent a setting of MetS by inhibition of LOOH-primed leukocyte chemotaxis/recruitment to target tissues. PMID:26090072

  2. The framingham risk score, diet, and inflammatory markers in Korean men with metabolic syndrome

    PubMed Central

    Kim, Juyong; Bae, Wookyung

    2012-01-01

    The Framingham risk score (FRS) has been used to assess the risk of a cardiovascular event and to identify patients for risk factor modifications. Therefore, the purpose of this study was to evaluate the relationship of the FRS with dietary intake and inflammatory biomarkers. We conducted a cross-sectional study of 180 men (49.2 ± 10.2 years) with MS. Serum levels of high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), and adiponectin were examined. Participants were asked to complete the food frequency questionnaire (FFQ) using the previous 1 year as a reference point. The absolute cardiovascular disease (CVD) risk percentage over 10 years was calculated to estimate the FRS, which was classified as low risk (< 10%), intermediate risk (10-20%), and high risk (> 20%). Mean intake of polyunsaturated fatty acids was lower in subjects who had > 20% FRS than in subjects who had < 10% FRS (3.7 ± 1.9 g/day vs. 4.7 ± 1.9 g/day; P < 0.05). Significant differences in the Index of Nutritional Quality of protein, phosphorus, iron, vitamin A, vitamin B1, niacin, vitamin B6, and vitamin C were observed between the > 20% FRS group and the < 10% FRS group (P < 0.05). IL-6 concentrations were significantly lower in subjects with a < 10% FRS than in subjects who were 10-20% FRS or > 20% FRS (0.91 ± 0.26 vs. 1.48 ± 033 vs. 2.72 ± 0.57 pg/mL, respectively; P < 0.05). IL-6 and dietary intake of polyunsaturated fatty acids together explained 6.6% of the variation in FRS levels in a stepwise multiple regression model. Our results provide some evidence that dietary intake in the higher CVD risk group was inferior to that in the lower risk group and that dietary fat intake and IL-6 were associated with FRS and MS in Korean men. PMID:22808350

  3. Cerebrospinal fluid cytokine profiles predict risk of early mortality and immune reconstitution inflammatory syndrome in HIV-associated cryptococcal meningitis.

    PubMed

    Jarvis, Joseph N; Meintjes, Graeme; Bicanic, Tihana; Buffa, Viviana; Hogan, Louise; Mo, Stephanie; Tomlinson, Gillian; Kropf, Pascale; Noursadeghi, Mahdad; Harrison, Thomas S

    2015-04-01

    Understanding the host immune response during cryptococcal meningitis (CM) is of critical importance for the development of immunomodulatory therapies. We profiled the cerebrospinal fluid (CSF) immune-response in ninety patients with HIV-associated CM, and examined associations between immune phenotype and clinical outcome. CSF cytokine, chemokine, and macrophage activation marker concentrations were assayed at disease presentation, and associations between these parameters and microbiological and clinical outcomes were examined using principal component analysis (PCA). PCA demonstrated a co-correlated CSF cytokine and chemokine response consisting primarily of Th1, Th2, and Th17-type cytokines. The presence of this CSF cytokine response was associated with evidence of increased macrophage activation, more rapid clearance of Cryptococci from CSF, and survival at 2 weeks. The key components of this protective immune-response were interleukin (IL)-6 and interferon-γ, IL-4, IL-10 and IL-17 levels also made a modest positive contribution to the PC1 score. A second component of co-correlated chemokines was identified by PCA, consisting primarily of monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α). High CSF chemokine concentrations were associated with low peripheral CD4 cell counts and CSF lymphocyte counts and were predictive of immune reconstitution inflammatory syndrome (IRIS). In conclusion CSF cytokine and chemokine profiles predict risk of early mortality and IRIS in HIV-associated CM. We speculate that the presence of even minimal Cryptococcus-specific Th1-type CD4+ T-cell responses lead to increased recruitment of circulating lymphocytes and monocytes into the central nervous system (CNS), more effective activation of CNS macrophages and microglial cells, and faster organism clearance; while high CNS chemokine levels may predispose to over recruitment or inappropriate recruitment of immune cells to the CNS and IRIS following peripheral immune reconstitution with ART. These results provide a rational basis for future studies of immune modulation in CM, and demonstrate the potential of baseline immune profiling to identify CM patients most at risk of mortality and subsequent IRIS. PMID:25853653

  4. Cerebrospinal Fluid Cytokine Profiles Predict Risk of Early Mortality and Immune Reconstitution Inflammatory Syndrome in HIV-Associated Cryptococcal Meningitis

    PubMed Central

    Jarvis, Joseph N.; Meintjes, Graeme; Bicanic, Tihana; Buffa, Viviana; Hogan, Louise; Mo, Stephanie; Tomlinson, Gillian; Kropf, Pascale; Noursadeghi, Mahdad; Harrison, Thomas S.

    2015-01-01

    Understanding the host immune response during cryptococcal meningitis (CM) is of critical importance for the development of immunomodulatory therapies. We profiled the cerebrospinal fluid (CSF) immune-response in ninety patients with HIV-associated CM, and examined associations between immune phenotype and clinical outcome. CSF cytokine, chemokine, and macrophage activation marker concentrations were assayed at disease presentation, and associations between these parameters and microbiological and clinical outcomes were examined using principal component analysis (PCA). PCA demonstrated a co-correlated CSF cytokine and chemokine response consisting primarily of Th1, Th2, and Th17-type cytokines. The presence of this CSF cytokine response was associated with evidence of increased macrophage activation, more rapid clearance of Cryptococci from CSF, and survival at 2 weeks. The key components of this protective immune-response were interleukin (IL)-6 and interferon-?, IL-4, IL-10 and IL-17 levels also made a modest positive contribution to the PC1 score. A second component of co-correlated chemokines was identified by PCA, consisting primarily of monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-1? (MIP-1?). High CSF chemokine concentrations were associated with low peripheral CD4 cell counts and CSF lymphocyte counts and were predictive of immune reconstitution inflammatory syndrome (IRIS). In conclusion CSF cytokine and chemokine profiles predict risk of early mortality and IRIS in HIV-associated CM. We speculate that the presence of even minimal Cryptococcus-specific Th1-type CD4+ T-cell responses lead to increased recruitment of circulating lymphocytes and monocytes into the central nervous system (CNS), more effective activation of CNS macrophages and microglial cells, and faster organism clearance; while high CNS chemokine levels may predispose to over recruitment or inappropriate recruitment of immune cells to the CNS and IRIS following peripheral immune reconstitution with ART. These results provide a rational basis for future studies of immune modulation in CM, and demonstrate the potential of baseline immune profiling to identify CM patients most at risk of mortality and subsequent IRIS. PMID:25853653

  5. Relationship between heart rate recovery and inflammatory markers in patients with polycystic ovary syndrome: a cross-sectional study

    PubMed Central

    Giallauria, Francesco; Orio, Francesco; Lombardi, Gaetano; Colao, Annamaria; Vigorito, Carlo; Tafuri, Maria Giovanna; Palomba, Stefano

    2009-01-01

    Background Polycystic ovary syndrome (PCOS) is an endocrine disease closely related to several risk factors for cardiovascular disease. An abnormal heart rate recovery (HRR), an easily-obtained measure derived from exercise stress test and closely related to an increased risk for cardiovascular mortality, has been recently described in PCOS women. A subclinical increase of the inflammation markers has been also observed in the PCOS. This study was designed to study the relationships between HRR and inflammatory markers in PCOS women. Methods Two-hundred forty-three young PCOS patients without known risk factors for cardiovascular risk were enrolled. All patients underwent hormonal and metabolic profile, white blood cells (WBCs) count and C-reactive protein (CRP). HRR was calculated as the difference between heart rate at peak exercise and heart rate at first minute of the cool-down period. Abnormal HRR was defined as ≤18 beats/min for standard exercise testing. Results Eighty-nine out of 243 patients presented abnormal HRR. Serum CRP (1.8 ± 0.7 vs. 1.1 ± 0.4 mg/dl, p < 0.001) and WBCs (7.3 ± 1.8 vs. 6.6 ± 1.5 109 cells/l, p < 0.001) concentrations were significantly higher in PCOS patients with abnormal versus normal HRR. HRR was significantly associated with both CRP (r = -0.33, p < 0.001) and WBCs (r = -0.29, p < 0.001), although in a stepwise multiple regression HRR resulted independently associated with CRP (beta = -0.151, p = 0.001) alone. In a logistic multivariate model, the group within the highest quartile of CRP (odds ratio 1.59, 95% CI 1.07–2.33) was more likely to have abnormal HRR than those within the lowest quartile. Conclusion Abnormal HRR and inflammatory markers are closely associated in PCOS women acting probably in concert to increase the cardiovascular risk profile of these patients. PMID:19187547

  6. Predictors of Systemic Inflammatory Response Syndrome in Ischemic Stroke Undergoing Systemic Thrombolysis with Intravenous Tissue Plasminogen Activator

    PubMed Central

    Boehme, Amelia K.; Kapoor, Niren; Albright, Karen C.; Lyerly, Michael J.; Rawal, Pawan V.; Shahripour, Reza Bavarsad; Alvi, Muhammad; Houston, J. Thomas; Sisson, April; Beasley, T. Mark; Alexandrov, Anne W.; Alexandrov, Andrei V.; Miller, David W.

    2016-01-01

    Background Systemic inflammatory response syndrome (SIRS) is an inflammatory process associated with poor outcomes in acute ischemic stroke (AIS) patients. However, no study to date has investigated predictors of SIRS in AIS patients treated with intravenous (IV) tissue plasminogen activator (tPA). Methods Consecutive patients were retrospectively reviewed for evidence of SIRS during their acute hospitalization. SIRS was defined as the presence of 2 or more of the following: (1) body temperature less than 36C or greater than 38C, (2) heart rate greater than 90, (3) respiratory rate greater than 20, or (4) white blood cell count less than 4000/mm or greater than 12,000/mm or more than 10% bands for more than 24 hours. Those diagnosed with an infection were excluded. A scoring system was created to predict SIRS based on patient characteristics available at the time of admission. Logistic regression was used to evaluate potential predictors of SIRS using a sensitivity cutoff of ?65% or area under the curve of .6 or more. Results Of 212 patients, 44 had evidence of SIRS (21%). Patients with SIRS were more likely to be black (61% versus 54%; P = .011), have lower median total cholesterol at baseline (143 versus 167 mg/dL; P = .0207), and have history of previous stroke (51% versus 35%; P = .0810). Ranging from 0 to 6, the SIRS prediction score consists of African American (2 points), history of hypertension (1 point), history of previous stroke (1 point), and admission total cholesterol less than 200 (2 points). Patients with an SIRS score of 4 or more were 3 times as likely to develop SIRS when compared with patients with a score of ?3 (odds ratio = 2.815, 95% confidence interval 1.435.56, P = .0029). Conclusions In our sample of IV tPA-treated AIS patients, clinical and laboratory characteristics available on presentation were able to identify patients likely to develop SIRS during their acute hospitalization. Validation is required in other populations. If validated, this score could assist providers in predicting who will develop SIRS after treatment with IV tPA. PMID:24424334

  7. Presence of Systemic Inflammatory Response Syndrome Predicts a Poor Clinical Outcome in Dogs with a Primary Hepatitis.

    PubMed

    Kilpatrick, Scott; Dreistadt, Margaret; Frowde, Polly; Powell, Roger; Milne, Elspeth; Smith, Sionagh; Morrison, Linda; Gow, Adam G; Handel, Ian; Mellanby, Richard J

    2016-01-01

    Primary hepatopathies are a common cause of morbidity and mortality in dogs. The underlying aetiology of most cases of canine hepatitis is unknown. Consequently, treatments are typically palliative and it is difficult to provide accurate prognostic information to owners. In human hepatology there is accumulating data which indicates that the presence of systemic inflammatory response syndrome (SIRS) is a common and debilitating event in patients with liver diseases. For example, the presence of SIRS has been linked to the development of complications such as hepatic encephalopathy (HE) and is associated with a poor clinical outcome in humans with liver diseases. In contrast, the relationship between SIRS and clinical outcome in dogs with a primary hepatitis is unknown. Seventy dogs with histologically confirmed primary hepatitis were enrolled into the study. Additional clinical and clinicopathological information including respiratory rate, heart rate, temperature, white blood cell count, sodium, potassium, sex, presence of ascites, HE score, alanine aminotransferase (ALT), alkaline phosphatase (ALP), bilirubin and red blood cell concentration were available in all cases. The median survival of dogs with a SIRS score of 0 or 1 (SIRS low) was 231 days compared to a median survival of 7 days for dogs with a SIRS score of 2, 3 or 4 (SIRS high) (p<0.001). A Cox proportional hazard model, which included all other co-variables, revealed that a SIRS high score was an independent predictor of a poor clinical outcome. The effect of modulating inflammation on treatment outcomes in dogs with a primary hepatitis is deserving of further study. PMID:26808672

  8. Elevated serum complement factors 3 and 4 are strong inflammatory markers of the metabolic syndrome development: a longitudinal cohort study.

    PubMed

    Liu, Zhenfang; Tang, Qin; Wen, Jing; Tang, Yan; Huang, DaMin; Huang, Yuzhen; Xie, Jinling; Luo, Yawen; Liang, Min; Wu, Chunlei; Lu, Zheng; Tan, Aihua; Gao, Yong; Wang, Qiuyan; Jiang, Yonghua; Yao, Ziting; Lin, Xinggu; Zhang, Haiying; Mo, Zengnan; Yang, Xiaobo

    2016-01-01

    An epidemiological design, consisting of cross-sectional (n?=?2376) and cohort (n?=?976) studies, was adopted to investigate the association between complement factors 3 (C3) and 4, and the metabolic syndrome (MetS) development. In the cross-sectional study, the C3 and C4 concentrations in the MetS group were higher than those in the non-MetS group (all P??0.050). After multi-factor adjustment, the odds ratios (ORs) in the highest quartile of C3 and C4 concentrations were 7.047 (4.664, 10.648) and 1.961 (1.349, 2.849), respectively, both Ptrend?inflammatory processes, and our results indicated that the elevated C3 and C4 levels were independent risk factors for MetS development. PMID:26726922

  9. Impact of vitamin C on the cardiometabolic and inflammatory profiles of mice lacking a functional Werner syndrome protein helicase.

    PubMed

    Aumailley, Lucie; Dubois, Marie Julie; Garand, Chantal; Marette, Andr; Lebel, Michel

    2015-12-01

    Werner syndrome (WS) is a premature aging disorder caused by mutations in a DNA helicase/exonuclease. Mice lacking the helicase domain of this protein exhibit metabolic abnormalities that are reversed by vitamin C. In this study, we used a targeted metabolomic approach to identify serum metabolites significantly altered in young mutant mice treated with or without vitamin C. We also measured several serum inflammatory and cardiometabolic factors. We show that young mutant mice exhibit an increase in serum hydroxyproline and plasminogen activator inhibitor-1 (PAI-1), markers of cardiovascular diseases and inflammation, before they exhibit morphological anomalies in different tissues. We also observed an increase in three very long chain lysophosphatidylcholines underlying peroxisome perturbation. Vitamin C reversed the concentrations of these metabolites and PAI-1 to wild type values. Transcriptomic analyses on the liver of mutant mice revealed a decrease in the expression of genes involved in fatty acid degradation compared to wild type animals. Vitamin C treatment increased the expression of genes involved in glutathione metabolism and the synthesis of unsaturated fatty acids in these mice. These results show that changes at the transcriptomic level concord with the alterations of several serum metabolites in these mice. Finally, we found that a mislocalization of the Wrn mutant protein in the liver endoplasmic reticulum fraction increased oxidative stress in that cellular compartment. Vitamin C reversed this oxidative stress. To conclude, this study provides novel potential predictive cardiometabolic biomarkers in WS that will allow the assessment of the impact of vitamin C on patients with WS. PMID:26521679

  10. Elevated serum complement factors 3 and 4 are strong inflammatory markers of the metabolic syndrome development: a longitudinal cohort study

    PubMed Central

    Liu, Zhenfang; Tang, Qin; Wen, Jing; Tang, Yan; Huang, DaMin; Huang, Yuzhen; Xie, Jinling; Luo, Yawen; Liang, Min; Wu, Chunlei; Lu, Zheng; Tan, Aihua; Gao, Yong; Wang, Qiuyan; Jiang, Yonghua; Yao, Ziting; Lin, Xinggu; Zhang, Haiying; Mo, Zengnan; Yang, Xiaobo

    2016-01-01

    An epidemiological design, consisting of cross-sectional (n = 2376) and cohort (n = 976) studies, was adopted to investigate the association between complement factors 3 (C3) and 4, and the metabolic syndrome (MetS) development. In the cross-sectional study, the C3 and C4 concentrations in the MetS group were higher than those in the non-MetS group (all P < 0.001), and the levels of immune globulin M (IgM), IgA, IgE, and IgG exhibited no significant differences between MetS and non-MetS (all P > 0.050). After multi-factor adjustment, the odds ratios (ORs) in the highest quartile of C3 and C4 concentrations were 7.047 (4.664, 10.648) and 1.961 (1.349, 2.849), respectively, both Ptrend < 0.050. After a 4 years follow-up, total 166 subjects were diagnosed with MetS, and the complement baseline levels from 2009 were used to predict the MetS risk in 2013. In the adjusted model, the relative risks (RRs) in the highest quartile of C3 and C4 levels were 4.779 (2.854, 8.003) and 2.590 (1.567, 4.280), respectively, both Ptrend < 0.001. Activation of complement factors may be an important part of inflammatory processes, and our results indicated that the elevated C3 and C4 levels were independent risk factors for MetS development. PMID:26726922

  11. Presence of Systemic Inflammatory Response Syndrome Predicts a Poor Clinical Outcome in Dogs with a Primary Hepatitis

    PubMed Central

    Kilpatrick, Scott; Dreistadt, Margaret; Frowde, Polly; Powell, Roger; Milne, Elspeth; Smith, Sionagh; Morrison, Linda; Gow, Adam G.; Handel, Ian; Mellanby, Richard J.

    2016-01-01

    Primary hepatopathies are a common cause of morbidity and mortality in dogs. The underlying aetiology of most cases of canine hepatitis is unknown. Consequently, treatments are typically palliative and it is difficult to provide accurate prognostic information to owners. In human hepatology there is accumulating data which indicates that the presence of systemic inflammatory response syndrome (SIRS) is a common and debilitating event in patients with liver diseases. For example, the presence of SIRS has been linked to the development of complications such as hepatic encephalopathy (HE) and is associated with a poor clinical outcome in humans with liver diseases. In contrast, the relationship between SIRS and clinical outcome in dogs with a primary hepatitis is unknown. Seventy dogs with histologically confirmed primary hepatitis were enrolled into the study. Additional clinical and clinicopathological information including respiratory rate, heart rate, temperature, white blood cell count, sodium, potassium, sex, presence of ascites, HE score, alanine aminotransferase (ALT), alkaline phosphatase (ALP), bilirubin and red blood cell concentration were available in all cases. The median survival of dogs with a SIRS score of 0 or 1 (SIRS low) was 231 days compared to a median survival of 7 days for dogs with a SIRS score of 2, 3 or 4 (SIRS high) (p<0.001). A Cox proportional hazard model, which included all other co-variables, revealed that a SIRS high score was an independent predictor of a poor clinical outcome. The effect of modulating inflammation on treatment outcomes in dogs with a primary hepatitis is deserving of further study. PMID:26808672

  12. The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X.

    PubMed

    Black, Paul H

    2003-10-01

    In previous publications, we presented the hypothesis that repeated episodes of acute or chronic psychological stress could induce an acute phase response (APR) and subsequently a chronic inflammatory process such as atherosclerosis. In this paper, that hypothesis, namely that such stress can induce an APR and inflammation, has been extended to include a chronic inflammatory process(s), characterized by the presence of certain cytokines and acute phase reactants (APR), which is associated with certain metabolic diseases. The loci of origin of these cytokines, particularly interleukin 6 (IL-6), and their induction, has been considered. Evidence is presented that the liver, the endothelium, and fat cell depots are the primary sources of cytokines, particularly IL-6, and that IL-6 and the acute phase protein (APP), C-reactive protein (CRP), are strongly associated with, and likely play a dominant role in, the development of this inflammatory process which leads to insulin resistance, non-insulin dependent diabetes mellitus type II, and Metabolic syndrome X. The possible role of psychological stress and the major stress-related hormones as etiologic factors in the pathogenesis of these metabolic diseases, as well as atherosclerosis, is discussed. The fact that stress can activate an APR, which is part of the innate immune inflammatory response, is evidence that the inflammatory response is contained within the stress response or that stress can induce an inflammatory response. The evidence that the stress, inflammatory, and immune systems all evolved from a single cell, the phagocyte, is further evidence for their intimate relationship which almost certainly was maintained throughout evolution. PMID:12946657

  13. Monocyte chemoattractant protein-1 (MCP) and macrophage inflammatory protein-1α (MIP) as possible biomarkers for the chronic pelvic pain syndrome

    PubMed Central

    Desireddi, Naresh V.; Campbell, Phillip L.; Stern, Jeffrey A.; Sobkoviak, Rudina; Chuai, Shannon; Shahrara, Shiva; Thumbikat, Praveen; Pope, Richard M.; Landis, J. Richard; Koch, Alisa E.; Schaeffer, Anthony J.

    2009-01-01

    PURPOSE The chronic pelvic pain syndrome (CPPS) is characterized by pelvic pain, voiding symptoms and varying degrees of inflammation within expressed prostatic secretions (EPS). We evaluated the chemokines MCP-1 (CCL2) and MIP-1α (CCL3) in EPS to identify marker elevations associated with both inflammatory (IIIA) and non-inflammatory (IIIB) CPPS. In addition, chemokine levels were correlated with clinical pain as determined by the NIH chronic prostatitis symptom index (CPSI). MATERIALS AND METHODS EPS were collected by digital rectal examination and evaluated by ELISA for MCP-1 and MIP-1α in 154 patients; controls (n = 13), BPH (n = 54), CPPS IIIA (n = 37), CPPS IIIB (n = 50). MCP-1 and MIP-1α levels were compared between IIIA, IIIB, and the control subgroups and correlated against the CPSI and pain sub-score using a Spearman test. RESULTS Mean levels of MCP-1 in the control, inflammatory BPH, non-inflammatory BPH, inflammatory CPPS, and non-inflammatory CPPS were 599.4, 886.0, 1636.5, 3261.2, and 2272.7 pg/ml, respectively. Mean levels of MIP-1α in the control, inflammatory BPH, non-inflammatory BPH, IIIA CPPS, and IIIB CPPS were 140.1, 299.4, 238.7, 1057.8, and 978.4 pg/ml, respectively. For each cytokine, both CPPS subtypes had statistically higher levels than the control group and BPH patients (p=0.0002). Receiver operating curves utilizing MCP-1 levels greater than 704 pg/ml and MIP-1α greater than 146 pg/ml identified patients with CPPS with an accuracy of 90% from control patients. MIP-1α levels (p=0.0007) correlated with the pain sub-score of the CPSI while MCP-1 (p=0.71) did not. CONCLUSIONS MCP-1 and MIP-1α within the prostatic fluid in both CPPS subtypes provide candidate future biomarkers for CPPS. In addition, MIP-1α elevation in EPS provides a new marker for clinical pain in CPPS patients. Given these findings, prostatic dysfunction likely plays a role in the pathophysiology of some patients with this syndrome. These chemokines may serve as effective diagnostic markers and modulators against the chemokines could provide an attractive treatment strategy in individuals with CPPS. PMID:18353390

  14. Acute and chronic neuropathies: new aspects of Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy, an overview and an update.

    PubMed

    Trojaborg, W

    1998-11-01

    During the last 15 years new information about clinical, electrophysiological, immunological and histopathological features of acute and chronic inflammatory neuropathies have emerged. Thus, the Guillain-Barré syndrome (GBS) is no longer considered a simple entity. Subtypes of the disorder besides the typical predominant motor manifestation, are recognized, i.e. a cranial nerve variant with ophthalmoplegia, ataxia and areflexia, an immune-mediated primary motor axonal neuropathy (AMAN), and a motor-sensory syndrome (AMSAN). Also, the clinical pattern of GBS is related to preceding viral or bacterial infections. Two types of acute motor paralysis have been described, one with slow and incomplete recovery, another with recovery times identical with acute inflammatory demyelinating polyneuropathy (AIDP). Histologically, the first is characterized by Wallerian degeneration of motor roots and peripheral motor nerve fibres. In the latter anti-GM antibodies bind to the nodes of Ranvier producing a failure of impulse transmission. Motor-point biopsies have shown denervated neuromuscular junctions and a reduced number of intramuscular nerve fibres. Molecular mimicry has been postulated as a possible mechanism triggering GBS. Thus, in the cranial variant antibodies to ganglioside GQ1b recognizes similar epitopes on Campylobacter jejuni strains and similar observations apply to anti-GM1 antibodies. Chronic inflammatory demyelinating polyneuropathy (CIDP) also has several different clinical presentations such as a pure motor syndrome, a sensory ataxic variant, a mononeuritis multiplex pattern, relapsing GBS, and a paraparetic subtype. Each of the acute and the subtypes have different, more or less distinct, electrophysiologic and pathological findings. Instructive patient stories are presented together with there electrophysiologic and biopsy findings. PMID:9872432

  15. Curcumin modulates the inflammatory response and inhibits subsequent fibrosis in a mouse model of viral-induced acute respiratory distress syndrome.

    PubMed

    Avasarala, Sreedevi; Zhang, Fangfang; Liu, Guangliang; Wang, Ruixue; London, Steven D; London, Lucille

    2013-01-01

    Acute Respiratory Distress Syndrome (ARDS) is a clinical syndrome characterized by diffuse alveolar damage usually secondary to an intense host inflammatory response of the lung to a pulmonary or extrapulmonary infectious or non-infectious insult often leading to the development of intra-alveolar and interstitial fibrosis. Curcumin, the principal curcumoid of the popular Indian spice turmeric, has been demonstrated as an anti-oxidant and anti-inflammatory agent in a broad spectrum of diseases. Using our well-established model of reovirus 1/L-induced acute viral pneumonia, which displays many of the characteristics of the human ALI/ARDS, we evaluated the anti-inflammatory and anti-fibrotic effects of curcumin. Female CBA/J mice were treated with curcumin (50 mg/kg) 5 days prior to intranasal inoculation with 10(7)pfu reovirus 1/L and daily, thereafter. Mice were evaluated for key features associated with ALI/ARDS. Administration of curcumin significantly modulated inflammation and fibrosis, as revealed by histological and biochemical analysis. The expression of IL-6, IL-10, IFN?, and MCP-1, key chemokines/cytokines implicated in the development of ALI/ARDS, from both the inflammatory infiltrate and whole lung tissue were modulated by curcumin potentially through a reduction in the phosphorylated form of NF?B p65. While the expression of TGF1 was not modulated by curcumin, TGF Receptor II, which is required for TGF signaling, was significantly reduced. In addition, curcumin also significantly inhibited the expression of ?-smooth muscle actin and Tenascin-C, key markers of myofibroblast activation. This data strongly supports a role for curcumin in modulating the pathogenesis of viral-induced ALI/ARDS in a pre-clinical model potentially manifested through the alteration of inflammation and myofibroblast differentiation. PMID:23437361

  16. Autoimmune/auto-inflammatory syndrome induced by adjuvants (ASIA) after quadrivalent human papillomavirus vaccination in Colombians: a call for personalised medicine.

    PubMed

    Anaya, Juan-Manuel; Reyes, Benjamin; Perdomo-Arciniegas, Ana M; Camacho-Rodrguez, Bernardo; Rojas-Villarraga, Adriana

    2015-01-01

    This was a case study in which 3 patients with autoimmune/auto-inflammatory syndrome induced by adjuvants (ASIA) after quadrivalent human papillomavirus vaccination (HPV) were evaluated and described. All the patients were women. Diagnosis consisted of HLA-B27 enthesitis related arthritis, rheumatoid arthritis and systemic lupus erythematous, respectively. Our results highlight the risk of developing ASIA after HPV vaccination and may serve to increase the awareness of such a complication. Factors that are predictive of developing autoimmune diseases should be examined at the population level in order to establish preventive measures in at-risk individuals for whom healthcare should be personalized and participatory. PMID:25962455

  17. Grape Consumption Increases Anti-Inflammatory Markers and Upregulates Peripheral Nitric Oxide Synthase in the Absence of Dyslipidemias in Men with Metabolic Syndrome

    PubMed Central

    Barona, Jacqueline; Blesso, Christopher N.; Andersen, Catherine J.; Park, Youngki; Lee, Jiyoung; Fernandez, Maria Luz

    2012-01-01

    We evaluated the effects of grape consumption on inflammation and oxidation in the presence or absence of dyslipidemias in metabolic syndrome (MetS). Men with MetS (n = 24), 11 with high triglycerides and low HDL and 13 with no dyslipidemia were recruited and randomly allocated to consume daily either 46 g of lyophilized grape powder (GRAPE), equivalent to 252 g fresh grapes, or placebo with an identical macronutrient composition and caloric value as GRAPE for four weeks. After a three-week washout, participants followed the alternate treatment. We measured changes between placebo and GRAPE periods in inflammatory and oxidative stress markers both in circulation and in gene expression. Changes in plasma adiponectin (p < 0.05), interleukin (IL)-10 (p < 0.005) and in mRNA expression of the inducible isoform of nitric oxide synthase (iNOS) (p < 0.25) were increased in the GRAPE compared to the placebo period only in those individuals without dyslipidemia. Additionally, plasma IL-10 was negatively correlated with NOX2 expression, a marker of oxidative stress (r = ?0.55, p < 0.01), while iNOS expression was positively correlated with the expression of superoxide dismutase 2 (r = 0.642, p < 0.01), a key anti-oxidative enzyme. Grape consumption displayed anti-oxidative and increased anti-inflammatory markers in the absence of the inflammatory milieu associated with dyslipidemias. PMID:23222963

  18. Grape consumption increases anti-inflammatory markers and upregulates peripheral nitric oxide synthase in the absence of dyslipidemias in men with metabolic syndrome.

    PubMed

    Barona, Jacqueline; Blesso, Christopher N; Andersen, Catherine J; Park, Youngki; Lee, Jiyoung; Fernandez, Maria Luz

    2012-12-01

    We evaluated the effects of grape consumption on inflammation and oxidation in the presence or absence of dyslipidemias in metabolic syndrome (MetS). Men with MetS (n = 24), 11 with high triglycerides and low HDL and 13 with no dyslipidemia were recruited and randomly allocated to consume daily either 46 g of lyophilized grape powder (GRAPE), equivalent to 252 g fresh grapes, or placebo with an identical macronutrient composition and caloric value as GRAPE for four weeks. After a three-week washout, participants followed the alternate treatment. We measured changes between placebo and GRAPE periods in inflammatory and oxidative stress markers both in circulation and in gene expression. Changes in plasma adiponectin (p < 0.05), interleukin (IL)-10 (p < 0.005) and in mRNA expression of the inducible isoform of nitric oxide synthase (iNOS) (p < 0.25) were increased in the GRAPE compared to the placebo period only in those individuals without dyslipidemia. Additionally, plasma IL-10 was negatively correlated with NOX2 expression, a marker of oxidative stress (r = -0.55, p < 0.01), while iNOS expression was positively correlated with the expression of superoxide dismutase 2 (r = 0.642, p < 0.01), a key anti-oxidative enzyme. Grape consumption displayed anti-oxidative and increased anti-inflammatory markers in the absence of the inflammatory milieu associated with dyslipidemias. PMID:23222963

  19. Postural Orthostatic Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants

    PubMed Central

    Tomljenovic, Lucija; Colafrancesco, Serena; Perricone, Carlo

    2014-01-01

    We report the case of a 14-year-old girl who developed postural orthostatic tachycardia syndrome (POTS) with chronic fatigue 2 months following Gardasil vaccination. The patient suffered from persistent headaches, dizziness, recurrent syncope, poor motor coordination, weakness, fatigue, myalgias, numbness, tachycardia, dyspnea, visual disturbances, phonophobia, cognitive impairment, insomnia, gastrointestinal disturbances, and a weight loss of 20 pounds. The psychiatric evaluation ruled out the possibility that her symptoms were psychogenic or related to anxiety disorders. Furthermore, the patient tested positive for ANA (1:1280), lupus anticoagulant, and antiphospholipid. On clinical examination she presented livedo reticularis and was diagnosed with Raynauds syndrome. This case fulfills the criteria for the autoimmune/auto-inflammatory syndrome induced by adjuvants (ASIA). Because human papillomavirus vaccination is universally recommended to teenagers and because POTS frequently results in long-term disabilities (as was the case in our patient), a thorough follow-up of patients who present with relevant complaints after vaccination is strongly recommended. PMID:26425598

  20. Postural Orthostatic Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the "Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants": Case Report and Literature Review.

    PubMed

    Tomljenovic, Lucija; Colafrancesco, Serena; Perricone, Carlo; Shoenfeld, Yehuda

    2014-01-01

    We report the case of a 14-year-old girl who developed postural orthostatic tachycardia syndrome (POTS) with chronic fatigue 2 months following Gardasil vaccination. The patient suffered from persistent headaches, dizziness, recurrent syncope, poor motor coordination, weakness, fatigue, myalgias, numbness, tachycardia, dyspnea, visual disturbances, phonophobia, cognitive impairment, insomnia, gastrointestinal disturbances, and a weight loss of 20 pounds. The psychiatric evaluation ruled out the possibility that her symptoms were psychogenic or related to anxiety disorders. Furthermore, the patient tested positive for ANA (1:1280), lupus anticoagulant, and antiphospholipid. On clinical examination she presented livedo reticularis and was diagnosed with Raynaud's syndrome. This case fulfills the criteria for the autoimmune/auto-inflammatory syndrome induced by adjuvants (ASIA). Because human papillomavirus vaccination is universally recommended to teenagers and because POTS frequently results in long-term disabilities (as was the case in our patient), a thorough follow-up of patients who present with relevant complaints after vaccination is strongly recommended. PMID:26425598

  1. Genetics Home Reference: Wiskott-Aldrich syndrome

    MedlinePLUS

    ... inflammatory disorders. Many people with this condition develop eczema, an inflammatory skin disorder characterized by abnormal patches ... names do people use for Wiskott-Aldrich syndrome? eczema-thrombocytopenia-immunodeficiency syndrome IMD2 immunodeficiency 2 Wiskott syndrome ...

  2. Immune reconstitution inflammatory syndrome involving the central nervous system in a patient with HIV infection: a case report and review of literature.

    PubMed

    Zaffiri, Lorenzo; Verma, Rajanshu; Struzzieri, Kevin; Monterroso, Joanne; Batts, Donald H; Loehrke, Mark E

    2013-01-01

    IRIS is described as a paradoxical deterioration of clinical status upon initiation of combined anti-retroviral therapy (cART) in patients with HIV infection. Immune reconstitution inflammatory syndrome (CNS-IRIS) involving the central nervous system is rarely reported. We describe the case of 57-year-old man who developed a fatal case of CNS- IRIS. A rapid deterioration of neurological status was associated with progression of patchy T2-weighted hyperintensities involving different vascular territories on brain MRI. Diagnosis of CNS-IRIS is based of laboratory and radiologic findings, however brain biopsy is supportive. Despite immune restoration being involved in clinical deterioration, discontinuation of cART is not recommended. The use of corticosteroids is highly controversial. Prompt recognition of CNS-IRIS is crucial for preventing neurological complications and ensuing sequelae. PMID:23435821

  3. Treatment of progressive multifocal leukoencephalopathy-immune reconstitution inflammatory syndrome with intravenous immunoglobulin in a patient with multiple sclerosis treated with fingolimod after discontinuation of natalizumab.

    PubMed

    Calic, Z; Cappelen-Smith, C; Hodgkinson, S J; McDougall, A; Cuganesan, R; Brew, B J

    2015-03-01

    We report a case of progressive multifocal leukoencephalopathy-immune reconstitution inflammatory syndrome in a multiple sclerosis (MS) patient 3.5 months after fingolimod commencement and 4.5 months after natalizumab (NTZ) cessation. Three cerebrospinal fluid analyses were required before a definitive diagnosis of progressive multifocal leukoencephalopathy was reached. Intravenous immunoglobulin (IVIG) was subsequently given as the sole MS treatment along with mirtazapine and mefloquine. There has been improvement and subsequent clinical stabilization. The notable features are the difficult timing of fingolimod commencement in the context of previous NTZ therapy, the role of repeated cerebrospinal fluid John Cunningham virus analyses in progressive multifocal leukoencephalopathy diagnosis, and the role of IVIG. PMID:25523125

  4. PROCLAIM: pilot study to examine the effects of clopidogrel on inflammatory markers in patients with metabolic syndrome receiving low-dose aspirin.

    PubMed

    Willerson, James T; Cable, Greg; Yeh, Edward T H

    2009-01-01

    Metabolic syndrome is associated with intravascular inflammation, as determined by increased levels of inflammatory biomarkers and an increased risk of ischemic atherothrombotic events. Evidence suggests that atherothrombosis and intravascular inflammation share predictive biomarkers, including high-sensitivity C-reactive protein, CD40 ligand, P-selectin, and N-terminal pro-brain natriuretic peptide. Patients who had metabolic syndrome were randomized to receive clopidogrel 75 mg/day plus aspirin 81 mg/day (n = 89) or placebo plus aspirin 81 mg/day (n = 92) for 9 weeks to assess the efficacy of each treatment in suppression of inflammatory markers. Change from baseline in the levels of high-sensitivity C-reactive protein, CD40 ligand, P-selectin, and N-terminal pro-brain natriuretic peptide at 6 weeks was assessed to evaluate each treatment. There was a significant difference at Week 6 in model-adjusted CD40-ligand levels in favor of clopidogrel plus aspirin compared with placebo plus aspirin in both the intent-to-treat population (difference between least-squares means = -186.5; 95% confidence interval, -342.3 to -30.8; P = 0.02) and the per-protocol population (P = 0.05). No significant differences were observed between the treatment arms for high-sensitivity C-reactive protein, P-selectin, and N-terminal pro-brain natriuretic peptide. There were no deaths or serious adverse events in either treatment arm. Data from this study suggest that clopidogrel can decrease the expression of the CD40-ligand biomarker. PMID:20069077

  5. Selective expansion of polyfunctional pathogen-specific CD4+ T cells in HIV-1infected patients with immune reconstitution inflammatory syndrome

    PubMed Central

    Mahnke, Yolanda D.; Greenwald, Jamieson H.; DerSimonian, Rebecca; Roby, Gregg; Antonelli, Lis R. V.; Sher, Alan; Roederer, Mario

    2012-01-01

    Since the introduction of highly active antiretroviral therapies (ART), the prognosis for HIV-1 patients has improved immensely. However, approximately 25% of patients can experience a variety of inflammatory symptoms that are collectively known as immune reconstitution inflammatory syndrome (IRIS). Studying the etiology and immunopathology of IRIS has been hampered by the fact that the symptoms and associated opportunistic infections are highly varied. We hypothesized that there is a common mechanism underlying IRIS pathogenesis and investigated a patient group with IRIS related to different pathogens. Functional and phenotypic characterization of PBMC samples was performed by polychromatic flow cytometry after in vitro stimulation with relevant antigenic preparations. In most patients, IRIS events were characterized by the robust increase of preexisting polyfunctional, highly differentiated effector CD4+ T-cell responses that specifically targeted the antigens of the underlying co-infection. T-cell responses to HIV-1 or other underlying infections were not affected and did not differ between IRIS and non-IRIS patients. These data suggest that patients with IRIS do not have a generalized T-cell dysfunction; instead, IRIS represents a dysregulated CD4+ T-cell response against residual opportunistic infection antigen. These studies were registered at www.clinical-trials.gov as NCT00557570 and NCT00286767. PMID:22219223

  6. Xanthine Oxidase Activity Is Associated with Risk Factors for Cardiovascular Disease and Inflammatory and Oxidative Status Markers in Metabolic Syndrome: Effects of a Single Exercise Session

    PubMed Central

    Feoli, Ana Maria Pandolfo; Macagnan, Fabrcio Edler; Piovesan, Carla Haas; Bodanese, Luiz Carlos; Siqueira, Ionara Rodrigues

    2014-01-01

    Objective. The main goal of the present study was to investigate the xanthine oxidase (XO) activity in metabolic syndrome in subjects submitted to a single exercise session. We also investigated parameters of oxidative and inflammatory status. Materials/Methods. A case-control study (9 healthy and 8 MS volunteers) was performed to measure XO, superoxide dismutase (SOD), glutathione peroxidase activities, lipid peroxidation, high-sensitivity C-reactive protein (hsCRP) content, glucose levels, and lipid profile. Body mass indices, abdominal circumference, systolic and diastolic blood pressure, and TG levels were also determined. The exercise session consisted of 3 minutes of stretching, 3 minutes of warm-up, 30 minutes at a constant dynamic workload at a moderate intensity, and 3 minutes at a low speed. The blood samples were collected before and 15 minutes after the exercise session. Results. Serum XO activity was higher in MS group compared to control group. SOD activity was lower in MS subjects. XO activity was correlated with SOD, abdominal circumference, body mass indices, and hsCRP. The single exercise session reduced the SOD activity in the control group. Conclusions. Our data support the association between oxidative stress and risk factors for cardiovascular diseases and suggest XO is present in the pathogenesis of metabolic syndrome. PMID:24967004

  7. [Lactate kinetics during constant hemodiafiltration in critically severe patients with the systemic inflammatory response syndrome and multiple organ failure].

    PubMed

    Iakovleva, I I; Timokhov, V S; Pestriakov, E V; Moroz, V V; Molchanova, L V; Murav'ev, O B; Sergeev, A Iu

    2000-01-01

    High-volume hemodiafiltration is a new approach to the treatment of critical patients with generalized inflammatory reaction and multiple organ failure. Increase of the liquid exchange during the procedure is fraught with the development of secondary metabolic disorders in cases when lactate-based buffer is used (with high amounts of lactate). This study was undertaken to evaluate the consequences for the acid-base balance in patients with hypoxia and circulatory failure. Twelve patients (6 men and 6 women) with APACHE II score 25 were examined. The major treatment modality was continuous hemodiafiltration. The results indicate that lactate-buffered solutions can be used in critical patients, because they do not cause a notable increase in the blood lactate levels due to its good utilization. Moreover, it is associated with correction of disorders in acid-base balance. No negative clinical consequences were observed after using lactate anion in high concentrations as the major buffer compound. PMID:10900718

  8. The exaggerated inflammatory response in Behet's syndrome: identification of dysfunctional post-transcriptional regulation of the IFN-?/CXCL10 IP-10 pathway.

    PubMed

    Ambrose, N; Khan, E; Ravindran, R; Lightstone, L; Abraham, S; Botto, M; Johns, M; Haskard, D O

    2015-09-01

    The mechanisms underlying the exaggerated inflammatory response in Behet's syndrome (BS) remain poorly understood. We investigated the response of CD14(+) blood monocytes to interferon (IFN)-?, focusing on the chemokine CXCL10. Chemokine synthesis and release were analysed at a protein and mRNA level following stimulation with IFN-?. Findings in BS patients were compared with 25 healthy controls (HC), 15 rheumatoid arthritis (RA) and 15 systemic lupus erythematosus (SLE) disease control patients. BS monocytes produced significantly more CXCL10 protein than HC monocytes from 2h following IFN-? stimulation, despite equivalent quantities of mRNA, suggesting more efficient translation. This was significantly more pronounced in BS with high disease activity and in those with ocular and neurological clinical manifestations. The imbalance between CXCL10 protein and mRNA expression was not observed in either RA or SLE patients, and was not seen with other chemokines studied (CXCL9, CXCL11 and CCL2). Furthermore, BS monocytes treated with an alternative stimulant (LPS) did not show abnormal tumour necrosis factor (TNF)-? release. Sucrose density gradients to segregate monocyte CXCL10 mRNA into free RNA or polysome-associated RNA showed equal proportions in BS and HC samples, suggesting that the difference between BS and HC may be due to reduced negative control of CXCL10 translation in BS at a post-initiation level. We conclude that BS monocytes have dysfunctional post-transcriptional regulation of CXCL10 mRNA, resulting in over-expression of CXCL10 protein upon IFN-? stimulation. As CXCL10 is a chemokine that recruits mononuclear cells, this abnormality may contribute to the exaggerated inflammatory responses that characterizes BS. PMID:25982097

  9. Hypoxia inducible factor-1? inhibition produced anti-allodynia effect and suppressed inflammatory cytokine production in early stage of mouse complex regional pain syndrome model.

    PubMed

    Hsiao, Hung-Tsung; Lin, Ya-Chi; Wang, Jeffrey Chi-Fei; Tsai, Yu-Chuan; Liu, Yen-Chin

    2016-03-01

    Complex regional pain syndrome (CRPS) is related to microcirculation impairment associated with tissue hypoxia and peripheral cytokine overproduction in the affected limb. Previous studies suggest that the pathogenesis involves hypoxia inducible factor-1? (HIF-1?) and exaggerated regional inflammatory response. 1-methylpropyl 2-imidazolyl disulfide (PX-12) acts as the thioredoxin-1 (Trx-1) inhibitor and decreases the level of HIF-1?, and can rapidly be metabolized for Trx-1 redox inactivation. This study hypothesized that PX-12 can decrease the cytokine production for nociceptive sensitization in the hypoxia-induced pain model. CD1 mice weighing around 30g were used. The animal CRPS model was developed via the chronic post-ischaemic pain (CPIP) model. The model was induced by using O-rings on the ankles of the mice hind limbs to produce 3-h ischaemia-reperfusion injury on the paw. PX-12 (25mg/kg, 5mg/kg) was given through tail vein injection immediately after ischaemia. Animal behaviour was tested using the von Frey method for 7days. Local paw skin tissue was harvest from three groups (control, 5mg/kg, 25mg/kg) 2h after injection of PX-12. The protein expression of interleukin-1? (IL-1?) and HIF-1? was analysed with the Western blotting method. Mice significantly present an anti-allodynia effect in a dose-related manner after the PX-12 administration. Furthermore, PX-12 not only decreased the expression of HIF-1? but also decreased the expression of IL-1? over the injured palm. This study, therefore, shows the first evidence of the anti-allodynia effect of PX-12 in a CPIP animal model for pain behaviour. The study concluded that inhibition of HIF-1? may produce an analgesic effect and the associated suppression of inflammatory cytokine IL-1? in a CPIP model. PMID:26711019

  10. Mesenchymal Stem/Progenitors and Other Endometrial Cell Types From Women With Polycystic Ovary Syndrome (PCOS) Display Inflammatory and Oncogenic Potential

    PubMed Central

    Piltonen, T. T.; Chen, J.; Erikson, D. W.; Spitzer, T. L. B.; Barragan, F.; Rabban, J. T.; Huddleston, H.; Irwin, J. C.

    2013-01-01

    Context: Endometrium in polycystic ovary syndrome (PCOS) presents altered gene expression indicating progesterone resistance and predisposing to reduced endometrial receptivity and endometrial cancer. Objective: We hypothesized that an altered endocrine/metabolic environment in PCOS may result in an endometrial “disease phenotype” affecting the gene expression of different endometrial cell populations, including stem cells and their differentiated progeny. Design and Setting: This was a prospective study conducted at an academic medical center. Patients and Main Outcome Measures: Proliferative-phase endometrium was obtained from 6 overweight/obese PCOS (National Institutes of Health criteria) and 6 overweight/obese controls. Microarray analysis was performed on fluorescence-activated cell sorting-isolated endometrial epithelial cells (eEPs), endothelial cells, stromal fibroblasts (eSFs), and mesenchymal stem cells (eMSCs). Gene expression data were validated using microfluidic quantitative RT-PCR and immunohistochemistry. Results: The comparison between eEPPCOS and eEPCtrl showed dysregulation of inflammatory genes and genes with oncogenic potential (CCL2, IL-6, ORM1, TNAIFP6, SFRP4, SPARC). eSFPCOS and eSFCtrl showed up-regulation of inflammatory genes (C4A/B, CCL2, ICAM1, TNFAIP3). Similarly, in eMSCPCOS vs eMSCCtrl, the most up-regulated genes were related to inflammation and cancer (IL-8, ICAM1, SPRR3, LCN2). Immunohistochemistry scoring showed increased expression of CCL2 in eEPPCOS and eSFPCOS compared with eEPCtrl and eSFCtrl and IL-6 in eEPPCOS compared with eEPCtrl. Conclusions: Isolated endometrial cell populations in women with PCOS showed altered gene expression revealing inflammation and prooncogenic changes, independent of body mass index, especially in eEPPCOS and eMSCPCOS, compared with controls. The study reveals an endometrial disease phenotype in women with PCOS with potential negative effects on endometrial function and long-term health. PMID:23824412

  11. Associations of erythrocyte palmitoleic acid with adipokines, inflammatory markers, and the metabolic syndrome in middle-aged and older Chinese123

    PubMed Central

    Zong, Geng; Ye, Xingwang; Sun, Liang; Li, Huaixing; Yu, Zhijie; Hu, Frank B

    2012-01-01

    Background: Palmitoleic acid has been shown to regulate adipokine expression and systemic metabolic homeostasis in animal studies. However, its association with human metabolic diseases remains controversial. Objective: We aimed to investigate associations of erythrocyte palmitoleic acid with adipokines, inflammatory markers, and metabolic syndrome (MetS) in a Chinese population. Design: Erythrocyte fatty acids were measured in a population-based sample of 3107 men and women aged 5070 y, for whom plasma glucose, insulin, lipid profile, adiponectin, retinol binding protein 4 (RBP-4), plasminogen activator inhibitor type 1, and high-sensitivity C-reactive protein (hsCRP) were measured. MetS was defined according to the updated National Cholesterol Education Program Adult Treatment Panel III criteria for Asian Americans. Results: The mean (SD) erythrocyte palmitoleic acid value was 0.41 0.20% of total fatty acids. Palmitoleic acid was positively correlated with RBP-4 (r = 0.14, P < 0.001) and inversely correlated with adiponectin (r = ?0.15, P < 0.001). After multivariable adjustment, palmitoleic acid was strongly associated with MetS and its components. ORs (95% CIs) for comparisons of extreme quartiles of palmitoleic acid were 3.50 (2.66, 4.59) for MetS, 7.88 (5.90, 10.52) for hypertriglyceridemia, 2.13 (1.66, 2.72) for reduced HDL cholesterol, 1.99 (1.60, 2.48) for central obesity, and 1.86 (1.41, 2.44) for elevated blood pressure (all P < 0.001). Further control for adipokines and hsCRP abolished the association of palmitoleic acid with central obesity but not with other MetS components. Conclusion: Erythrocyte palmitoleic acid is associated with an adverse profile of adipokines and inflammatory markers and an increased risk of MetS in this Chinese population. PMID:23015321

  12. Genomic and Clinical Effects Associated with a Relaxation Response Mind-Body Intervention in Patients with Irritable Bowel Syndrome and Inflammatory Bowel Disease

    PubMed Central

    Jacquart, Jolene; Scult, Matthew A.; Slipp, Lauren; Riklin, Eric Isaac Kagan; Lepoutre, Veronique; Comosa, Nicole; Norton, Beth-Ann; Dassatti, Allison; Rosenblum, Jessica; Thurler, Andrea H.; Surjanhata, Brian C.; Hasheminejad, Nicole N.; Kagan, Leslee; Slawsby, Ellen; Rao, Sowmya R.; Macklin, Eric A.; Fricchione, Gregory L.; Benson, Herbert; Libermann, Towia A.; Korzenik, Joshua; Denninger, John W.

    2015-01-01

    Introduction Irritable Bowel Syndrome (IBS) and Inflammatory Bowel Disease (IBD) can profoundly affect quality of life and are influenced by stress and resiliency. The impact of mind-body interventions (MBIs) on IBS and IBD patients has not previously been examined. Methods Nineteen IBS and 29 IBD patients were enrolled in a 9-week relaxation response based mind-body group intervention (RR-MBI), focusing on elicitation of the RR and cognitive skill building. Symptom questionnaires and inflammatory markers were assessed pre- and post-intervention, and at short-term follow-up. Peripheral blood transcriptome analysis was performed to identify genomic correlates of the RR-MBI. Results Pain Catastrophizing Scale scores improved significantly post-intervention for IBD and at short-term follow-up for IBS and IBD. Trait Anxiety scores, IBS Quality of Life, IBS Symptom Severity Index, and IBD Questionnaire scores improved significantly post-intervention and at short-term follow-up for IBS and IBD, respectively. RR-MBI altered expression of more genes in IBD (1059 genes) than in IBS (119 genes). In IBD, reduced expression of RR-MBI response genes was most significantly linked to inflammatory response, cell growth, proliferation, and oxidative stress-related pathways. In IBS, cell cycle regulation and DNA damage related gene sets were significantly upregulated after RR-MBI. Interactive network analysis of RR-affected pathways identified TNF, AKT and NF-?B as top focus molecules in IBS, while in IBD kinases (e.g. MAPK, P38 MAPK), inflammation (e.g. VEGF-C, NF-?B) and cell cycle and proliferation (e.g. UBC, APP) related genes emerged as top focus molecules. Conclusions In this uncontrolled pilot study, participation in an RR-MBI was associated with improvements in disease-specific measures, trait anxiety, and pain catastrophizing in IBS and IBD patients. Moreover, observed gene expression changes suggest that NF-?B is a target focus molecule in both IBS and IBDand that its regulation may contribute to counteracting the harmful effects of stress in both diseases. Larger, controlled studies are needed to confirm this preliminary finding. Trial Registration ClinicalTrials.Gov NCT02136745 PMID:25927528

  13. Isoniazid-resistant Mycobacterium kansasii in an HIV-positive patient, and possible development of immune reconstitution inflammatory syndrome after initiation of highly active antiretroviral therapy: case report.

    PubMed

    Despotovic, A; Savic, B; Salemovic, D; Ranin, J; Jevtovic, Dj

    2016-01-01

    Non-tuberculous mycobacteria are rare but important causes of infection in HIV-positive individuals. A 28-year-old HIV-positive male presented with a high fever, non-productive cough, right subcostal pain, splenomegaly, a very low CD4 count, elevated C-reactive protein and erythrocyte sedimentation rate, and a normal white blood cell count. The suspicion of tuberculosis (TB) was very high, and sputum samples were positive for acid-fast bacilli. Standard quadruple anti-TB therapy was initiated, but once culture of the sample revealed Mycobacterium kansasii, pyrazinamide was withdrawn. Highly active antiretroviral therapy (HAART) was initiated soon after, consisting of abacavir/lamivudine and efavirenz. The patient's general condition deteriorated 2 weeks after HAART initiation, which could have been due to the development of immune reconstitution inflammatory syndrome (IRIS). The patient recovered and was discharged in good condition. However, the results of resistance testing of the isolated organism arrived after discharge, and showed isoniazid and streptomycin resistance. This is the first case report of M. kansasii infection from Serbia and shows the difficulties encountered during the course of treatment. PMID:26603644

  14. Angiogenic and inflammatory markers in acute respiratory distress syndrome and renal injury associated to A/H1N1 virus infection.

    PubMed

    Bautista, Edgar; Arcos, Magali; Jimenez-Alvarez, Lus; Garca-Sancho, Ma Cecilia; Vzquez, Mara E; Pea, Erika; Higuera, Anjarath; Ramrez, Gustavo; Fernndez-Plata, Rosario; Cruz-Lagunas, Alfredo; Garca-Moreno, Sara A; Urrea, Francisco; Ramrez, Remedios; Correa-Rotter, Ricardo; Prez-Padilla, Jos Rogelio; Ziga, Joaqun

    2013-06-01

    Acute kidney injury (AKI) is often associated to acute respiratory distress syndrome (ARDS) due to influenza A/H1N1 virus infection. The profile of angiogenic and inflammatory factors in ARDS patients may be relevant for AKI. We analyzed the serum levels of several angiogenic factors, cytokines, and chemokines in 32 patients with A/H1N1 virus infection (17 with ARDS/AKI and 15 ARDS patients who did not developed AKI) and in 18 healthy controls. Significantly higher levels of VEGF, MCP-1, IL-6, IL-8 and IP-10 in ARDS/AKI patients were detected. Adjusting by confusing variables, levels of MCP-1 ?150 pg/mL (OR=12.0, p=0.04) and VEGF ?225 pg/mL (OR=6.4, p=0.03) were associated with the development of AKI in ARDS patients. Higher levels of MCP-1 and IP-10 were significantly associated with a higher risk of death in patients with ARDS (hazard ratio (HR)=10.0, p=0.02; HR=25.5, p=0.03, respectively) even taking into account AKI. Patients with influenza A/H1N1 infection and ARDS/AKI have an over-production of MCP-1, VEGF and IP-10 possibly contributing to kidney injury and are associated to a higher risk of death. PMID:23542734

  15. Using the polymerase chain reaction coupled with denaturing gradient gel electrophoresis to investigate the association between bacterial translocation and systemic inflammatory response syndrome in predicted acute severe pancreatitis

    PubMed Central

    Pearce, Callum B; Zinkevich, Vitaly; Beech, Iwona; Funjika, Viera; Ruiz, Ana Garcia; Aladawi, Afraa; Duncan, Hamish D

    2005-01-01

    AIM: To investigate the use of PCR and DGGE to investigate the association between bacterial translocation and systemic inflammatory response syndrome in predicted severe AP. METHODS: Patients with biochemical and clinical evidence of acute pancreatitis and an APACHE II score ?8 were enrolled. PCR and DGGE were employed to detect bacterial translocation in blood samples collected on d 1, 3, and 8 after the admission. Standard microbial blood cultures were taken when there was clinical evidence of sepsis or when felt to be clinically indicated by the supervising team. RESULTS: Six patients were included. Of all the patients investigated, only one developed septic complications; the others had uneventful illness. Bacteria were detected using PCR in 4 of the 17 collected blood samples. The patient with sepsis was PCR-positive in two samples (taken on d 1 and 3), despite three negative blood cultures. Using DGGE and specific primers, the bacteria in all blood specimens which tested positive for the presence of bacterial DNA were identified as E coli. CONCLUSION: Our study confirmed that unlike traditional microbiological techniques, PCR can detect the presence of bacteria in the blood of patients with severe AP. Therefore, this latter method in conjunction with DGGE is potentially an extremely useful tool in predicting septic morbidity and evaluating patients with the disease. Further research using increased numbers of patients, in particular those patients with necrosis and sepsis, is required to assess the reliability of PCR and DGGE in the rapid diagnosis of infection in AP. PMID:16437661

  16. Branched DNA-based Alu quantitative assay for cell-free plasma DNA levels in patients with sepsis or systemic inflammatory response syndrome.

    PubMed

    Hou, Yan-Qiang; Liang, Dong-Yu; Lou, Xiao-Li; Zhang, Mei; Zhang, Zhen-Huan; Zhang, Lu-Rong

    2016-02-01

    Cell-free circulating DNA (cf-DNA) can be detected by various of laboratory techniques. We described a branched DNA-based Alu assay for measuring cf-DNA in septic patients. Compared to healthy controls and systemic inflammatory response syndrome (SIRS) patients, serum cf-DNA levels were significantly higher in septic patients (1426.54 863.79 vs 692.02 703.06 and 69.66 24.66 ng/mL). The areas under the receiver operating characteristic curve of cf-DNA for normal vs sepsis and SIRS vs sepsis were 0.955 (0.884-1.025), and 0.856 (0.749-0.929), respectively. There was a positive correlation between cf-DNA and interleukin 6 or procalcitonin or Acute Physiology and Chronic Health Evaluation II. The cf-DNA concentration was higher in intensive care unit nonsurviving patients compared to surviving patients (2183.33 615.26 vs 972.46 648.36 ng/mL; P < .05). Branched DNA-based Alu assays are feasible and useful to quantify serum cf-DNA levels. Increased cf-DNA levels in septic patients might complement C-reactive protein and procalcitonin in a multiple marker format. Cell-free circulating DNA might be a new marker in discrimination of sepsis and SIRS. PMID:26589770

  17. Inflammatory-metabolic parameters in obese and nonobese normoandrogenemic polycystic ovary syndrome during metformin and oral contraceptive treatment.

    PubMed

    Kilic, Sevtap; Yilmaz, Nafiye; Zulfikaroglu, Ebru; Erdogan, Gokcen; Aydin, Murat; Batioglu, Sertac

    2011-09-01

    Our aim was to evaluate the optimal treatment strategy addressing cardiovascular risk in obese and nonobese patients with polycystic ovary syndrome (PCOS). We planned a prospect?ve randomized clinical study. Normoandrogenemic and oligoamenorrheic women with PCOS and impaired glucose tolerance (n = 96) were enrolled in the study. Six months of treatment with metformin HCL or oral contraceptive pills (OCPs) were given to the patients. Group 1 were obese and receiving metformin. Group 2 were obese and receiving OCPs. Group 3 were nonobese and receiving metformin, and Group 4 were nonobese receiving OCPs. ADMA, homocysteine, high sensitive C-reactive protein (hs-CRP) and homeostasis model assessment estimate of insulin resistance (HOMA-IR) were investigated. ADMA, homocysteine, hs-CRP and HOMA-IR were similar in obese and nonobese groups before the treatment. After 6 months of treatment, a significant decrease was observed in ADMA, homocysteine and HOMA-IR levels in Groups 1 and 3. An increase in ADMA and hs-CRP levels was observed in Groups 2 and 4. In this study, metformin treatment leads to improvement in hormonal and metabolic parameters and decreases ADMA and homocysteine levels possibly independent of BMI. However, the use of oral contraceptives in obese and nonobese patients with PCOS with impaired glucose tolerance increases ADMA and hs-CRP levels and creates an increase in the metabolic risk. PMID:21105835

  18. Positive effect of combined exercise training in a model of metabolic syndrome and menopause: autonomic, inflammatory, and oxidative stress evaluations.

    PubMed

    Conti, Filipe Fernandes; Brito, Janaina de Oliveira; Bernardes, Nathalia; Dias, Danielle da Silva; Malfitano, Christiane; Morris, Mariana; Llesuy, Susana Francisca; Irigoyen, Maria-Cludia; De Angelis, Ktia

    2015-12-15

    It is now well established that after menopause cardiometabolic disorders become more common. Recently, resistance exercise has been recommended as a complement to aerobic (combined training, CT) for the treatment of cardiometabolic diseases. The aim of this study was to evaluate the effects of CT in hypertensive ovariectomized rats undergoing fructose overload in blood pressure variability (BPV), inflammation, and oxidative stress parameters. Female rats were divided into the following groups (n = 8/group): sedentary normotensive Wistar rats (C), and sedentary (FHO) or trained (FHOT) ovariectomized spontaneously hypertensive rats undergoing and fructose overload. CT was performed on a treadmill and ladder adapted to rats in alternate days (8 wk; 40-60% maximal capacity). Arterial pressure (AP) was directly measured. Oxidative stress and inflammation were measured on cardiac and renal tissues. The association of risk factors (hypertension + ovariectomy + fructose) promoted increase in insulin resistance, mean AP (FHO: 174 4 vs. C: 108 1 mmHg), heart rate (FHO: 403 12 vs. C: 352 11 beats/min), BPV, cardiac inflammation (tumor necrosis factor-?-FHO: 65.8 9.9 vs. C: 23.3 4.3 pg/mg protein), and oxidative stress cardiac and renal tissues. However, CT was able to reduce mean AP (FHOT: 158 4 mmHg), heart rate (FHOT: 303 5 beats/min), insulin resistance, and sympathetic modulation. Moreover, the trained rats presented increased nitric oxide bioavailability, reduced tumor necrosis factor-? (FHOT: 33.1 4.9 pg/mg protein), increased IL-10 in cardiac tissue and reduced lipoperoxidation, and increased antioxidant defenses in cardiac and renal tissues. In conclusion, the association of risk factors promoted an additional impairment in metabolic, cardiovascular, autonomic, inflammatory, and oxidative stress parameters and combined exercise training was able to attenuate these dysfunctions. PMID:26423710

  19. Clinical Criteria Replenish High-Sensitive Troponin and Inflammatory Markers in the Stratification of Patients with Suspected Acute Coronary Syndrome

    PubMed Central

    Sthli, Barbara Elisabeth; Yonekawa, Keiko; Altwegg, Lukas Andreas; Wyss, Christophe; Hof, Danielle; Fischbacher, Philipp; Brauchlin, Andreas; Schulthess, Georg; Krayenbhl, Pierre-Alexandre; von Eckardstein, Arnold; Hersberger, Martin; Neidhart, Michel; Gay, Steffen; Novopashenny, Igor; Wolters, Regine; Frank, Michelle; Wischnewsky, Manfred Bernd; Lscher, Thomas Felix; Maier, Willibald

    2014-01-01

    Objectives In patients with suspected acute coronary syndrome (ACS), rapid triage is essential. The aim of this study was to establish a tool for risk prediction of 30-day cardiac events (CE) on admission. 30-day cardiac events (CE) were defined as early coronary revascularization, subsequent myocardial infarction, or cardiovascular death within 30 days. Methods and Results This single-centre, prospective cohort study included 377 consecutive patients presenting to the emergency department with suspected ACS and for whom troponin T measurements were requested on clinical grounds. Fifteen biomarkers were analyzed in the admission sample, and clinical parameters were assessed by the TIMI risk score for unstable angina/Non-ST myocardial infarction and the GRACE risk score. Sixty-nine (18%) patients presented with and 308 (82%) without ST-elevations, respectively. Coronary angiography was performed in 165 (44%) patients with subsequent percutaneous coronary intervention accounting for the majority of CE in 123 (33%) patients, respectively. Eleven out of 15 biomarkers were elevated in patients with CE compared to those without. High-sensitive troponin T (hs-cTnT) was the best univariate biomarker to predict CE in Non-ST-elevation patients (AUC 0.80), but did not yield incremental information above clinical TIMI risk score (AUC 0.80 vs 0.82, p?=?0.69). Equivalence testing of AUCs of risk models and non-inferiority testing demonstrated that the clinical TIMI risk score alone was non-inferior to its combination with hs-cTnT in predicting CE. Conclusions In patients presenting without ST-elevations, identification of those prone to CE is best based on clinical assessment based on TIMI risk score criteria and hs-cTnT. PMID:24892556

  20. Associations of retinol-binding protein 4 with oxidative stress, inflammatory markers, and metabolic syndrome in a middle-aged and elderly Chinese population

    PubMed Central

    2014-01-01

    Background Retinol-binding protein 4 (RBP4), a novel adipokine secreted by adipocytes and the liver, has elevated levels in type 2 diabetes mellitus (T2DM). However, its association with human metabolic diseases remains controversial. The present study was designed to investigate the associations of plasma RBP4 levels with oxidative stress, inflammatory markers, and metabolic syndrome (MetS) in a Chinese population. Method We evaluated plasma RBP4 levels in a cross-sectional sample of 1748 Chinese men and women aged 50 to 70 years in Guangzhou using an in-house developed and validated sandwich ELISA. Plasma glucose, insulin, lipid profile, serum adiponectin, adipocyte fatty acid-binding protein (A-FABP), 8-iso-prostaglandin F2α (8-iso PGF2α), 13-(S)-hydroxyoctadecadienoic acid (13-HODE), high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL6), monocyte chemotactic protein 1 (MCP1) and tumor necrosis factor α (TNFα) were all measured. MetS was defined according to the updated National Cholesterol Education Program Adult Treatment Panel III criteria for Asian Americans. Results Circulating RBP4 levels were positively correlated with A-FABP (r = 0.104, P < 0.001), 8-iso PGF2α (0.236, P < 0.001), and 13-HODE (0.204, P < 0.001) and were inversely correlated with HDL cholesterol (r = −0.072, P = 0.004). After multivariable adjustment, the RBP4 levels were strongly associated with MetS and its components. The ORs (95% CIs) for the comparisons of the extreme quartiles of RBP4 were 3.46 (2.87, 4.42) for MetS, 5.92 (4.47, 8.02) for hypertriglyceridemia, 1.42 (1.11, 1.68) for reduced HDL cholesterol, 1.87 (1.48, 2.36) for central obesity and 2.74 (2.15, 3.36) for hyperglycemia (all P < 0.001). When we further controlled for adipokines, markers of oxidative stress and proinflammatory response, the association of RBP4 with central obesity was abolished but not the association with other MetS components. Conclusions Plasma RBP4 levels are associated with an adverse profile of oxidative stress and inflammatory markers and an increased risk of MetS in this Chinese population. These associations are independent of conventional risk factors. PMID:24559154

  1. Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells.

    PubMed

    Tsilioni, Irene; Russell, Irwin J; Stewart, Julia M; Gleason, Rae M; Theoharides, Theoharis C

    2016-03-01

    Fibromyalgia syndrome (FMS) is a chronic, idiopathic condition of widespread musculoskeletal pain affecting more women than men. Even though clinical studies have provided evidence of altered central pain pathways, the lack of definitive pathogenesis or reliable objective markers has hampered development of effective treatments. Here we report that the neuropeptides corticotropin-releasing hormone (CRH), substance P (SP), and SP-structurally-related hemokinin-1 (HK-1) were significantly (P = 0.026, P < 0.0001, and P = 0.002, respectively) elevated (0.82 ± 0.57 ng/ml, 0.39 ± 0.18 ng/ml, and 7.98 ± 3.12 ng/ml, respectively) in the serum of patients with FMS compared with healthy controls (0.49 ± 0.26 ng/ml, 0.12 ± 0.1 ng/ml, and 5.71 ± 1.08 ng/ml, respectively). Moreover, SP and HK-1 levels were positively correlated (Pearson r = 0.45, P = 0.002) in FMS. The serum concentrations of the inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF) were also significantly (P = 0.029 and P = 0.006, respectively) higher (2.97 ± 2.35 pg/ml and 0.92 ± 0.31 pg/ml, respectively) in the FMS group compared with healthy subjects (1.79 ± 0.62 pg/ml and 0.69 ± 0.16 pg/ml, respectively). In contrast, serum IL-31 and IL-33 levels were significantly lower (P = 0.0001 and P = 0.044, respectively) in the FMS patients (849.5 ± 1005 pg/ml and 923.2 ± 1284 pg/ml, respectively) in comparison with healthy controls (1281 ± 806.4 pg/ml and 3149 ± 4073 pg/ml, respectively). FMS serum levels of neurotensin were not different from controls. We had previously shown that CRH and SP stimulate IL-6 and TNF release from mast cells (MCs). Our current results indicate that neuropeptides could stimulate MCs to secrete inflammatory cytokines that contribute importantly to the symptoms of FMS. Treatment directed at preventing the secretion or antagonizing these elevated neuroimmune markers, both centrally and peripherally, may prove to be useful in the management of FMS. PMID:26763911

  2. Serum Concentrations of Interleukin-6, Procalcitonin, and C-Reactive Protein: Discrimination of Septical Complications and Systemic Inflammatory Response Syndrome after Pediatric Surgery.

    PubMed

    Neunhoeffer, Felix; Plinke, Swantje; Renk, Hanna; Hofbeck, Michael; Fuchs, Jörg; Kumpf, Matthias; Zundel, Sabine; Seitz, Guido

    2016-04-01

    Background Early differentiation between sepsis and systemic inflammatory response syndrome (SIRS) is useful for therapeutic management in neonates and infants after surgery. Objective To compare the early (first 2 days) diagnostic value of interleukin-6 (IL-6), procalcitonin (PCT), and C-reactive protein (CRP) after surgery in the differentiation of subsequent SIRS and septic complications. Methods IL-6, PCT, and CRP were measured 0, 24, and 48 hours after surgery in neonates and infants with clinical suspicion of postoperative sepsis. Sensitivity, specificity, and predictive values for SIRS/septic complications were calculated. Results A total of 31 out of 205 neonates and infants showed clinical signs for postoperative sepsis and underwent sepsis work-up. Nine patients developed septic complications, sixteen patients met criteria for SIRS, and six patients showed an uneventful postoperative course during the first five postoperative days. IL-6, PCT, and CRP levels increased in all subgroups after surgery and were significantly higher in the sepsis group (p < 0.05). IL-6 peaked immediately, CRP at 24 to 48 hours, and PCT at 24 hours after surgery. Sensitivity and specificity (area under the curve) for IL-6 (cutoff 673 ng/dL) were 94.4 and 75% (86.2%), for CRP (cutoff 1.48 mg/dL) 76.2 and 75.0% (88.1%), and for PCT (cutoff 16.1 mg/L) 66.7 and 57.1% (65.6%). Conclusion IL-6 appears to be an early marker for severe bacterial infections with high sensitivity. IL-6 and CRP were the most reliable markers for the discrimination between SIRS and sepsis within the postoperative period. PMID:25643248

  3. Treatment of irritable bowel syndrome in outpatients with inflammatory bowel disease using a food and beverage intolerance, food and beverage avoidance diet.

    PubMed

    MacDermott, Richard P

    2007-01-01

    Irritable bowel syndrome (IBS) in the outpatient with chronic inflammatory bowel disease (IBD) is a difficult but important challenge to recognize and treat. It is very helpful to have effective treatment approaches for IBS that are practical and use minimal medications. Because of the underlying chronic inflammation in IBD, IBS symptoms occur with increased frequency and severity, secondary to increased hypersensitivity to foods and beverages that stimulate the gastrointestinal tract. This paper discusses how to treat IBS in the IBD outpatient, with emphasis on using a food and beverage intolerance, avoidance diet. The adverse effects of many foods and beverages are amount dependent and can be delayed, additive, and cumulative. The specific types of foods and beverages that can induce IBS symptoms include milk and milk containing products; caffeine containing products; alcoholic beverages; fruits; fruit juices; spices; seasonings; diet beverages; diet foods; diet candies; diet gum; fast foods; condiments; fried foods; fatty foods; multigrain breads; sourdough breads; bagels; salads; salad dressings; vegetables; beans; red meats; gravies; spaghetti sauce; stews; nuts; popcorn; high fiber; and cookies, crackers, pretzels, cakes, and pies. The types of foods and beverages that are better tolerated include water; rice; plain pasta or noodles; baked or broiled potatoes; white breads; plain fish, chicken, turkey, or ham; eggs; dry cereals; soy or rice based products; peas; applesauce; cantaloupe; watermelon; fruit cocktail; margarine; jams; jellies; and peanut butter. Handouts that were developed based upon what worsens or helps IBS symptoms in patients are included to help patients learn which foods and beverages to avoid and which are better tolerated. PMID:17206644

  4. Can mean platelet volume and mean platelet volume/platelet count ratio be used as a diagnostic marker for sepsis and systemic inflammatory response syndrome?

    PubMed Central

    Ates, Selma; Oksuz, Haf?ze; Dogu, B?rsen; Bozkus, Fulsen; Ucmak, Hasan; Yan?t, Fadime

    2015-01-01

    Objectives: To determine whether the mean platelet volume (MPV) and MPV/platelet (PLT) values can be used in the study of sepsis and systemic inflammatory response syndrome (SIRS). Methods: In this retrospective case-controlled study, 69 sepsis, 69 SIRS patients, and 72 control group who were treated in the years 2012-2013 were reviewed, and both the MPV and MPV/PLT rates were evaluated in all groups at Kahramanmaras Sutcu Imam University Intensive Care Unit, Kahramanmaras, Turkey. Results: Statistically significant difference was found between sepsis, SIRS, and control groups when comparing the MPV and MPV/PLT ratio (p<0.05), and no significant difference was found between sepsis and SIRS groups in terms of MPV and MPV/PLT ratio (p>0.05). Mean platelet volume values for sepsis and control groups was 10.07/8.731 femtoliter (fL) (p=0.000), and 9.45/8.731 fL (p=0.000) for SIRS and control groups. In the group of sepsis patients, the MPV was found to be at cut-off 8.915, sensitivity 71%, and specificity 63.9%. In the group of patients with SIRS, MPV was found to be at cut-off 8.85, sensitivity 69.6%, and specificity 62.5%. For the MPV/PLT values, the specificity and sensitivity were found to be insignificant. Conclusion: This study shows that although there was no significant reduction in the PLT values between the sepsis and SIRS patients, the MPV and MPV/PLT ratio values were found to have significant differences. However, the specificity and sensitivity of the values were not reliable standard to be used as a test. PMID:26446329

  5. Immune reconstitution inflammatory syndrome mimicking progressive multifocal leucoencephalopathy in a multiple sclerosis patient treated with natalizumab: a case report and review of the literature.

    PubMed

    Evangelopoulos, Maria-Eleptheria; Koutoulidis, Vasilios; Kilidireas, Kostas; Evangelopoulos, Dimitrios-Stergios; Nakas, Georgios; Andreadou, Elisabeth; Moulopoulos, Lia-Angela

    2015-01-01

    Natalizumab (NTM) represents an effective drug for the treatment of relapsing-remitting multiple sclerosis (RRMS). Progressive multifocal leucoencephalopathy (PML) is a potential life-threatening complication of NTM treatment. A close follow-up and MRI monitoring of patients under NTM are required to avoid such devastating complications. The case of a 47-year-old woman with RRMS (EDSS 1.5) treated with NTM for 44 months is reported. The patient had a relapse with mild cerebellar symptomatology and visual complaints. MRI revealed a new area of abnormal signal intensity in the subcortical white matter of the right parietal lobe with mild peripheral enhancement. Visual fields showed scotomata mostly of the left eye. NTM was discontinued. JC virus (JCV) polymerase chain reaction (PCR) in cerebrospinal fluid was negative. The patient received IV corticosteroids for 5 days and then monthly for 2 months with subsequent clinical and MRI improvement. On month 4, she presented with a new relapse with severe ataxia, mild behavioral change, increase of cerebellar symptoms and internuclear opthalmoplegia (EDSS 3.5). MRI showed reappearance of the right parietal lobe lesion, with decreased size and less pronounced contrast enhancement. A new 2-cm lesion was noted in the left cerebellar hemisphere with a speckled pattern of contrast enhancement. JCV PCR was negative and the patient was treated with IV corticosteroids. On month 12, she demonstrated clinical and MRI improvement. Although initially PML was highly suspected in this patient, the clinical and MRI findings were supportive of the presence of immune reconstitution inflammatory syndrome (IRIS). PMID:25368707

  6. Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways

    PubMed Central

    2010-01-01

    Background In a recently published paper, Harvey and Wessely put forward a 'biopsychosocial' explanatory model for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is proposed to be applicable to (chronic) fatigue even when apparent medical causes are present. Methods Here, we review the model proposed by Harvey and Wessely, which is the rationale for behaviourally oriented interventions, such as cognitive behaviour therapy (CBT) and graded exercise therapy (GET), and compare this model with a biological model, in which inflammatory, immune, oxidative and nitrosative (IO&NS) pathways are key elements. Discussion Although human and animal studies have established that the pathophysiology of ME/CFS includes IO&NS pathways, these abnormalities are not included in the model proposed by Harvey and Wessely. Activation of IO&NS pathways is known to induce fatigue and somatic (F&S) symptoms and can be induced or maintained by viral and bacterial infections, physical and psychosocial stressors, or organic disorders such as (auto)immune disorders. Studies have shown that ME/CFS and major depression are both clinical manifestations of shared IO&NS pathways, and that both disorders can be discriminated by specific symptoms and unshared or differentiating pathways. Interventions with CBT/GET are potentially harmful for many patients with ME/CFS, since the underlying pathophysiological abnormalities may be intensified by physical stressors. Conclusions In contrast to Harvey and Wessely's (bio)psychosocial model for ME/CFS a bio(psychosocial) model based upon IO&NS abnormalities is likely more appropriate to this complex disorder. In clinical practice, we suggest physicians should also explore the IO&NS pathophysiology by applying laboratory tests that examine the pathways involved. PMID:20550693

  7. Inflammatory Myopathies

    MedlinePLUS

    ... or persistent, inflammatory myopathy are polymyositis, dermatomyositis, and inclusion body myositis (IBM). These rare disorders may affect ... Institute of Neurological Disorders and Stroke (NINDS). NINDS Inclusion Body Myositis Information Page Inclusion Body Myositis (Inflammatory ...

  8. UPREGULATION OF MICRO RNA-146a (miRNA-146a), A MARKER FOR INFLAMMATORY NEURODEGENERATION, IN SPORADIC CREUTZFELDT-JAKOB DISEASE (sCJD) AND GERSTMANNSTRAUSSLERSCHEINKER (GSS) SYNDROME

    PubMed Central

    Lukiw, W.J.; Dua, P.; Pogue, A. I.; Eicken, C.; Hill, J. M.

    2013-01-01

    A mouse- and human-brain-abundant, nuclear factor (NF)-?B-regulated, micro RNA-146a (miRNA-146a) is an important modulator of the innate immune response and inflammatory signaling in specific immunological and brain cell types. Levels of miRNA-146a are induced in human brain cells challenged with at least five different species of single- or double-stranded DNA or RNA neurotrophic viruses, suggesting a broad role for miRNA-146a in the brains innate immune response and antiviral immunity. Upregulated miRNA-146a is also observed in pro-inflammatory cytokine-, A?42 peptide- and neurotoxic metal-induced, oxidatively stressed human neuronal-glial primary cell cocultures, in murine scrapie and in Alzheimers disease (AD) brain. In AD, miRNA-146a levels are found to progressively increase with disease severity and co-localize to brain regions enriched in inflammatory neuropathology. This study provides evidence of upregulation of miRNA-146a in extremely rare (incidence 110 per 100 million) human prion-based neurodegenerative disorders, including sporadic CreutzfeldtJakob disease (sCJD) and GerstmannStraussler-Scheinker syndrome (GSS). The findings suggest that an upregulated miRNA-146a may be integral to innate immune or inflammatory brain cell responses in prion-mediated infections and to progressive and irreversible neurodegeneration of both the murine and human brain. PMID:22043907

  9. Utility of Sepsis Biomarkers and the Infection Probability Score to Discriminate Sepsis and Systemic Inflammatory Response Syndrome in Standard Care Patients

    PubMed Central

    Ratzinger, Franz; Schuardt, Michael; Eichbichler, Katherina; Tsirkinidou, Irene; Bauer, Marlene; Haslacher, Helmuth; Mitteregger, Dieter; Binder, Michael; Burgmann, Heinz

    2013-01-01

    Physicians are regularly faced with severely ill patients at risk of developing infections. In literature, standard care wards are often neglected, although their patients frequently suffer from a systemic inflammatory response syndrome (SIRS) of unknown origin. Fast identification of patients with infections is vital, as they immediately require appropriate therapy. Further, tools with a high negative predictive value (NPV) to exclude infection or bacteremia are important to increase the cost effectiveness of microbiological examinations and to avoid inappropriate antibiotic treatment. In this prospective cohort study, 2,384 patients with suspected infections were screened for suffering from two or more SIRS criteria on standard care wards. The infection probability score (IPS) and sepsis biomarkers with discriminatory power were assessed regarding their capacity to identify infection or bacteremia. In this cohort finally consisting of 298 SIRS-patients, the infection prevalence was 72%. Bacteremia was found in 25% of cases. For the prediction of infection, the IPS yielded 0.51 ROC-AUC (30.1% sensitivity, 64.6% specificity). Among sepsis biomarkers, lipopolysaccharide binding protein (LBP) was the best parameter with 0.63 ROC-AUC (57.5% sensitivity, 67.1% specificity). For the prediction of bacteremia, the IPS performed slightly better with a ROC-AUC of 0.58 (21.3% sensitivity, 65% specificity). Procalcitonin was the best discriminator with 0.78 ROC-AUC, 86.3% sensitivity, 59.6% specificity and 92.9% NPV. Furthermore, bilirubin and LBP (ROC-AUC: 0.65, 0.62) might also be considered as useful parameters. In summary, the IPS and widely used infection parameters, including CRP or WBC, yielded a poor diagnostic performance for the detection of infection or bacteremia. Additional sepsis biomarkers do not aid in discriminating inflammation from infection. For the prediction of bacteremia procalcitonin, and bilirubin were the most promising parameters, which might be used as a rule for when to take blood cultures or using nucleic acid amplification tests for microbiological diagnostics. PMID:24349403

  10. Geraniol, Alone and in Combination with Pioglitazone, Ameliorates Fructose-Induced Metabolic Syndrome in Rats via the Modulation of Both Inflammatory and Oxidative Stress Status

    PubMed Central

    Ibrahim, Sherehan M.; El- Denshary, Ezzedin S.; Abdallah, Dalaal M.

    2015-01-01

    Geraniol (GO) potent antitumor and chemopreventive effects are attributed to its antioxidant and anti-inflammatory properties. In the current study, the potential efficacy of GO (250 mg/kg) in ameliorating metabolic syndrome (MetS) induced by fructose in drinking water was elucidated. Moreover, the effect of pioglitazone (5 and 10 mg/kg; PIO) and the possible interaction of the co-treatment of GO with PIO5 were studied in the MetS model. After 4 weeks of treatment, GO and/or PIO reduced the fasting blood glucose and the glycemic excursion in the intraperitoneal glucose tolerance test. GO and PIO5/10 restrained visceral adiposity and partly the body weight gain. The decreased level of peroxisome proliferator activated receptor (PPAR)-? transcriptional activity in the visceral adipose tissue of MetS rats was increased by single treatment regimens. Though GO did not affect MetS-induced hyperinsulinemia, PIO5/10 lowered it. Additionally, GO and PIO5/10 suppressed glycated hemoglobin and the receptor for advanced glycated end products (RAGE). These single regimens also ameliorated hyperuricemia, the disrupted lipid profile, and the elevated systolic blood pressure evoked by MetS. The rise in serum transaminases, interleukin-1?, and tumor necrosis factor-?, as well as hepatic lipid peroxides and nitric oxide (NO) was lowered by the single treatments to different extents. Moreover, hepatic non-protein thiols, as well as serum NO and adiponectin were enhanced by single regimens. Similar effects were reached by the combination of GO with PIO5; however, a potentiative interaction was noted on fasting serum insulin level, while synergistic effects were reflected as improved insulin sensitivity, as well as reduced RAGE and triglycerides. Therefore, GO via the transcriptional activation of PPAR-? reduces inflammation and free radical injury produced by MetS. Thereby, these effects provide novel mechanistic insights on GO management of MetS associated critical risk factors. Moreover, the co-administration of GO to PIO5 exalted the antidiabetic drug anti-MetS efficacy. PMID:25679220

  11. A Prospective Follow-Up of Adipocytokines in Cohort Patients With Gout: Association With Metabolic Syndrome But Not With Clinical Inflammatory Findings: Strobe-Compliant Article.

    PubMed

    Garca-Mndez, Sergio; Rivera-Bahena, Carolina Bustos; Montiel-Hernndez, Jos Luis; Xibill-Friedmann, Daniel; lvarez-Hernndez, Everardo; Pelez-Ballestas, Ingris; Burgos-Vargas, Rubn; Vzquez-Mellado, Janitzia

    2015-07-01

    The aim of this study was to determine the levels of leptin (Lep) and adiponectin (AdipoQ) in patients with gout and its relationship with joint inflammatory data and/or with metabolic syndrome (MetS) variables, during 1 year follow-up.Forty-one patients (40 males) with gout diagnosis, attending for the first time to a rheumatology department, were included. Evaluations were performed baseline, at 6 and 12 months. Variables included the following: demographic, clinical and laboratory data related to gout and associated diseases. Lep and AdipoQ determinations by the ELISA method were performed in frozen serum from each visit. The pharmacological and no-pharmacological treatment for gout and associated diseases was individualized for each patient according to published guidelines. Statistical analysis included Mann-Whitney U test, Fisher test, x, ANOVA, Cochran Q, Pearson and Spearman correlation tests, as well as linear regression.In the baseline evaluation, 29.2% had MetS (hypertriglyceridemia 66%, hypertension 44% and obesity 37%); patients with MetS had higher C reactive protein (CRP) levels [34.1 28.6 vs. 12.2 11.2 mg/dL, P = 0.033]. Although not significant, also had higher Lep and lower AdipoQ levels (3.2 3.0 vs. 1.9 1.2 ng/mL, P = 0.142 and 40.5 26.8 vs. 38.0 24.9 ng/mL, P = 0.877, respectively). During follow-up, our patients had significant improvement in serum uric acid (sUA) levels and variables evaluating pain and joint swelling (P ? 0.05). Metabolic abnormalities tended to persist or even worsen during the monitoring period: significant increase in total cholesterol (P = 0.004), tendency to higher triglycerides (P = 0.883) and slight improvement in glycaemia (P = 0.052). Lep values increased significantly during follow-up (P = 0.001) while AdipoQ levels diminished slightly (P = 0.317). Neither Lep nor AdipoQ values showed important correlation (r > 0.5) with metabolic variables or joint swelling.This study suggests that in patients with gout, concentrations of Lep and AdipoQ are more in line with the metabolic state than with clinical disease activity. PMID:26131838

  12. AB165. The role of inflammatory cytokines and MAPK signaling in chronic prostatitis/chronic pelvic pain syndrome with related mental health disorders

    PubMed Central

    Hu, Chao; Yang, Hualan; Zhao, Yanfang; Chen, Xiang; Dong, Yinying; Dong, Yehao; Cui, Jiefeng; Zhu, Tongyu; Zheng, Ping; Lin, Ching-Shwun; Dai, Jican

    2015-01-01

    Objective Mental health disorders (MHD) in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) have been widely studied. However, the underlying molecular mechanisms and, in particular, role of inflammatory cytokines and their associated signaling pathways has not been investigated in detail. To determine the potential role of cytokines and associated signaling pathways in CP/CPPS patients with MHD and in a CP/CPPS animal model. Methods Between July 2012 and August 2013, 810 CP/CPPS patients and 992 control subjects were enrolled in this case-control multicenter study, and serum cytokine levels were measured. Male Sprague-Dawley rats received multiple intracutaneous injections (neck, tail, and pelvic limbs) of an immuno-agent along with a pertussis-diphtheria-tetanus triple vaccine for autoimmune CP/CPPS development. After 45 and 60 days behavioral analysis was performed, and prostate and specific brain areas related to MHD were subjected to RT-qPCR and Western blot analysis of cytokine signaling pathways. Moreover, histological prostate examination, and detection of IL-1? levels in serum and cerebrospinal fluid (CSF) was performed. Results In CP/CPPS patients with significant MHD, elevated IL-1?, IL-1?, IL-4, IL-13, and TNF-? serum levels were observed. The above five cytokines in CP/CPPS rats were significantly elevated in prostate tissue (P<0.05), and IL-1? levels were elevated in serum and CSF. In behavioral tests, CP/CPPS rats showed anxiety- and depression-like symptoms, and impaired spatial and associative memory performance (P<0.05). In the CP/CPPS group ERK1/2 phosphorylation levels were increased in the amygdala and nucleus accumbens, and decreased in the hippocampus and caudate nucleus. Lack of human CSF data in present research may limit the translational values of the results. Conclusions These data suggest that prostate-derived cytokines, especially IL-1?, cross the blood brain barrier and may lead to enhanced ERK1/2 signaling in several brain areas, possibly underlying induction of CP/CPPS-related MHD.

  13. A Prospective Follow-Up of Adipocytokines in Cohort Patients With Gout: Association With Metabolic Syndrome But Not With Clinical Inflammatory Findings

    PubMed Central

    García-Méndez, Sergio; Rivera-Bahena, Carolina Bustos; Montiel-Hernández, José Luis; Xibillé-Friedmann, Daniel; Álvarez-Hernández, Everardo; Peláez-Ballestas, Ingris; Burgos-Vargas, Rubén; Vázquez-Mellado, Janitzia

    2015-01-01

    Abstract The aim of this study was to determine the levels of leptin (Lep) and adiponectin (AdipoQ) in patients with gout and its relationship with joint inflammatory data and/or with metabolic syndrome (MetS) variables, during 1 year follow-up. Forty-one patients (40 males) with gout diagnosis, attending for the first time to a rheumatology department, were included. Evaluations were performed baseline, at 6 and 12 months. Variables included the following: demographic, clinical and laboratory data related to gout and associated diseases. Lep and AdipoQ determinations by the ELISA method were performed in frozen serum from each visit. The pharmacological and no-pharmacological treatment for gout and associated diseases was individualized for each patient according to published guidelines. Statistical analysis included Mann–Whitney U test, Fisher test, x2, ANOVA, Cochran Q, Pearson and Spearman correlation tests, as well as linear regression. In the baseline evaluation, 29.2% had MetS (hypertriglyceridemia 66%, hypertension 44% and obesity 37%); patients with MetS had higher C reactive protein (CRP) levels [34.1 ± 28.6 vs. 12.2 ± 11.2 mg/dL, P = 0.033]. Although not significant, also had higher Lep and lower AdipoQ levels (3.2 ± 3.0 vs. 1.9 ± 1.2 ng/mL, P = 0.142 and 40.5 ± 26.8 vs. 38.0 ± 24.9 ng/mL, P = 0.877, respectively). During follow-up, our patients had significant improvement in serum uric acid (sUA) levels and variables evaluating pain and joint swelling (P ≤ 0.05). Metabolic abnormalities tended to persist or even worsen during the monitoring period: significant increase in total cholesterol (P = 0.004), tendency to higher triglycerides (P = 0.883) and slight improvement in glycaemia (P = 0.052). Lep values increased significantly during follow-up (P = 0.001) while AdipoQ levels diminished slightly (P = 0.317). Neither Lep nor AdipoQ values showed important correlation (r > 0.5) with metabolic variables or joint swelling. This study suggests that in patients with gout, concentrations of Lep and AdipoQ are more in line with the metabolic state than with clinical disease activity. PMID:26131838

  14. Enhancing of Women Functional Status with Metabolic Syndrome by Cardioprotective and Anti-Inflammatory Effects of Combined Aerobic and Resistance Training

    PubMed Central

    Alsamir Tibana, Ramires; da Cunha Nascimento, Dahan; Frade de Sousa, Nuno Manuel; de Souza, Vinicius Carolino; Durigan, Joo; Vieira, Amilton; Bottaro, Martim; de Toledo Nbrega, Otvio; de Almeida, Jeeser Alves; Navalta, James Wilfred; Franco, Octavio Luiz; Prestes, Jonato

    2014-01-01

    These data describe the effects of combined aerobic plus resistance training (CT) with regards to risk factors of metabolic syndrome (MetS), quality of life, functional capacity, and pro- and anti-inflammatory cytokines in women with MetS. In this context, thirteen women (35.46.2 yr) completed 10 weeks of CT consisting of three weekly sessions of ?60 min aerobic training (treadmill at 6570% of reserve heart rate, 30 min) and resistance training (3 sets of 812 repetitions maximum for main muscle groups). Dependent variables were maximum chest press strength; isometric hand-grip strength; 30 s chair stand test; six minute walk test; body mass; body mass index; body adiposity index; waist circumference; systolic (SBP), diastolic and mean blood pressure (MBP); blood glucose; HDL-C; triglycerides; interleukins (IL) 6, 10 and 12, osteoprotegerin (OPG) and serum nitric oxide metabolite (NOx); quality of life (SF-36) and Z-Score of MetS. There was an improvement in muscle strength on chest press (p?=?0.009), isometric hand-grip strength (p?=?0.03) and 30 s chair stand (p?=?0.007). There was a decrease in SBP (p?=?0.049), MBP (p?=?0.041), Z-Score of MetS (p?=?0.046), OPG (0.420.26 to 0.380.19 ng/mL, p<0.05) and NOx (13.32.3 mol/L to 9.12.3 mol/L; p<0.0005). IL-10 displayed an increase (13.67.5 to 17.212.3 pg/mL, p<0.05) after 10 weeks of training. Combined training also increased the perception of physical capacity (p?=?0.011). This study endorses CT as an efficient tool to improve blood pressure, functional capacity, quality of life and reduce blood markers of inflammation, which has a clinical relevance in the prevention and treatment of MetS. Trial Registration Brazilian Clinical Trials Registry (ReBec) - RBR-6gdyvz - http://www.ensaiosclinicos.gov.br/rg/?q=RBR-6gdyvz PMID:25379699

  15. Genetics Home Reference: Majeed syndrome

    MedlinePLUS

    ... inflammatory bone condition known as chronic recurrent multifocal osteomyelitis (CRMO). This condition causes recurrent episodes of pain ... Syndrome Genetic Testing Registry: Majeed syndrome MedlinePlus Encyclopedia: Osteomyelitis MedlinePlus Encyclopedia: Psoriasis You might also find information ...

  16. Genetics Home Reference: Majeed syndrome

    MedlinePLUS

    ... syndrome have had an inflammatory skin disorder called psoriasis. Where can I find information about diagnosis or ... Registry: Majeed syndrome MedlinePlus Encyclopedia: Osteomyelitis MedlinePlus Encyclopedia: Psoriasis You might also find information on the diagnosis ...

  17. Nutrition in inflammatory bowel disease.

    PubMed

    Kelly, D G

    1999-08-01

    The nutritional impact of inflammatory bowel disease is notable, both in Crohn's disease and ulcerative colitis. The causes of malnutrition include decreased intake, maldigestion, malabsorption, accelerated nutrient losses, increased requirements, and drug-nutrient interactions. Inflammatory bowel disease causes alterations in body composition and, because of these changes, affects energy expenditure. Various approaches have been most effective in correcting malnutrition, supporting growth, and managing short-bowel syndrome, but the success of primary therapy has been limited. PMID:10980968

  18. DRESS syndrome as a complication of treatment of hepatitis C virus-associated post-inflammatory liver cirrhosis with peginterferon α2a and ribavirin

    PubMed Central

    Pazgan-Simon, Monika; Simon, Krzysztof

    2014-01-01

    Various skin and systemic symptoms may develop as a complication of treatment with different medications and medicinal substances. One of them is a relatively rare drug reaction with eosinophilia and systemic symptoms, referred to as DRESS syndrome. The morphology of skin lesions and the patient's general health can differ; the management involves withdrawal of drugs suspected of triggering DRESS syndrome, and administration of local and systemic glucocorticosteroids. In this paper we present a case of a patient with HCV associated chronic hepatitis, treated with peginterferon α2a (PEG-IFN-α2a) and ribavirin, who developed skin lesions and systemic symptoms typical of DRESS syndrome. PMID:25610356

  19. Allergic acute coronary syndrome (Kounis syndrome)

    PubMed Central

    Chhabra, Lovely; Masrur, Shihab; Parker, Matthew W.

    2015-01-01

    Anaphylaxis rarely manifests as a vasospastic acute coronary syndrome with or without the presence of underlying coronary artery disease. The variability in the underlying pathogenesis produces a wide clinical spectrum of this syndrome. We present three cases of anaphylactic acute coronary syndrome that display different clinical variants of this phenomenon. The main pathophysiological mechanism of the allergic anginal syndromes is the inflammatory mediators released during a hypersensitivity reaction triggered by food, insect bites, or drugs. It is important to appropriately recognize and treat Kounis syndrome in patients with exposure to a documented allergen. PMID:26130889

  20. Why myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) may kill you: disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways may explain cardiovascular disorders in ME/CFS.

    PubMed

    Maes, Michael; Twisk, Frank Nm

    2009-01-01

    There is evidence that disorders in inflammatory and oxidative and nitrosative (IO&NS) pathways and a lowered antioxidant status are important pathophysiological mechanisms underpinning myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS). Important precipitating and perpetuating factors for ME/CFS are (amongst others) bacterial and viral infections; bacterial translocation due to an increased gut permeability; and psychological stress. Recently, Jason et al (2006) reported that the mean age of patients with myalgic encephalomyelitis/chronic fatigue syndrome dying from heart failure, i.e. 58.7 years, is significantly lower than the age of those dying from heart failure in the general US population, i.e. 83.1 years. These findings implicate that ME/CFS is a risk factor to cardio-vascular disorder. This review demonstrates that disorders in various IO&NS pathways provide explanations for the earlier mortality due to cardiovascular disorders in ME/CFS. These pathways are: a) chronic low grade inflammation with extended production of nuclear factor kappa B and COX-2 and increased levels of tumour necrosis factor alpha; b) increased O&NS with increased peroxide levels, and phospholipid oxidation including oxidative damage to phosphatidylinositol; c) decreased levels of specific antioxidants, i.e. coenzyme Q10, zinc and dehydroepiandrosterone-sulphate; d) bacterial translocation as a result of leaky gut; e) decreased omega-3 polyunsatutared fatty acids (PUFAs), and increased omega-6 PUFA and saturated fatty acid levels; and f) the presence of viral and bacterial infections and psychological stressors. The mechanisms whereby each of these factors may contribute towards cardio-vascular disorder in ME/CFS are discussed. ME/CFS is a multisystemic metabolic-inflammatory disorder. The aberrations in IO&NS pathways may increase the risk for cardiovascular disorders. PMID:20038921

  1. Effect of amino acids residues 323-433 and 628-747 in Nsp2 of representative porcine reproductive and respiratory syndrome virus strains on inflammatory response in vitro.

    PubMed

    Liu, Xing; Bai, Juan; Wang, Haiyan; Fan, Baochao; Li, Yufeng; Jiang, Ping

    2015-10-01

    Porcine reproductive and respiratory syndrome virus (PRRSV) is an important pathogen that is responsible for large economic losses in the swine industry worldwide. In PRRSV strains, many genetic variations occur in the central hypervariable region (HV2) of the Nsp2 gene, which encodes non-structural protein 2. For example, PRRSV strains VR2332, Em2007, MN184C, and TJM-F92 contained variations in the Nsp2 sequences and exhibited differing levels of virulence in adult pigs. However, the role of HV2 with respect to PRRSV immunity is unclear. In this study, four recombinant PRRSV strains (rBB/+30aa, rBB/?68aa, rBB/?111aa, and rBB/?120aa) were rescued using a highly pathogenic type 2 PRRSV cDNA clone (pBB). All rescued strains displayed similar growth characteristics to the parental rBB virus in pulmonary alveolar macrophages (PAMs). Expression levels of inflammatory cytokines IL-?, IL-6, and TNF-? were significantly lower, at the mRNA and protein level, for groups infected with rBB/?111aa and rBB/?120aa than those in the rBB group. Levels of these inflammatory cytokines in the rBB/+30aa and rBB/?68aa groups were not significantly different with those in the rBB group. Phosphorylation levels of I?B were decreased to a greater extent in the rBB/?111aa and rBB/?120aa groups compared with those in the rBB/+30aa, rBB/?68aa, and rBB groups. Our results indicate that amino acids 323-433 and 628-747 of Nsp2 failed to exert significant effects on PRRSV replication in PAMs, but modulated the expression of inflammatory cytokines in vitro. PMID:26043979

  2. Clinical particularities and response to the anti-inflammatory effect of antiviral treatment in patients with chronic hepatitis C and rheumatoid syndrome.

    PubMed

    Lilea, G C; Streba, C T; Baloseanu, C L; Vere, C C; Rogoveanu, I

    2012-12-15

    Hepatitis C virus (HCV) is an important cause for the development of serious hepatic disease such as chronic hepatitis and liver cirrhosis. Though the pathological mechanisms are poorly understood, it is well established that CHC plays an important role in several immune mediated conditions, including rheumatoid arthritis. We focused on the clinical particularities of patients with CHC and associated RS and we specifically investigated the anti-inflammatory role of IFN-alpha concerning the rheumatic symptoms. PMID:23346247

  3. HIV protease inhibitors alter innate immune response signaling to double-stranded RNA in oral epithelial cells: implications for immune reconstitution inflammatory syndrome?

    PubMed

    Danaher, Robert J; Kaetzel, Charlotte S; Greenberg, Richard N; Wang, Chunmei; Bruno, Maria E C; Miller, Craig S

    2010-10-23

    In this investigation, several HIV protease inhibitors altered the virally associated, double-stranded RNA (dsRNA)-stimulated, innate immune response. Lopinavir, the most potent inducer of interleukin (IL)-8 expression, also inhibited dsRNA-induced monocyte chemotactic protein 1 expression. Further analyses demonstrated that nuclear factor-κB is required for lopinavir's induction of IL-8. These findings demonstrate that protease inhibitors, such as lopinavir, differentially dysregulate innate immune signaling in a manner that could affect immune (reconstitution) inflammatory responses in oral epithelium. PMID:20841991

  4. [Inflammatory cerebral amyloid angiopathy].

    PubMed

    Ii, Yuichiro; Tomimoto, Hidekazu

    2015-03-01

    Inflammatory cerebral amyloid angiopathy (CAA) typically affects older patients who present with acute or subacute cognitive decline, headache, behavioral change, seizures, and focal neurological deficits. Brain magnetic resonance imaging (MRI) reveals patchy or confluent asymmetric white matter hyperintensities on T2-weighted or fluid-attenuated inversion recovery images, which indicates vasogenic edema, and previous lobar hemorrhages and/or multiple lobar microbleeds on T2*-weighted gradient-recalled echo or susceptibility-weighted imaging. Neuropathological findings include frank vasculitis and/or perivascular inflammation with mononuclear or multinucleated giant cells that are associated with amyloid-beta (A?)-laden vessels. Importantly, these findings suggest that these patients may respond well to immunosuppressive treatment with high-dose corticosteroids and/or cyclophosphamide. The pathogenesis of this syndrome is still unknown, although anti-A? autoantibodies in the cerebrospinal fluid may mediate inflammatory processes against cerebrovascular A?. Moreover, MRI findings in patients with inflammatory CAA are very similar to those in patients with Alzheimer's disease who were treated with a monoclonal anti-A? antibody, and these findings are called amyloid-related imaging abnormalities (ARIA). Anti-A? autoantibodies in the cerebrospinal fluid might be a biomarker of future disease-modifying therapies for patients with Alzheimer's disease and CAA. PMID:25846442

  5. Acute inflammatory myelopathies.

    PubMed

    Cree, Bruce A C

    2014-01-01

    Inflammatory injury to the spinal cord causes a well-recognized clinical syndrome. Patients typically develop bilateral weakness, usually involving the legs, although the arms may also become affected, in association with a pattern of sensory changes that suggests a spinal cord dermatomal level. Bowel and bladder impairment is also common in many patients. Recognition of the clinical pattern of spinal cord injury should lead clinicians to perform imaging studies to evaluate for compressive etiologies. MRI of the spine is particularly useful in helping visualize intraparenchymal lesions and when these lesions enhance following contrast administration a diagnosis of myelitis is made. Cerebrospinal fluid analysis can also confirm a diagnosis of myelitis when a leukocytosis is present. There are many causes of non-compressive spinal cord injury including infectious, parainfectious, toxic, nutritional, vascular, systemic as well as idiopathic inflammatory etiologies. This review focuses on inflammatory spinal cord injury and its relationships with multiple sclerosis, neuromyelitis optica, acute disseminated encephalomyelitis and systemic collagen vascular and paraneoplastic diseases. PMID:24507538

  6. Syndromic Scoliosis

    MedlinePLUS

    ... Neurofibromatosis (NF) Noonan Syndrome VATER/VACTERL Syndrome Angelman Syndrome Rett Prader Willi Osteogenesis Imperfecta Trisomy 21 (Down's Syndrome) Symptoms Highly variable based on underlying syndrome and ...

  7. The rate of bloodstream infection is high in infants with short bowel syndrome: Relationship with small bowel bacterial overgrowth, enteral feeding and inflammatory and immune responses

    PubMed Central

    Cole, Conrad R.; Frem, Juliana C.; Schmotzer, Brian; Gewirtz, Andrew T.; Meddings, Jonathan B.; Gold, Benjamin D.; Ziegler, Thomas R.

    2009-01-01

    Objective This pilot study in parenteral nutrition (PN) dependent infants with short bowel syndrome (SBS) evaluated the impact of feeding route and intestinal permeability on bloodstream infection (BSI), small bowel bacterial overgrowth (SBBO) and systemic immune responses, and fecal calprotectin as a biomarker for SBBO. Study design 10 infants (ages 4.2-15.4 months) with SBS due to necrotizing enterocolitis were evaluated. Nutritional assessment, breath hydrogen testing, intestinal permeability, fecal calprotectin, serum flagellin- and LPS- specific antibody titers, and proinflammatory cytokine concentrations (TNF-?, IL-1 ?, IL-6, IL-8) were performed at baseline, 60 and 120 days. Healthy, age-matched controls (n=5) were recruited. Results BSI incidence was high (80%) and SBBO was common (50%). SBBO increased the odds for BSI (> 7-fold; p=0.009). Calprotectin levels were higher in children with SBS and SBBO versus those without SBBO and healthy controls (p<0.05). Serum TNF-?, was elevated at baseline versus controls. Serum TNF-?, IL-1 ?, IL-6 and IL-8 levels diminished with increased enteral nutrition. Anti-flagellin and anti-LPS IgG levels in children with SBSwere lower versus controls and rose over time. Conclusion In children with SBS, SBBO increases the risk for BSI and systemic proinflammatory response decreases with increasing enteral feeding and weaning PN. PMID:20171649

  8. [Mirizzi's syndrome].

    PubMed

    Roullet-Audy, J C; Guivarc'h, M; Mosnier, H

    1989-04-15

    Six cases of Mirizzi syndrome are reported. The syndrome consists of a special anatomical variant of the cystic duct, which has a low opening but runs side-by-side with the common bile duct, associated with entrapment of a gallstone in the cystic duct or the neck of the gallbladder, partial or total obstruction of the hepatic duct by the stone and by inflammatory lesions, and recurrent cholangitis. Clinical signs are non-specific and suggest at first sight an obstructive jaundice. Pre-operative morphological examination seldom provide a diagnosis before surgery. In the most typical cases ultrasonography shows dilatation of the upper biliary tract with narrowing of the hepatic duct below the dilatation, due to a stone located outside the common bile duct. Opacification of the biliary tract by endoscopic retrograde catheterization of the papilla duodeni or by transparietohepatic puncture give suggestive images (non-opacification of the cystic duct, narrowing of the hepatic duct opposite the extrinsic compression, with overlying dilatation), but these images are not specific. The per-operative diagnosis is difficult owing to the inflammatory lesions, and a diagnosis of cholangiocarcinoma may be envisaged. Cholecystectomy with recanalization of the cystic duct suppresses the extrinsic compression and helps the inflammatory lesions to regress. However, opening and draining the common bile duct is often necessary. PMID:2524051

  9. Inflammatory glaucoma

    PubMed Central

    Bodh, Sonam A.; Kumar, Vasu; Raina, Usha K.; Ghosh, B.; Thakar, Meenakshi

    2011-01-01

    Glaucoma is seen in about 20% of the patients with uveitis. Anterior uveitis may be acute, subacute, or chronic. The mechanisms by which iridocyclitis leads to obstruction of aqueous outflow include acute, usually reversible forms (e.g., accumulation of inflammatory elements in the intertrabecular spaces, edema of the trabecular lamellae, or angle closure due to ciliary body swelling) and chronic forms (e.g., scar formation or membrane overgrowth in the anterior chamber angle). Careful history and follow-up helps distinguish steroid-induced glaucoma from uveitic glaucoma. Treatment of combined iridocyclitis and glaucoma involves steroidal and nonsteroidal antiinflammatory agents and antiglaucoma drugs. However, glaucoma drugs can often have an unpredictable effect on intraocular pressure (IOP) in the setting of uveitis. Surgical intervention is required in case of medical failure. Method of Literature Search: Literature on the Medline database was searched using the PubMed interface. PMID:21713239

  10. Anti-inflammatory actions of acupuncture.

    PubMed Central

    Zijlstra, Freek J; van den Berg-de Lange, Ineke; Huygen, Frank J P M; Klein, Jan

    2003-01-01

    Acupuncture has a beneficial effect when treating many diseases and painful conditions, and therefore is thought to be useful as a complementary therapy or to replace generally accepted pharmacological intervention. The attributive effect of acupuncture has been investigated in inflammatory diseases, including asthma, rhinitis, inflammatory bowel disease, rheumatoid arthritis, epicondylitis, complex regional pain syndrome type 1 and vasculitis. Large randomised trials demonstrating the immediate and sustained effect of acupuncture are missing. Mechanisms underlying the ascribed immunosuppressive actions of acupuncture are reviewed in this communication. The acupuncture-controlled release of neuropeptides from nerve endings and subsequent vasodilative and anti-inflammatory effects through calcitonine gene-related peptide is hypothesised. The complex interactions with substance P, the analgesic contribution of beta-endorphin and the balance between cell-specific pro-inflammatory and anti-inflammatory cytokines tumour necrosis factor-alpha and interleukin-10 are discussed. PMID:12775355

  11. A non-synonymous polymorphism in IL-23R Gene (rs1884444) is associated with reduced risk to schistosomiasis-associated Immune Reconstitution Inflammatory Syndrome in a Kenyan population

    PubMed Central

    2014-01-01

    Background Human Immunodeficiency Virus (HIV) and Schistosomiasis co-infection is common among residents at the shores of Lake Victoria in Kenya. About 36% of this population initiating antiretroviral therapy (ART) experience Immune Reconstitution Inflammatory Syndrome (IRIS) that complicates recovery. Several IL-23R alleles have been associated with susceptibility to both autoimmune and inflammatory diseases through T-helper type 17 (TH17) cells. However, whether or not variants within the IL-23R increase susceptibility to IRIS in western Kenya is unknown. The objective of the current study was to determine the association between IL-23R gene polymorphisms, CD4+ cell counts and HIV RNA levels and IRIS in HIV and Schistosoma mansoni co-infected patients undergoing highly active anti-retroviral therapy (HAART). Methods A three-month case–control study was conducted on antiretroviral naïve schistosomiasis/HIV co-infected fishermen starting HAART in Uyoma Rarieda, Siaya County, Kenya. Seventy one patients were sampled at baseline and followed up for three months, to establish if they developed Schistosoma-related IRIS. In addition, the CD4+ cell counts and HIV RNA levels were determined in pre- and post-administration of HAART. Variations at five polymorphic sites of IL-23R (rs1884444, rs11465754, rs6682925, rs7530511 and rs7539625) based on >10% minor allele frequency in Yoruban reference population was determined using Allelic Discrimination Assay. The association between the five variants and susceptibility to IRIS was determined using logistic regression while controlling for potential confounders. In addition, the functional differences between the baseline CD4 + Cell counts and viral loads were determined using medians while across IL-23R genotypes were determined using Kruskal-Wallis tests. Results Overall, 26 (36.6%) patients developed schistosomiasis-associated IRIS at a median age of 35.5 years. Carriage of the TT genotype at the non-synonymous rs1884444 T > G relative to GG, was associated with a decreased risk of schistosomiasis-associated IRIS (OR, 0.25, 95% CI, 0.07-0.96, P = 0.043) while both baseline CD4+ cell counts and viral loads had no association with IRIS. Conclusion These findings indicate that the non-synonymous variant rs1884444 T > G of IL-23R is associated with a decreased risk to schistosomiasis-associated IRIS. However, additional studies in a larger cohort and with an all inclusive polymorphic variants in the synonymous and non-synonymous regions need to be evaluated. PMID:24912586

  12. SAPHO syndrome associated spondylitis

    PubMed Central

    Tanaka, Masato; Nakanishi, Kazuo; Misawa, Haruo; Sugimoto, Yoshihisa; Takahata, Tomohiro; Nakahara, Hiroyuki; Nakahara, Shinnosuke; Ozaki, Toshifumi

    2008-01-01

    The concept of synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome has been well clarified, after Chamot et al. suggested this peculiar disorder in 1987. The most commonly affected site in SAPHO syndrome is the anterior chest, followed by the spine. However, the clinical course and taxonomic concept of SAPHO spinal lesions are poorly understood. This study was performed to analyze: (1) the detailed clinical course of spinal lesions in SAPHO syndrome, and (2) the relationship between SAPHO syndrome with spinal lesions and seronegative spondyloarthropathy. Thirteen patients with spondylitis in SAPHO syndrome were analyzed. The features of spinal lesions were a chronic onset with a slight inflammatory reaction, and slowly progressing non-marginal syndesmophytes at multi spinal levels, besides the coexistence of specific skin lesions. SAPHO syndrome, especially spinal lesions related to palmoplantar pustulosis, can be recognized as a subtype of seronegative spondyloarthropathy. PMID:18642032

  13. [SAPHO syndrome].

    PubMed

    Heldmann, F; Kiltz, U; Baraliakos, X; Braun, J

    2014-10-01

    The SAPHO syndrome, an acronym for synovitis, acne, pustulosis, hyperostosis and osteitis, is a rare disease which affects bones, joints and the skin. The main osteoarticular features are hyperostosis and osteitis. Osteoarticular symptoms predominantly occur on the anterior chest wall but the spine and the peripheral skeleton can also be involved. The most important skin affections are palmoplantar pustulosis and severe acne. The etiology of this syndrome remains unclear but infectious, immunological and genetic factors are involved. The diagnostic features of SAPHO syndrome are clinical and radiological. The most important diagnostic procedure is Tc-99 m bone scintigraphy but conventional x-rays as well as computed tomography (CT) and magnetic resonance imaging (MRI) can also contribute to the final diagnosis. Bone histology and positron emission tomography CT (PET-CT) may help to differentiate SAPHO syndrome from malignancies and infectious osteomyelitis. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the cornerstone of treatment. The results obtained using antibiotics and disease-modifying antirheumatic drugs (DMARDs), such as sulfasalazine and methotrexate are inconsistent. Bisphosphonates and anti-tumor necrosis factor (anti-TNF) drugs have shown promising results in small studies but further research is still necessary. PMID:25260820

  14. A Randomized, Double-Blind, Placebo-Controlled Clinical Trial of a Chemokine Receptor 5 (CCR5) Antagonist to Decrease the Occurrence of Immune Reconstitution Inflammatory Syndrome in HIV-Infection: The CADIRIS Study

    PubMed Central

    Sierra-Madero, Juan G.; Ellenberg, Susan; Rassool, Mohammed S.; Tierney, Ann; Belaunzarn-Zamudio, Pablo F.; Lpez-Martnez, Alondra; Pieira-Menndez, Alicia; Montaner, Luis J.; Azzoni, Livio; Bentez, Csar Rivera; Sereti, Irini; Andrade-Villanueva, Jaime; Mosqueda-Gmez, Juan L.; Rodriguez, Benigno; Sanne, Ian; Lederman, Michael M.

    2015-01-01

    Background Immune Reconstitution Inflammatory Syndrome (IRIS) is a common complication of antiretroviral therapy (ART) in HIV-infected patients. IRIS is associated with an increased risk of hospitalization and death. We ascertained whether CCR5 blockade using maraviroc reduces the risk of IRIS. Methods The CADIRIS study was a randomized, double-blind, placebo-controlled, clinical trial that accrued subjects from five clinical sites in Mexico and one in South Africa between November 2009 and January 2012, and followed them for one year. The primary outcome was occurrence of IRIS by 24 weeks. HIV-infected adults, nave to ART, with CD4 cells <100/?L, and HIVRNA >1,000 copies/mL were eligible. We screened 362 subjects; 279 met inclusion criteria, 3 refused participation, and 276 were randomized. Participants received maraviroc 600 mg twice daily or placebo added to an ART regimen that included tenofovir, emtricitabine, and efavirenz for 48 weeks. Findings There were 276 patients randomized (140 received maraviroc and 136 placebo). There was no difference in the time to IRIS events between treatment arms (HR 108, 95% CI (066, 177), log-rank test p=0743). In total, 64 (23%) patients had IRIS events, 33 (24%) in the maraviroc arm and 31 (23%) in the placebo arm (p=088). Interpretation Maraviroc had no significant effect on frequency, time or severity of IRIS events after ART initiation. Including a CCR5 inhibitor in an initial treatment regimen does not confer a meaningful protection from the occurrence of IRIS in persons with advanced HIV infection. Funding The trial was funded as investigator initiated research by Pfizer Inc, New York, NY, USA. Trial Registration ClinicalTrials.gov. ID: NCT00988780 (http://clinicaltrials.gov/ct2/show/NCT00988780) PMID:26366430

  15. Nutrition in inflammatory bowel diseases.

    PubMed

    Mihai, C?t?lina; Prelipcean, Cristina Cijevschi; Pintilie, Iulia; Nedelciuc, Otilia; Jigaranu, Anca-Olivia; Dranga, Mihaela; Mihai, B

    2013-01-01

    The relationship between nutrition and inflammatory bowel disease (IBD) is a complex one, the evaluation and correction of nutritional deficits being integral part of therapy in these patients. The diet that consists in excessive consumption of meat, sugar, fats (with a higher 0 6 /o) 3 polyunsaturated fatty acids ratio) are factors involved in the epidemiology and pathogenesis of IBD. Malnutrition is present among most IBD patients, being the result of multiple mechanisms from digestive symptoms to inflammatory process, intestinal resection and administration of medications. Oral diet is high-calorie, high protein at correcting the vitamin and mineral deficiencies. Enteral diet has both an adjuvant role and that of inducing and maintaining remission as single treatment, particularly in children. Parenteral nutrition is reserved for patients with obstruction, fistula, toxic megacolon, short bowel syndrome, severe malabsorption, and other conditions that make enteral nutrition impossible or inefficient. PMID:24502032

  16. Nonsteroidal anti-inflammatory drugs.

    PubMed

    Dugowson, Carin E; Gnanashanmugam, Priya

    2006-05-01

    Nonsteroidal anti-inflammatory drugs, including COX-2 selective drugs, are often used for acute and chronic musculoskeletal pain,including osteoarthritis, trauma, overuse syndromes, and compression fractures. Although these medications are often well tolerated in the young and otherwise healthy patient, the chronic use of these medications can lead to multiple medical problems, most commonly related to the gastrointestinal tract. Recently, concerns about cardiovascular adverse effects have been raised, particularly in the COX-2 drugs. Dosing and duration of therapy should be adjusted for comorbidities. CBC and renal and hepatic function should be checked at intervals of 3 to 6 months, depending on the patient. PMID:16616271

  17. Sweet's syndrome.

    PubMed

    Limdiwala, Piyush G; Parikh, Shilpa J; Shah, Jigna S

    2014-01-01

    Acute febrile neutrophilic dermatosis or Sweet's syndrome (SS) is characterized by painful, erythematous plaques of rapid onset accompanied by fever. The etiology of SS is unknown and it may be associated with antecedent infections, malignancies, autoimmune diseases, drugs and vaccines, upper respiratory or gastrointestinal infection, pregnancy, inflammatory bowel disease as well as chemotherapy or idiopathic. The standard therapy for SS is systemic corticosteroids. We report a rare case of 19-year-old young male patient with complaint of severe ill-defined type of pain in both jaws associated with plaques and papules on extensor surfaces of upper and lower extremities with bodyache and myalgia. Histopathological examination suggested perivascular neutrophilic infiltration with scattered eosinophils. Sweet syndrome has rare oral manifestations secondary to hematological changes. It can also present as a paraneoplastic syndrome (malignancy-associated form of condition, which is most commonly related to acute myelogenous leukemia), which leads to poor prognosis and thus it requires careful examination, early diagnosis and long-term follow-up. PMID:25099003

  18. Metabolic Syndrome

    MedlinePLUS

    ... How Can I Help a Friend Who Cuts? Metabolic Syndrome KidsHealth > For Teens > Metabolic Syndrome Print A A ... applies to a condition known as metabolic syndrome. Metabolic Syndrome Is an Early Warning Sign Metabolic syndrome isn' ...

  19. Action of antiproteases on the inflammatory response in acute pancreatitis.

    PubMed

    Chen, Chun-Chia; Wang, Sun Sang; Lee, Fa-Yauh

    2007-01-01

    The spectrum of acute pancreatitis ranges from mild edematous disease to a severe necrotizing process which is usually accompanied by local or systemic complications and even mortality. Early deaths (within the first week) due to severe acute pancreatitis are generally caused by massive inflammatory responses which result in multiple organ failure. Although the exact mechanisms which trigger the inflammatory and necrotizing processes are not completely understood, it is generally accepted that autodigestion and activated leukocytes play important roles in the pathogenesis of acute pancreatitis. Proinflammatory cytokines are associated with systemic inflammatory response syndrome and multiple organ failure syndrome in acute pancreatitis. A compensatory anti-inflammatory response occurs in parallel with systemic inflammatory response syndrome. Trypsin secreted by the pancreatic acinar cells activates protease-activated receptor-2 which can result in the production of cytokines. Protease inhibitors such as aprotinin, gabexate mesilate, nafamostat mesilate, ulinastatin, etc. can inhibit the various enzymes and inflammatory response in experimental and clinical studies. Thus, protease inhibitors have been considered as a potential treatment to inhibit the pancreatic inflammation in acute pancreatitis. The beneficial effects of antiproteases on experimental severe acute pancreatitis may be, in part, due to the modulation of inflammatory cytokine responses. The effect of protease inhibitors on the inflammatory response in human acute pancreatitis deserves further study. PMID:17625305

  20. Coexistence of Ankylosing Spondylitis and Klinefelter's Syndrome

    PubMed Central

    Kobak, ?enol; Yalin, Murat; Karadeniz, Muamer; Oncel, Guray

    2013-01-01

    Ankylosing spondylitis is a chronic inflammatory disease characterized by inflammatory lower back pain and morning stiffness and accompanied by spine and sacroiliac joint involvement. Klinefelter's syndrome is a genetic condition that only affects males. Affected males have an extra X chromosome. This paper reports a 30-years-old male on followup with the diagnosis of Klinefelters syndrome. The patient admitted with complaints of inflammatory lower back, and neck pain and morning stiffness and was diagnosed with ankylosing spondylitis. Nonsteroidal anti-inflammatory drug and salazopyrine treatment resulted in significant regression in his complaints. PMID:23762731

  1. Coexistence of Ankylosing Spondylitis and Klinefelter's Syndrome.

    PubMed

    Kobak, Senol; Yalin, Murat; Karadeniz, Muamer; Oncel, Guray

    2013-01-01

    Ankylosing spondylitis is a chronic inflammatory disease characterized by inflammatory lower back pain and morning stiffness and accompanied by spine and sacroiliac joint involvement. Klinefelter's syndrome is a genetic condition that only affects males. Affected males have an extra X chromosome. This paper reports a 30-years-old male on followup with the diagnosis of Klinefelters syndrome. The patient admitted with complaints of inflammatory lower back, and neck pain and morning stiffness and was diagnosed with ankylosing spondylitis. Nonsteroidal anti-inflammatory drug and salazopyrine treatment resulted in significant regression in his complaints. PMID:23762731

  2. Classification and prognosis of inflammatory muscle disease.

    PubMed

    Miller, F W

    1994-11-01

    Although our understanding of the inflammatory myopathies is still evolving, it is becoming increasingly clear that these syndromes are composed of many separate and distinct disorders with widely divergent clinical signs, symptoms, laboratory abnormalities, and prognoses. Their classification remains controversial, but three approaches of dividing the myositis syndromes appear useful in helping to group disorders with similar features together. The three approaches divide these syndromes on the basis of clinical and histopathologic findings, by serology, and by exposures to known environmental agents. Studies of the prognosis of these disorders are limited by the rarity and heterogeneity of the myositis syndromes. Taken together, however, they suggest that a variety of demographic, clinical, and serologic features are associated with a poor outcome. These include older age at myositis onset, severe myositis, delay to diagnosis and therapy, significant cardiac, pulmonary or gastrointestinal involvement, and the presence of cancer, inclusion body myositis, or antisynthetase or anti-SRP auto-antibodies. It is hoped that our understanding of the classification and prognosis of the inflammatory myopathies will become more complete as we perceive more fully the interrelationships between the genetic and environmental risk factors necessary for the induction of myositis and develop more rational ways of dividing and treating these increasingly recognized syndromes. PMID:7855323

  3. Inflammatory Bowel Disease

    MedlinePLUS

    ... do I have a higher chance of getting colon cancer? Can my inflammatory bowel disease make it harder ... do I have a higher chance of getting colon cancer? Yes. Inflammatory bowel disease (IBD) can increase your ...

  4. How I Manage Heel Spur Syndrome.

    ERIC Educational Resources Information Center

    Seder, Joseph I.

    1987-01-01

    This article discusses plantar fascitis and heel spurs, the two contributing causes of heel spur syndrome. Treatment methods, which include rest, anti-inflammatory medication, shoe padding, and, as a last resort, surgery are described. (Author/MT)

  5. Complete remission of Sweet's syndrome after azacytidine treatment for concomitant myelodysplastic syndrome.

    PubMed

    Martinelli, Sara; Rigolin, Gian Matteo; Leo, Genesio; Gaf, Roberta; Lista, Enrico; Cibien, Francesca; Sofritti, Olga; Daghia, Giulia; Cavazzini, Francesco; Cuneo, Antonio

    2014-01-01

    Sweet's syndrome is a rare condition with potentially disabling implications, characterized by painful skin lesions due to neutrophilic dermal infiltration and systemic inflammatory symptoms. A significant proportion of cases is malignancy associated. Hematologic neoplasms, particularly acute myeloid leukemia and myelodysplastic syndromes, are the most commonly associated malignant conditions. Here, we describe the first case of clinical remission of refractory Sweet's syndrome following hypomethylating therapy with azacytidine in a patient with myelodysplastic syndrome who concurrently obtained a complete hematologic response. PMID:24554168

  6. Anti-Inflammatory Iridoids of Botanical Origin

    PubMed Central

    Viljoen, A; Mncwangi, N; Vermaak, I

    2012-01-01

    Inflammation is a manifestation of a wide range of disorders which include; arthritis, atherosclerosis, Alzheimer’s disease, inflammatory bowel syndrome, physical injury and infection amongst many others. Common treatment modalities are usually non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, paracetamol, indomethacin and ibuprofen as well as corticosteroids such as prednisone. These however, may be associated with a host of side effects due to non-selectivity for cyclooxygenase (COX) enzymes involved in inflammation and those with selectivity may be highly priced. Thus, there is a continuing search for safe and effective anti-inflammatory molecules from natural sources. Research has confirmed that iridoids exhibit promising anti-inflammatory activity which may be beneficial in the treatment of inflammation. Iridoids are secondary metabolites present in various plants, especially in species belonging to the Apocynaceae, Lamiaceae, Loganiaceae, Rubiaceae, Scrophulariaceae and Verbenaceae families. Many of these ethnobotanicals have an illustrious history of traditional use alluding to their use to treat inflammation. Although iridoids exhibit a wide range of pharmacological activities such as cardiovascular, hepatoprotection, hypoglycaemic, antimutagenic, antispasmodic, anti-tumour, antiviral, immunomodulation and purgative effects this review will acutely focus on their anti-inflammatory properties. The paper aims to present a summary for the most prominent iridoid-containing plants for which anti-inflammatory activity has been demonstrated in vitro and / or in vivo. PMID:22414102

  7. Metabolic Syndrome

    MedlinePLUS

    ... Th M e etabolic Syndrome What is the metabolic syndrome? The term metabolic syndrome describes a cluster of risk factors that increase ... high blood sugar). The exact cause of the metabolic syndrome is not known but genetic factors, too much ...

  8. Antiphospholipid Syndrome

    MedlinePLUS

    ... Awards Enhancing Diversity Find People About NINDS NINDS Antiphospholipid Syndrome Information Page Synonym(s): Hughes Syndrome Table of Contents ( ... research is being done? Clinical Trials What is Antiphospholipid Syndrome? Antiphospholipid syndrome (APS) is an autoimmune disorder caused ...

  9. Cushing's Syndrome

    MedlinePLUS

    MENU Return to Web version Cushing's Syndrome Overview What is Cushing's syndrome? Cushing's syndrome occurs when your body is exposed to high levels ... they can cause problems with your eyesight. Diagnosis & Tests How is Cushing's syndrome diagnosed? Your doctor may ...

  10. Down Syndrome

    MedlinePLUS

    ... Sledding, Skiing, Snowboarding, Skating Crushes What's a Booger? Down Syndrome KidsHealth > For Kids > Down Syndrome Print A A ... skills. continue Do a Lot of People Have Down Syndrome? Down syndrome is not contagious , so you can' ...

  11. Observational Study of the Genetic Architecture of Neutrophil-Mediated Inflammatory Skin Diseases

    ClinicalTrials.gov

    2014-06-11

    Other Specified Inflammatory Disorders of Skin or Subcutaneous Tissue; Pyoderma Gangrenosum; Erosive Pustular Dermatosis of the Scalp; Sweet's Syndrome; Behcet's Disease; Bowel-associated Dermatosis-arthritis Syndrome; Pustular Psoriasis; Acute Generalized Exanthematous Pustulosis; Keratoderma Blenorrhagicum; Sneddon-Wilkinson Disease; IgA Pemphigus; Amicrobial Pustulosis of the Folds; Infantile Acropustulosis; Transient Neonatal Pustulosis; Neutrophilic Eccrine Hidradenitis; Rheumatoid Neutrophilic Dermatitis; Neutrophilic Urticaria; Still's Disease; Erythema Marginatum; Unclassified Periodic Fever Syndromes / Autoinflammatory Syndromes; Dermatitis Herpetiformis; Linear IgA Bullous Dermatosis; Bullous Systemic Lupus Erythematosus; Inflammatory Epidermolysis Bullosa Aquisita; Neutrophilic Dermatosis of the Dorsal Hands (Pustular Vasculitis); Small Vessel Vasculitis Including Urticarial Vasculitis; Erythema Elevatum Diutinum; Medium Vessel Vasculitis

  12. Anti-inflammatory effects of insulin.

    TOXLINE Toxicology Bibliographic Information

    Dandona P; Chaudhuri A; Mohanty P; Ghanim H

    2007-07-01

    PURPOSE OF REVIEW: This review deals with the recent observations on the pro-inflammatory effects of glucose and the anti-inflammatory actions of insulin. Apart from being novel, they are central to our understanding of why hyperglycemia is a prognosticator of bad clinical outcomes including patients with acute coronary syndromes, stroke and in patients in the intensive care unit.RECENT FINDINGS: The pro-inflammatory effect of glucose as well as that of other macronutrients including fast food meals provides the basis of chronic oxidative stress and inflammation in the obese and their propensity to atherosclerotic disease. The anti-inflammatory action of insulin provides a neutralizing effect to balance macronutrient induced inflammation on the one hand and the possibility of using insulin as an anti-inflammatory drug on the other.SUMMARY: The actions of macronutrients and insulin described above explain why insulin resistant states like obesity and type 2 diabetes are associated with oxidative stress, inflammation and atherosclerosis. They also suggest that insulin may be antiatherogenic.

  13. Conjugated linoleic acid and inflammatory cell signalling.

    PubMed

    Reynolds, C M; Roche, H M

    2010-01-01

    Conjugated linoleic acids (CLA) are a family of polyunsaturated fatty acids (PUFA), some isomers occurring naturally in beef and dairy products and others being formed as a result of bihydrogenation of vegetable oils to form margarine. Synthetic and natural sources of CLA may have beneficial effects in a range of inflammatory conditions including colitis, atherosclerosis, metabolic syndrome and rheumatoid arthritis. Most of the biological effects have been attributed to the cis9, trans11- (c9, t11-) and the trans10, cis12- (t10, c12-) isomers. Evidence suggests that c9, t11-CLA is responsible for the anti-inflammatory effect attributed to CLA while t10, t12-CLA appears to be responsible for anti-adipogenic effects. This review will focus on the effects of CLA on the inflammatory components associated with insulin resistance, atherosclerosis and Th1 mediated inflammatory disease, at a cellular, systemic and clinical level. Whist CLA may ameliorate certain aspects of the inflammatory response, particularly within cellular and animal models, the relevance of this has yet to be clarified within the context of human health. PMID:20207526

  14. Curcumin in inflammatory diseases.

    PubMed

    Shehzad, Adeeb; Rehman, Gauhar; Lee, Young Sup

    2013-01-01

    Curcumin (diferuloylmethane), a yellow coloring agent extracted from turmeric is also used as a remedy for the treatment and prevention of inflammatory diseases. Acute and chronic inflammation is a major factor in the progression of obesity, type II diabetes, arthritis, pancreatitis, cardiovascular, neurodegenerative and metabolic diseases, as well as certain types of cancer. Turmeric has a long history of use in Ayurvedic medicine for the treatment of inflammatory disorders. Recent studies on the efficacy and therapeutic applicability of turmeric have suggested that the active ingredient of tumeric is curcumin. Further, compelling evidence has shown that curcumin has the ability to inhibit inflammatory cell proliferation, invasion, and angiogenesis through multiple molecular targets and mechanisms of action. Curcumin is safe, non-toxic, and mediates its anti-inflammatory effects through the down-regulation of inflammatory transcription factors, cytokines, redox status, protein kinases, and enzymes that all promote inflammation. In addition, curcumin induces apoptosis through mitochondrial and receptor-mediated pathways, as well as activation of caspase cascades. In the current study, the anti-inflammatory effects of curcumin were evaluated relative to various chronic inflammatory diseases. Based on the available pharmacological data obtained from in vitro and in vivo research, as well as clinical trials, an opportunity exists to translate curcumin into clinics for the prevention of inflammatory diseases in the near future. PMID:23281076

  15. Effect and Treatment of Chronic Pain in Inflammatory Arthritis

    PubMed Central

    2013-01-01

    Pain is the most common reason patients with inflammatory arthritis see a rheumatologist. Patients consistently rate pain as one of their highest priorities, and pain is the single most important determinant of patient global assessment of disease activity. Although pain is commonly interpreted as a marker of inflammation, the correlation between pain intensity and measures of peripheral inflammation is imperfect. The prevalence of chronic, non-inflammatory pain syndromes such as fibromyalgia is higher among patients with inflammatory arthritis than in the general population. Inflammatory arthritis patients with fibromyalgia have higher measures of disease activity and lower quality of life than inflammatory patients who do not have fibromyalgia. This review article focuses on current literature involving the effects of pain on disease assessment and quality of life for patients with inflammatory arthritis. It also reviews non-pharmacologic and pharmacologic options for treatment of pain for patients with inflammatory arthritis, focusing on the implications of comorbidities and concurrent disease-modifying antirheumatic drug therapy. Although several studies have examined the effects of reducing inflammation for patients with inflammatory arthritis, very few clinical trials have examined the safety and efficacy of treatment directed specifically towards pain pathways. Most studies have been small, have focused on rheumatoid arthritis or mixed populations (e.g., rheumatoid arthritis plus osteoarthritis), and have been at high risk of bias. Larger, longitudinal studies are needed to examine the mechanisms of pain in inflammatory arthritis and to determine the safety and efficacy of analgesic medications in this specific patient population. PMID:23292816

  16. Pediatric inflammatory bowel disease

    PubMed Central

    Diefenbach, Karen A; Breuer, Christopher K

    2006-01-01

    Inflammatory bowel disease is an important cause of gastrointestinal pathology in children and adolescents. The incidence of pediatric inflammatory bowel disease is increasing; therefore, it is important for the clinician to be aware of the presentation of this disease in the pediatric population. Laboratory tests, radiology studies, and endoscopic procedures are helpful in diagnosing inflammatory bowel disease and differentiating between Crohn’s disease and ulcerative colitis. Once diagnosed, the goal of medical management is to induce remission of disease while minimizing the side effects of the medication. Specific attention needs to be paid to achieving normal growth in this susceptible population. Surgical management is usually indicated for failure of medical management, complication, or malignancy. Algorithms for diagnostic evaluation and treatment of pediatric inflammatory bowel disease are presented. The specific psychosocial issues facing these patients are also discussed in this review as are the future goals of research in the complex problem of pediatric inflammatory bowel disease. PMID:16718840

  17. Dravet Syndrome

    MedlinePLUS

    ... NINDS Dravet Syndrome Information Page Synonym(s): Severe Myoclonic Epilepsy of Infancy (SMEI) Table of Contents (click to ... Dravet Syndrome? Dravet syndrome, also called severe myoclonic epilepsy of infancy (SMEI), is a severe form of ...

  18. Metabolic syndrome

    MedlinePLUS

    Metabolic syndrome is a name for a group of risk factors that occur together and increase the chance ... Metabolic syndrome is becoming very common in the United States. Doctors are not sure whether the syndrome is ...

  19. Down Syndrome

    MedlinePLUS

    ... NICHD Research Information Clinical Trials Resources and Publications Down Syndrome: Condition Information Skip sharing on social media links Share this: Page Content What is Down syndrome? Down syndrome describes a set of cognitive and ...

  20. Piriformis Syndrome

    MedlinePLUS

    ... Awards Enhancing Diversity Find People About NINDS NINDS Piriformis Syndrome Information Page Table of Contents (click to jump ... is being done? Clinical Trials Organizations What is Piriformis Syndrome? Piriformis syndrome is a rare neuromuscular disorder that ...

  1. Short communication: Camel milk ameliorates inflammatory responses and oxidative stress and downregulates mitogen-activated protein kinase signaling pathways in lipopolysaccharide-induced acute respiratory distress syndrome in rats.

    PubMed

    Zhu, Wei-Wei; Kong, Gui-Qing; Ma, Ming-Ming; Li, Yan; Huang, Xiao; Wang, Li-Peng; Peng, Zhen-Yi; Zhang, Xiao-Hua; Liu, Xiang-Yong; Wang, Xiao-Zhi

    2016-01-01

    Acute respiratory distress syndrome (ARDS) is a complex syndrome disorder with high mortality rate. Camel milk (CM) contains antiinflammatory and antioxidant properties and protects against numerous diseases. This study aimed to demonstrate the function of CM in lipopolysaccharide (LPS)-induced ARDS in rats. Camel milk reduced the lung wet:dry weight ratio and significantly reduced LPS-induced increases in neutrophil infiltration, interstitial and intra-alveolar edema, thickness of the alveolar wall, and lung injury scores of lung tissues. It also had antiinflammatory and antioxidant effects on LPS-induced ARDS. After LPS stimulation, the levels of proinflammatory cytokines (tumor necrosis factor-?, IL-10, and IL-1?) in serum and oxidative stress markers (malondialdehyde, myeloperoxidase, and total antioxidant capacity) in lung tissue were notably attenuated by CM. Camel milk also downregulated mitogen-activated protein kinase signaling pathways. Given these results, CM is a potential complementary food for ARDS treatment. PMID:26601576

  2. Phosphorylation site analysis of the anti-inflammatory and mRNA-destabilizing protein tristetraprolin

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Tristetraprolin (TTP/TIS11/ZFP36) is a member of the CCCH zinc finger proteins, and is an anti-inflammatory protein. Mice deficient in TTP develop a profound inflammatory syndrome with erosive arthritis, autoimmunity, and myeloid hyperplasia. TTP binds to AU-rich elements with high affinity for UUAU...

  3. Skin gangrene as an extraintestinal manifestation of inflammatory bowel disease.

    PubMed

    Komatsu, Yumi Cristina; Capareli, Gabriela Cunha; Boin, Maria Fernanda Feitosa de Camargo; Lellis, Rute; Freitas, Thas Helena Proena de; Simone, Karine

    2014-01-01

    Inflammatory bowel diseases can commonly present many cutaneous lesions which can contribute to the diagnosis of the disease or its activity. The most frequent cutaneous or mucocutaneous manifestations suggesting ulcerative rectocolitis activity are erythema nodosum (3-10%), pyoderma gangrenosum (5-12%) and aphthous stomatitis (4%). Other reactive skin manifestations related to immunological mechanisms associated with the inflammatory bowel disease are: Sweet's syndrome, arthritis-dermatitis syndrome associated with inflammatory bowel disease and leukocytoclastic vasculitis. We describe the case of a young man with diagnosis of ulcerative rectocolitis, which presented an extensive cutaneous gangrene secondary to microvascular thrombosis. The case represents a dermatologic rarity and should be recognized as a cutaneous manifestation related to the hypercoagulability state observed in the disease's activity. PMID:25387503

  4. Pelvic Inflammatory Disease

    MedlinePLUS

    Pelvic inflammatory disease (PID) is an infection and inflammation of the uterus, ovaries, and other female reproductive organs. It causes scarring ... United States. Gonorrhea and chlamydia, two sexually transmitted diseases, are the most common causes of PID. Other ...

  5. Inflammatory Concepts of Obesity

    PubMed Central

    Rocha, Viviane Zorzanelli; Folco, Eduardo J.

    2011-01-01

    Obesity, long considered a condition characterized by the deposition of inert fat, is now recognized as a chronic and systemic inflammatory disease, where adipose tissue plays a crucial endocrine role through the production of numerous bioactive molecules, collectively known as adipokines. These molecules regulate carbohydrate and lipid metabolism, immune function and blood coagulability, and may serve as blood markers of cardiometabolic risk. Local inflammatory loops operate in adipose tissue as a consequence of nutrient overload, and crosstalk among its cellular constituents-adipocytes, endothelial and immune cells-results in the elaboration of inflammatory mediators. These mediators promote important systemic effects that can result in insulin resistance, dysmetabolism and cardiovascular disease. The understanding that inflammation plays a critical role in the pathogenesis of obesity-derived disorders has led to therapeutic approaches that target different points of the inflammatory network induced by obesity. PMID:21837268

  6. Pelvic Inflammatory Disease (PID)

    MedlinePLUS

    ... Vietnamese) Recommend on Facebook Tweet Share Compartir Untreated sexually transmitted diseases (STDs) can cause pelvic inflammatory disease (PID), a ... plain language for individuals with general questions about sexually transmitted diseases. The content here can be syndicated (added to ...

  7. Breast Cancer -- Inflammatory

    MedlinePLUS

    ... medical, surgical, radiation, gynecologic, and pediatric oncologists, oncology nurses, physician assistants, social workers, and patient advocates. Cancer.Net Guide Breast Cancer - Inflammatory ... with Side Effects Follow-up Care and Monitoring ...

  8. Anti-inflammatory Diets.

    PubMed

    Sears, Barry

    2015-01-01

    Chronic disease is driven by inflammation. This article will provide an overview on how the balance of macronutrients and omega-6 and omega-3 fatty acids in the diet can alter the expression of inflammatory genes. In particular, how the balance of the protein to glycemic load of a meal can alter the generation of insulin and glucagon and the how the balance of omega-6 and omega-3 fatty acids can effect eicosanoid formation. Clinical results on the reduction of inflammation following anti-inflammatory diets are discussed as well as the molecular targets of anti-inflammatory nutrition. To overcome silent inflammation requires an anti-inflammatory diet (with omega-3s and polyphenols, in particular those of Maqui). The most important aspect of such an anti-inflammatory diet is the stabilization of insulin and reduced intake of omega-6 fatty acids. The ultimate treatment lies in reestablishing hormonal and genetic balance to generate satiety instead of constant hunger. Anti-inflammatory nutrition, balanced 40:30:30 with caloric restriction, should be considered as a form of gene silencing technology, in particular the silencing of the genes involved in the generation of silent inflammation. To this anti-inflammatory diet foundation supplemental omega-3 fatty acids at the level of 2-3g of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) per day should be added. Finally, a diet rich in colorful, nonstarchy vegetables would contribute adequate amounts of polyphenols to help not only to inhibit nuclear factor (NF)-?B (primary molecular target of inflammation) but also activate AMP kinase. Understanding the impact of an anti-inflammatory diet on silent inflammation can elevate the diet from simply a source of calories to being on the cutting edge of gene-silencing technology. PMID:26400429

  9. Nephrotoxicity of nonsteroidal anti-inflammatory drugs.

    PubMed

    Baisac, J; Henrich, W L

    1994-01-01

    Nonsteroidal anti-inflammatory drugs (NSAIDs) are important therapeutic agents in the management of rheumatologic disorders and other pain syndromes. Over the counter availability of the drugs has expanded the usage of the drugs. This article reviews the nephrotoxicity of these drugs, with some emphasis on NSAID-related proteinuria. Although reversibility of renal involvement upon drug discontinuance is the rule, progression to end-stage renal disease has occurred. A proposed guideline for monitoring renal impairment in low- and high-risk patients is also presented. PMID:7845321

  10. Fecal calprotectin in inflammatory bowel disease

    PubMed Central

    Walsham, Natalie E; Sherwood, Roy A

    2016-01-01

    Inflammatory bowel disease (IBD) and irritable bowel syndrome share many symptoms. While irritable bowel syndrome is a functional bowel disorder for which no specific treatment is available, the range of effective therapies for IBD is evolving rapidly. Accurate diagnosis of IBD is therefore essential. Clinical assessment, together with various imaging modalities and endoscopy, has been the mainstay of diagnosis for many years. Fecal biomarkers of gastrointestinal inflammation have appeared in the past decade, of which calprotectin, a neutrophil cytosolic protein, has been studied the most. Crohn’s disease and ulcerative colitis are chronic remitting and relapsing diseases, and objective assessment of disease activity and response to treatment are important. This review focuses on the use of fecal calprotectin measurements in the diagnosis and monitoring of patients with IBD. PMID:26869808

  11. [Proteus syndrome].

    PubMed

    Benichou, J J; Labrune, B; Formanek, A; Denoix, C; Oger, P

    1990-01-01

    Two new cases of Proteus syndrome are reported. This congenital syndrome, first described in 1983, comprises gigantism of extremities, body hemihypertrophy, pigmented nevi and multiple tumors (subcutaneous, lipomas, hamartomas). This syndrome belongs to the same group as Recklinghausen disease, Maffucci or Klippel-Trenaunay syndromes. The prognosis is not well known but mostly depends on functional and psychologic consequences of important deformations. PMID:2206106

  12. Evolution of Inflammatory Diseases

    PubMed Central

    Okin, Daniel

    2013-01-01

    The association of inflammation with modern human diseases (e.g. obesity, cardiovascular disease, type 2 diabetes mellitus, cancer) remains an unsolved mystery of current biology and medicine. Inflammation is a protective response to noxious stimuli that unavoidably occurs at a cost to normal tissue function. This fundamental tradeoff between the cost and benefit of the inflammatory response has been optimized over evolutionary time for specific environmental conditions. Rapid change of the human environment due to niche construction outpaces genetic adaptation through natural selection, leading increasingly to a mismatch between the modern environment and selected traits. Consequently, multiple tradeoffs that affect human physiology are not optimized to the modern environment, leading to increased disease susceptibility. Here we examine the inflammatory response from an evolutionary perspective. We discuss unique aspects of the inflammatory response and its evolutionary history that can help explain the association between inflammation and modern human diseases. PMID:22975004

  13. Desquamative inflammatory vaginitis.

    PubMed

    Reichman, Orna; Sobel, Jack

    2014-10-01

    Desquamative inflammatory vaginitis (DIV) is an uncommon form of chronic purulent vaginitis. It occurs mainly in Caucasians with a peak occurrence in the perimenopause. Symptoms and signs are nonspecific; DIV is a diagnosis of exclusion, and other causes of purulent vaginitis should be excluded. The main symptoms include purulent discharge, vestibulo-vaginal irritation, and dyspareunia. Examination of vaginal walls shows signs of inflammation with increased erythema and petechiae. Through microscopy (wet mount) of the vaginal secretions, DIV is defined by an increase in inflammatory cells and parabasal epithelial cells (immature squamous cells). Vaginal flora is abnormal and pH is always elevated above 4.5. Although etiology and pathogenesis remain unknown, the favorable response to anti-inflammatory agents suggests that the etiology is immune mediated. Either local vaginal clindamycin or vaginal corticosteroids are adequate treatment. As a chronic condition, maintenance treatment should be considered as relapse is common. PMID:25132275

  14. The Hyperferritinemic Syndrome: macrophage activation syndrome, Stills disease, septic shock and catastrophic antiphospholipid syndrome

    PubMed Central

    2013-01-01

    Background Over the last few years, accumulating data have implicated a role for ferritin as a signaling molecule and direct mediator of the immune system. Hyperferritinemia is associated with a multitude of clinical conditions and with worse prognosis in critically ill patients. Discussion There are four uncommon medical conditions characterized by high levels of ferritin, namely the macrophage activation syndrome (MAS), adult onset Stills disease (AOSD), catastrophic antiphospholipid syndrome (cAPS) and septic shock, that share a similar clinical and laboratory features, and also respond to similar treatments, suggesting a common pathogenic mechanism. Ferritin is known to be a pro-inflammatory mediator inducing expression of pro-inflammatory molecules, yet it has opposing actions as a pro-inflammatory and as an immunosuppressant. We propose that the exceptionally high ferritin levels observed in these uncommon clinical conditions are not just the product of the inflammation but rather may contribute to the development of a cytokine storm. Summary Here we review and compare four clinical conditions and the role of ferritin as an immunomodulator. We would like to propose including these four conditions under a common syndrome entity termed Hyperferritinemic Syndrome. PMID:23968282

  15. Inflammatory Monocyte Effector Mechanisms

    PubMed Central

    Lauvau, Gregoire; Chorro, Laurent; Spaulding, Emily; Soudja, Saidi M'Homa

    2014-01-01

    Monocytes are blood-derived mononuclear phagocytic cells that traffic throughout the body and can provide rapid innate immune effector responses in response to microbial pathogen infections. Amongst blood monocytes, the most abundant subset in mice is represented by inflammatory Ly6C+ CCR2+ monocytes and is the functional equivalent of the CD14+ monocytes in humans. Herein we focus on published evidence describing the exquisite functional plasticity of these cells, and we extend this overview to their multiples roles in vivo during host immune defenses against microbial pathogen infections, as antigen-presenting cells, inflammatory cells or Trojan horse cells. PMID:25205002

  16. Theodore Roosevelt's inflammatory rheumatism.

    PubMed

    Pinals, Robert S

    2008-02-01

    Theodore Roosevelt's death at age 60 was probably caused by a pulmonary embolus, but it was preceded by a 2 1/2-month illness described as inflammatory rheumatism. He had intermittent fever and acute arthritis in several joints leading to hospitalization and enforced bed rest for 6 weeks. The details of his illness and its possible etiology are reviewed. Inflammatory rheumatism was a descriptive term within which several modern diagnoses might be included. Although it is not possible to identify Roosevelt's illness with any certainty, it was most compatible with polyarticular gout, although reactive arthritis, rheumatic fever, and several other diagnoses cannot be ruled out. PMID:18431099

  17. Inflammatory bowel disease

    PubMed Central

    Beattie, R M; Croft, N M; Fell, J M; Afzal, N A; Heuschkel, R B

    2006-01-01

    Twenty five per cent of inflammatory bowel disease presents in childhood. Growth and nutrition are key issues in the management with the aim of treatment being to induce and then maintain disease remission with minimal side effects. Only 25% of Crohn's disease presents with the classic triad of abdominal pain, weight loss, and diarrhoea. Most children with ulcerative colitis have blood in the stool at presentation. Inflammatory markers are usually although not invariably raised at presentation (particularly in Crohn's disease). Full investigation includes upper gastrointestinal endoscopy and ileocolonoscopy. Treatment requires multidisciplinary input as part of a clinical network led by a paediatrician with special expertise in the management of the condition. PMID:16632672

  18. Histiocytoid Sweet's syndrome in a patient with myelodsyplastic syndrome: report and review of the literature.

    PubMed

    Shalaby, Michael M; Riahi, Ryan R; Rosen, Les B; Soine, Erik J

    2016-01-01

    The neutrophilic dermatoses are a group of disorders characterized by skin lesions for which histological examination reveals intense epidermal and/or dermal inflammatory infiltrates composed primarily of neutrophils without evidence of infection. The myelodysplastic syndromes consist of a heterogeneous group of malignant hematopoietic stem cell disorders characterized by dysplastic and inadequate blood cell production with a variable risk of transformation to acute leukemia. Rarely, histiocytoid Sweet's syndrome occurring in patients with myelodysplastic syndrome has been described. We present a case of a 66-year-old woman with a history of myelodysplastic syndrome who developed histiocytoid Sweet's syndrome. We also review the literature and characterize patients with myelodysplastic syndrome who have developed histiocytoid Sweet's syndrome. PMID:26937301

  19. Arterial Stiffness Alterations and Inflammatory Response Following Endovascular Aortic Repair

    PubMed Central

    Moulakakis, Konstantinos G.; Mylonas, Spyridon N.; Kakisis, John; Kadoglou, Nikolaos P.E.; Papadakis, Ioannis; Sfyroeras, George S.; Antonopoulos, Constantine C.N.; Mantas, George; Ikonomidis, Ignatios; Liapis, Christos D.

    2015-01-01

    Endovascular abdominal aortic aneurysm repair (EVAR) and thoracic aortic aneurysm repair (TEVAR) have been widely incorporated into clinical practice. However, changes in arterial stiffness and post-implantation syndrome after aortic endografting remain important issues under investigation. The aneurysm sac wall motion after successful EVAR and TEVAR reflects complex interactions between all the components of the excluded aneurysm, including true compliance of the aneurysm wall itself, intra-aneurysm sac pressure, remodeling of the thrombus, and mechanical characteristics of the endograft. Experimental and clinical studies have shown that aortic endografting results in increased arterial stiffness in animal models. It can be assumed that the alterations of aortic mechanical properties can have a direct impact on heart output. The long-term impact of these mechanical changes on cardiovascular outcomes and the potential effects of different endografts on hemodynamics are important issues under investigation. Post-implantation syndrome (PIS) is a systemic inflammatory response frequently observed after endovascular treatment of aortic pathologies. The main features of PIS include fever, leukocytosis, elevated C-reactive protein levels, and coagulation disturbances. Endograft design appears to influence this inflammatory response following aortic endografting; woven polyester endografts have been shown to be associated with greater inflammatory response compared to PTFE stent grafts. The purpose of this paper is to review the literature to elucidate arterial stiffness alterations and inflammatory response after EVAR and TEVAR and the impact of endograft design on aortic stiffness and the post-inflammatory response. PMID:26798761

  20. "SAPHO syndrome and infections".

    PubMed

    Govoni, Marcello; Colina, Matteo; Massara, Alfonso; Trotta, Francesco

    2009-01-01

    The syndrome of synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) encompasses a broad spectrum of cutaneous manifestations associated with osteitic and hyperostotic lesions, which typically may involve the anterior chest wall (ACW). The aetiopathogenetic mechanisms as well as the nosographic framing of the disease are still not fully defined although an important role has been suggested for Propionibacterium acnes (P. acnes). This germ might be able to stimulate both the innate and the T-cell-mediated immune system. The elicited immunological response could be an attempt to eliminate the germ thus inducing the perpetuation of the inflammation. Whether the osteo-articular changes seen in SAPHO could be attributable directly to the infection or to an inflammatory reaction induced by pathogenic material remains a debated issue. The current concept of SAPHO syndrome as a reactive infectious osteitis in genetic predisposed subjects seems appealing, but it has not been yet demonstrated. PMID:18721907

  1. [Papillary edema in Muckle-Wells syndrome].

    PubMed

    Wirths, G; Grenzebach, U; Eter, N

    2015-09-01

    Papillary edema may occur isolated without functional impairment or secondary related to various syndromes, increased intracerebral pressure or associated with medicinal treatment. The Muckle-Wells syndrome is a rare disease, which among many other symptoms can lead to optic disc swelling and recurrent increase in intracerebral pressure. Besides familial cold-induced autoinflammatory syndrome (FCAS) and neonatal onset multisystem inflammatory disease (NOMID), the Muckle-Wells syndrome also belongs to the cryopyrin-associated periodic syndromes (CAPS). In most cases of CAP syndromes there is an underlying genetic disorder that leads to overproduction of interleukin-1? (IL-1?); therefore, typical symptoms include inflammation reactions, such as repeated skin rash, fatigue, fever, joint pain and conjunctivitis. PMID:25614348

  2. Inverse relationship of interleukin-6 and mast cells in children with inflammatory and non-inflammatory abdominal pain phenotypes

    PubMed Central

    Henderson, Wendy A; Shankar, Ravi; Taylor, Tara J; Del Valle-Pinero, Arseima Y; Kleiner, David E; Kim, Kevin H; Youssef, Nader N

    2012-01-01

    AIM: To investigate interleukin-6 (IL-6), mast cells, enterochromaffin cells, 5-hydroxytryptamine, and substance P in the gastrointestinal mucosa of children with abdominal pain. METHODS: Formalin-fixed paraffin-embedded gastrointestinal biopsy blocks from patients (n = 48) with non-inflammatory bowel disease (irritable bowel syndrome and functional abdominal pain) and inflammatory bowel disease were sectioned and stained for IL-6, mast cells, enterochromaffin cells, 5-hydroxytryptamine, and substance P. All children had chronic abdominal pain as part of their presenting symptoms. Biopsy phenotype was confirmed by a pathologist, blinded to patient information. Descriptive statistics, chi-square, and independent sample t tests were used to compare differences between the inflammatory and non-inflammatory groups. RESULTS: The cohort (n = 48), mean age 11.9 years (SD = 2.9), 54.2% females, 90% Caucasian, was comprised of a non-inflammatory (n = 26) and an inflammatory (n = 22) phenotype. There was a significant negative correlation between substance P expression and mast cell count (P = 0.05, r = -0.373). Substance P was found to be expressed more often in female patient biopsies and more intensely in the upper gastrointestinal mucosa as compared to the lower mucosa. There were significantly increased gastrointestinal mucosal immunoreactivity to IL-6 (P = 0.004) in the inflammatory phenotype compared to non-inflammatory. Additionally, we found significantly increased mast cells (P = 0.049) in the mucosa of the non-inflammatory phenotype compared to the inflammatory group. This difference was particularly noted in the lower colon biopsies. CONCLUSION: The findings of this study yield preliminary evidence in identifying biomarkers of undiagnosed abdominal pain in children and may suggest candidate genes for future evaluation. PMID:23516176

  3. Prostacyclin: An Inflammatory Paradox

    PubMed Central

    Stitham, Jeremiah; Midgett, Charles; Martin, Kathleen A.; Hwa, John

    2011-01-01

    Prostacyclin (PGI2) is a member of the prostaglandin family of bioactive lipids. Its best-characterized role is in the cardiovascular system, where it is released by vascular endothelial cells, serving as a potent vasodilator and inhibitor of platelet aggregation. In recent years, prostacyclin (PGI2) has also been shown to promote differentiation and inhibit proliferation in vascular smooth muscle cells. In addition to these well-described homeostatic roles within the cardiovascular system, prostacyclin (PGI2) also plays an important role as an inflammatory mediator. In this review, we focus on the contribution of prostacyclin (PGI2) as both a pathophysiological mediator and therapeutic agent in three major inflammatory-mediated disease processes, namely rheumatoid arthritis, where it promotes disease progression (“pro-inflammatory”), along with pulmonary vascular disease and atherosclerosis, where it inhibits disease progression (“anti-inflammatory”). The emerging role of prostacyclin (PGI2) in this context provides new opportunities for understanding the complex molecular basis for inflammatory-related diseases, and insights into the development of current and future anti-inflammatory treatments. PMID:21687516

  4. Paraneoplastic Syndromes

    MedlinePLUS

    ... NINDS Funding Information Research Programs Training & Career Awards Enhancing Diversity Find People About NINDS NINDS Paraneoplastic Syndromes ... done? Research on paraneoplastic syndromes is aimed at enhancing scientific understanding and evaluating new therapeutic interventions. Researchers ...

  5. Angelman Syndrome

    MedlinePLUS

    ... heads, jerky movements, protruding tongues, and bouts of laughter." Infants with Angelman syndrome appear normal at birth, ... develop techniques to diagnose, treat, prevent, and ultimately cure them. NIH Patient Recruitment for Angelman Syndrome Clinical ...

  6. Marfan Syndrome

    MedlinePLUS

    ... Like for Kids With Marfan Syndrome? en espaol Sndrome de Marfan Evan couldn't wait for school ... for Marfan syndrome runs in families, getting passed down to children from parents who have the disease. ...

  7. Brown Syndrome

    MedlinePLUS

    ... poor binocular vision (which can result in poor depth perception) and/or amblyopia. Are there different kinds of Brown syndrome? Brown syndrome can be classified according to severity. In mild cases there is a reduced ability to look up ...

  8. LEOPARD syndrome

    MedlinePLUS

    LEOPARD syndrome is a very rare inherited disorder in which there are problems with the skin, face, ... LEOPARD syndrome is inherited as an autosomal dominant trait. This means the person only needs the abnormal ...

  9. Asperger syndrome

    MedlinePLUS

    Asperger syndrome is often considered a high functioning form of autism. It can lead to difficulty interacting socially, repeat behaviors, and clumsiness. Asperger syndrome is a part of the larger developmental ...

  10. Pseudoaminopterin syndrome.

    PubMed

    Kraoua, Lilia; Capri, Yline; Perrin, Laurence; Benmansour, Abdelmajjid; Verloes, Alain

    2012-09-01

    Pseudoaminopterin syndrome or aminopterin syndrome-like sine aminopterin (ASSA syndrome--OMIM 600325] is a rare autosomal recessive syndrome defined by characteristic dysmorphic features, skeletal defects, limb anomalies, cryptorchidism, and growth retardation. The syndrome owes its name to the fact that patients resemble the children exposed to aminopterin or to methotrexate, two dihydrofolate reductase inhibitors used for chemotherapy, or as an abortificient in early pregnancy. Ten patients have been described with pseudoaminopterin syndrome. Their phenotype is variable, and differs from the phenotype resulting from folic acid deprivation, leading to the notion that the pathogenesis may be more complex than simple vitamin deficiency. We report on an Algerian patient with pseudoaminopterin syndrome, review the previously reported cases and confirm that pseudoaminopterin syndrome does not result from a detectable contiguous gene imbalance as high resolution CGH array was normal in this child. PMID:22811276

  11. Fahr's Syndrome

    MedlinePLUS

    ... is Fahr's Syndrome? Fahr's Syndrome is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits ... the NINDS or the NIH is appreciated. Last Modified February 13, 2007 National Institute of Neurological Disorders ...

  12. Pendred Syndrome

    MedlinePLUS

    ... Pendred syndrome will show vestibular weakness when their balance is tested. However, the brain is very good at making up for a weak vestibular system, and most children and adults with Pendred syndrome don't have a problem ...

  13. Rett Syndrome

    MedlinePLUS

    Rett syndrome is a rare genetic disease that causes developmental and nervous system problems, mostly in girls. It's related to autism spectrum disorder. Babies with Rett syndrome seem to grow and develop normally at first. ...

  14. Rett Syndrome

    MedlinePLUS

    ... NICHD Research Information Clinical Trials Resources and Publications Rett Syndrome: Overview Skip sharing on social media links Share this: Page Content Rett syndrome is a neurological and developmental genetic disorder that ...

  15. Sweet's syndrome with idiopathic thrombocythemia.

    PubMed

    Kaszewski, Sebastian; Czajkowski, Rafa?; Protas-Drozd, Franciszka; Placek, Waldemar; Jakubowski, Sebastian

    2014-02-01

    Diagnosis of paraneoplastic skin syndromes associating neoplastic processes is assumed as the crucial aspect of dermatological practice. Knowledge of clinical findings of dermatoses suggesting coincidence of malignant proliferative processes facilitates diagnostic and therapeutic procedures. We would like to present a case of Sweet's syndrome, qualified for comparative paraneoplastic skin syndromes. Sweet's syndrome, acute, febrile neutrophilic dermatosis, was first described by Robert Douglas Sweet in 1964 as a disorder characterized by fever, skin lesions of erythematous-infiltrative character, leukocytosis with neutrophilia and dense infiltrations of dermis by mature neutrophils. Sweet's syndrome aetiology is not fully understood, although cytokine abnormalities suggest that Th1 lymphocytes play an important role in pathogenesis of the dermatosis. Factors inducing Sweet's syndrome include: haematopoietic hyperplasia; neoplasms: genitourinary, breast, gastrointestinal; infections of the respiratory and alimentary system; inflammatory bowel diseases; drugs; pregnancy and vaccinations. Systemic corticosteroids are the "gold standard" of Sweet's syndrome treatment; potassium iodide or colchicine may also be used. Indomethacin, clofazimine, cyclosporine A and sulfones are the second-line drugs. PMID:24683399

  16. Sweet's syndrome with idiopathic thrombocythemia

    PubMed Central

    Kaszewski, Sebastian; Protas-Drozd, Franciszka; Placek, Waldemar; Jakubowski, Sebastian

    2014-01-01

    Diagnosis of paraneoplastic skin syndromes associating neoplastic processes is assumed as the crucial aspect of dermatological practice. Knowledge of clinical findings of dermatoses suggesting coincidence of malignant proliferative processes facilitates diagnostic and therapeutic procedures. We would like to present a case of Sweet's syndrome, qualified for comparative paraneoplastic skin syndromes. Sweet's syndrome, acute, febrile neutrophilic dermatosis, was first described by Robert Douglas Sweet in 1964 as a disorder characterized by fever, skin lesions of erythematous-infiltrative character, leukocytosis with neutrophilia and dense infiltrations of dermis by mature neutrophils. Sweet's syndrome aetiology is not fully understood, although cytokine abnormalities suggest that Th1 lymphocytes play an important role in pathogenesis of the dermatosis. Factors inducing Sweet's syndrome include: haematopoietic hyperplasia; neoplasms: genitourinary, breast, gastrointestinal; infections of the respiratory and alimentary system; inflammatory bowel diseases; drugs; pregnancy and vaccinations. Systemic corticosteroids are the gold standard of Sweet's syndrome treatment; potassium iodide or colchicine may also be used. Indomethacin, clofazimine, cyclosporine A and sulfones are the second-line drugs. PMID:24683399

  17. Craniofacial Syndrome Descriptions

    MedlinePLUS

    ... Goldenhar/Hemifacial Moebius syndrome Pfeiffer syndrome Pierre Robin Sequence Treacher Collins syndrome Other syndromes Wonder News & Events ... of the radial limb. Pfeiffer syndrome Pierre Robin Sequence Saethre-Chotzen Saethre-Chotzen syndrome is a condition ...

  18. Can Probiotics Cure Inflammatory Bowel Diseases?

    PubMed

    Korada, Siva Kumar; Yarla, Nagendra Sastry; Bishayee, Anupam; Aliev, Gjumrakch; Aruna Lakshmi, K; Arunasree, M K; Dananajaya, B L; Mishra, Vijendra

    2016-01-01

    Gastrointestinal (GI) disorders, especially microbial dysbiosis play role in several GI ailments such as irritable bowel syndrome, colorectal cancer, inflammatory bowel diseases, and antibiotic-associated diarrhoea. Role of inflammatory bowel disease (IBD) is multifactorial as it involves loss of maintaining intestinal epithelial barrier integrity, increased release of pro-inflammatory molecules, and microbial dysbiosis in gut microflora. Some specific pathogens also play a key role in the IBD development. The origin and causation are still in unfathomable condition and the exact root cause is unknown. Recently probiotic studies have been gaining importance because of their positive responses in their IBD experimental results. According to joint Food and Agricultural Organisation/World Health Organisation working group, probiotics are defined as live microorganisms which when administered in adequate amount confer health benefit on the host. These live beneficial microorganisms are considered helpful in improving gut colonization and perseverance thereby improves prophylactic effect. In the direction of IBD research, a number of studies are needed to standardize its methodology and its applicability on human usage. The particular review presents an overview of gut microflora and its impact on host health, types of IBD and existing therapies to treat this disorder, mechanism of several probiotic actions, role of probiotics in IBD prevention with their supporting evidences. PMID:26648465

  19. Early Guillain-Barr syndrome without inflammation.

    PubMed

    Ropper, A H; Adelman, L

    1992-09-01

    A patient with typical acute Guillain-Barr syndrome died 72 hours after his first symptoms occurred, and an autopsy was performed 8 hours after his death. Extensive sampling of cranial and peripheral nerves, sensory ganglia, and autonomic nerves showed only minimal inflammatory lymphocytic and macrophage infiltrates. This case, one of the earliest studied extensively, represents an extreme example of a noninflammatory mechanism that has been proposed in some cases of Gullain-Barr syndrome. PMID:1325767

  20. Velocardiofacial Syndrome

    ERIC Educational Resources Information Center

    Gothelf, Doron; Frisch, Amos; Michaelovsky, Elena; Weizman, Abraham; Shprintzen, Robert J.

    2009-01-01

    Velocardiofacial syndrome (VCFS), also known as DiGeorge, conotruncal anomaly face, and Cayler syndromes, is caused by a microdeletion in the long arm of Chromosome 22. We review the history of the syndrome from the first clinical reports almost half a century ago to the current intriguing molecular findings associating genes from the

  1. Piriformis Syndrome

    MedlinePLUS

    ... the symptoms of piriformis syndrome? The most common symptom of piriformis syndrome is sciatica. This term describes pain, tingling or numbness that ... such as a car accident or a fall. ... something other than piriformis syndrome is causing your sciatica, he or she may order additional tests. Computerized ...

  2. Turcot Syndrome

    MedlinePLUS

    ... of colorectal cancer , and an increased risk of brain cancer . The type of brain cancer generally depends on whether the Turcot syndrome ... Lynch syndrome or FAP. The two most common types of brain tumors in Turcot syndrome are: Glioblastoma . This type ...

  3. Rowell syndrome

    PubMed Central

    Bhat, Ramesh Y; Varma, Chaitanya; Bhatt, Sonia; Balachandran, C

    2014-01-01

    Rowell syndrome is a rare disease consisting of erythema multiforme-like lesions associated with lupus erythematosus. The syndrome occurs mostly in middle-aged women. The authors describe the syndrome in a 15-year-old boy who responded well to systemic steroids and hydroxychloroquine. PMID:25506561

  4. Velocardiofacial Syndrome

    ERIC Educational Resources Information Center

    Gothelf, Doron; Frisch, Amos; Michaelovsky, Elena; Weizman, Abraham; Shprintzen, Robert J.

    2009-01-01

    Velocardiofacial syndrome (VCFS), also known as DiGeorge, conotruncal anomaly face, and Cayler syndromes, is caused by a microdeletion in the long arm of Chromosome 22. We review the history of the syndrome from the first clinical reports almost half a century ago to the current intriguing molecular findings associating genes from the…

  5. Aase syndrome

    MedlinePLUS

    Aase-Smith syndrome; Hypoplastic anemia/Triphalangeal thumb syndrome ... Jones KL, ed. Aase syndrome. In: Smith's Recognizable Patterns Of Human Malformation. 6th ed. Saunders. 2005. Clinton C, Gazda HT. Diamond-Blackfan Anemia. 2009 Jun 25 [Updated 2013 Jul ...

  6. Double pylorus in a patient with Behet's syndrome.

    PubMed

    Hatemi, Ibrahim; Hatemi, Gulen; Erzin, Yusuf Z; Celik, Aykut Ferhat

    2015-01-01

    We report a patient with Behet's syndrome who presented with upper gastrointestinal haemorrhage. Gastroduodenoscopy showed a gastroduodenal fistula which caused the appearance of double pylorus in the antrum. The possibility of peptic ulcer disease related to non-steroidal anti-inflammatory drug use or Behet's syndrome itself, as the cause of this rare condition in this patient is discussed. PMID:25664680

  7. Pelvic Inflammatory Disease (PID) Treatment

    MedlinePLUS

    ... Code: Follow STD STD on Twitter STD on Facebook Sexually Transmitted Diseases (STDs) Pelvic Inflammatory Disease (PID) Treatment and Care Recommend on Facebook Tweet Share Compartir How is pelvic inflammatory disease treated? Several types of antibiotics can cure PID. ...

  8. Follow-up in healthy schoolchildren and in adolescents with DOWN syndrome: psycho-environmental and genetic determinants of physical activity and its impact on fitness, cardiovascular diseases, inflammatory biomarkers and mental health; the UP&DOWN Study

    PubMed Central

    2014-01-01

    Background An objective diagnosis of sedentary behaviour as well as of the physical activity and fitness levels in youth and to better understand how lifestyle is associated with cardiovascular disease risk factors and other phenotypes is of clinical and public health interest, and might be informative for developing intervention studies focused on the promotion of physical activity in these population. The aim of this methodological paper is to describe the design and assessment in the UP&DOWN study. Methods/Design The UP&DOWN study is a multi-center follow-up design where 2225 Spanish primary and secondary schoolchildren from Cadiz and Madrid, respectively, as well as 110 Spanish adolescents with Down syndrome from Madrid and Toledo were recruited to be assessed. Nine main measurement categories are assessed: i) socio-demographic and early determinants; ii) environmental determinants; iii) physical activity and sedentary behaviour; iv) health-related fitness; v) blood pressure and resting heart rate; vi) mental health; vii) dietary patterns; viii) blood samples; and ix) genetic analysis. During the 3-yr follow-up study, socio-demographic and early determinants, and genetic analysis are only assessed in the first year. Blood sampling is assessed in the first year and the third year (2nd follow-up), and all the other measurements are assessed every year. Discussion The findings of the UP&DOWN study may help the Health Information Systems and policy makers to identify the target population for primary prevention and health promotion policies, and to develop and test preventive strategies. Moreover, these data will allow following the trends at population level, as well as to modify/adapt/create new evidence-based physical activity guidelines at national level. The findings will also serve as a scientific platform for interventional studies. PMID:24761982

  9. Compartmentalization of the inflammatory response in sepsis and SIRS.

    PubMed

    Cavaillon, Jean-Marc; Annane, Djillali

    2006-01-01

    Sepsis and systemic inflammatory response syndrome (SIRS) are associated with an exacerbated production of both pro- and anti-inflammatory mediators that are mainly produced within tissues. Although a systemic process, the pathophysiological events differ from organ to organ, and from organ to peripheral blood, leading to the concept of compartmentalization. The nature of the insult (e.g. burn, hemorrhage, trauma, peritonitis), the cellular composition of each compartment (e.g. nature of phagocytes, nature of endothelial cells), and its micro-environment (e.g. local presence of granulocyte-macrophage colony stimulating factor [GM-CSF] in the lungs, low levels of arginine in the liver, release of endotoxin from the gut), and leukocyte recruitment, have a great influence on local inflammation and on tissue injury. High levels of pro-inflammatory mediators (e.g. interleukin-1 [IL-1], tumor necrosis factor [TNF], gamma interferon [IFN-gamma], high mobility group protein-1 [HMGB1], macrophage migration inhibitory factor [MIF]) produced locally and released into the blood stream initiate remote organ injury as a consequence of an organ cross-talk. The inflammatory response within the tissues is greatly influenced by the local delivery of neuromediators by the cholinergic and sympathetic neurons. Acetylcholine and epinephrine contribute with IL-10 and other mediators to the anti-inflammatory compensatory response initiated to dampen the inflammatory process. Unfortunately, this regulatory response leads to an altered immune status of leukocytes that can increase the susceptibility to further infection. Again, the nature of the insult, the nature of the leukocytes, the presence of circulating microbial components, and the nature of the triggering agent employed to trigger cells, greatly influence the immune status of the leukocytes that may differ from one compartment to another. While anti-inflammatory mediators predominate within the blood stream to avoid igniting new inflammatory foci, their presence within tissues may not always be sufficient to prevent the initiation of a deleterious inflammatory response in the different compartments. PMID:16719987

  10. Chronic Inflammatory Demyelinating Polyneuropathy

    PubMed Central

    Dimachkie, Mazen M.; Barohn, Richard J.

    2014-01-01

    Opinion statement Chronic Inflammatory polyneuropathies are an important group of neuromuscular disorders that present chronically and progress over more than 8 weeks, being referred to as chronic inflammatory demyelinating polyneuropathy (CIDP). Despite tremendous progress in elucidating disease pathogenesis, the exact triggering event remains unknown. Our knowledge regarding diagnosis and management of CIDP and its variants continues to expand, resulting in improved opportunities for identification and treatment. Most clinical neurologists will be involved in the management of patients with these disorders, and should be familiar with available therapies for CIDP. We review the distinctive clinical, laboratory, and electro-diagnostic features that aid in diagnosis. We emphasize the importance of clinical patterns that define treatment responsiveness and the most appropriate therapies in order to improve prognosis. PMID:23564314

  11. Inflammatory mechanisms of endometritis.

    PubMed

    Woodward, E M; Troedsson, M H T

    2015-07-01

    Transient post breeding endometritis is a normal physiological reaction in the mare, as it is believed that an inflammatory response is necessary for the effective removal of contaminating bacteria and excess spermatozoa introduced into the uterus. While most mares can clear endometritis within a reasonable amount of time, persistent endometritis caused by either bacteria or spermatozoa can threaten the success of a pregnancy. A subpopulation of mares is susceptible to persistent endometritis, and these mares are a concern in equine reproductive medicine. Research has identified several factors that contribute to susceptibility; however, the exact mechanisms of the progression of the disease are still being elucidated. Current research focuses on endometrial gene expression during endometritis in an attempt to understand the timing of specific inflammatory processes involved with the development of susceptibility to persistent endometritis. With an increased understanding of the mechanisms involved with the disease, current treatments can be improved upon, and new treatments can be developed to target affected pathways. PMID:25537084

  12. Inflammatory bowel disease.

    PubMed

    Bowling, T E

    1995-06-01

    Since the early 1970s there has been considerable debate over the role of nutritional support in the treatment of patients with acute inflammatory bowel disease. The role of enteral feeding as a primary therapeutic option in patients with acute Crohn's disease remains controversial. This article reviews the role of nutritional support both as an adjunct to standard medical therapy and as a primary therapeutic option. PMID:7552633

  13. Keratoconus: an inflammatory disorder?

    PubMed

    Galvis, V; Sherwin, T; Tello, A; Merayo, J; Barrera, R; Acera, A

    2015-07-01

    Keratoconus has been classically defined as a progressive, non-inflammatory condition, which produces a thinning and steepening of the cornea. Its pathophysiological mechanisms have been investigated for a long time. Both genetic and environmental factors have been associated with the disease. Recent studies have shown a significant role of proteolytic enzymes, cytokines, and free radicals; therefore, although keratoconus does not meet all the classic criteria for an inflammatory disease, the lack of inflammation has been questioned. The majority of studies in the tears of patients with keratoconus have found increased levels of interleukin-6 (IL-6), tumor necrosis factor-?(TNF-?), and matrix metalloproteinase (MMP)-9. Eye rubbing, a proven risk factor for keratoconus, has been also shown recently to increase the tear levels of MMP-13, IL-6, and TNF-?. In the tear fluid of patients with ocular rosacea, IL-1? and MMP-9 have been reported to be significantly elevated, and cases of inferior corneal thinning, resembling keratoconus, have been reported. We performed a literature review of published biochemical changes in keratoconus that would support that this could be, at least in part, an inflammatory condition. PMID:25931166

  14. Inflammatory Septal Nasal Polyp

    PubMed Central

    Salaria, Neha; Sharma, Naveen; Garg, Uma; Saluja, Swaran Kaur; Agarwal, Ruchi

    2015-01-01

    Introduction: Nasal polyps are benign prolapsed mucosal lesions which commonly arise from the paranasal sinuses and lateral walls of the nose especially the contact areas of osteomeatal complex. Though nasal polyps arising from the nasal septum have been reported, those arising from its anterior part are extremely rare and present a diagnostic dilemma. Aetiology is multifactorial and is mainly a result of the inflammatory response of the lining mucosa. Case Report: The case of a 28-year-old male, with a history of progressively increasing nasal complaints since 4 months and with a nasal mass arising from the anterior nasal septum on examination, is reported. Diagnosis of an inflammatory nasal polyp was made on histopathological examination after surgical excision of the mass. Conclusion: The diagnosis of an inflammatory nasal polyp was not only unusual in terms of its location but also in its appearance on anterior rhinoscopy and tomographic scanning images. The definitive diagnosis in such cases can only be achieved through surgical resection and detailed histopathological examination.

  15. Pelvic inflammatory disease.

    PubMed

    Gradison, Margaret

    2012-04-15

    Pelvic inflammatory disease is a polymicrobial infection of the upper genital tract. It primarily affects young, sexually active women. The diagnosis is made clinically; no single test or study is sensitive or specific enough for a definitive diagnosis. Pelvic inflammatory disease should be suspected in at-risk patients who present with pelvic or lower abdominal pain with no identified etiology, and who have cervical motion, uterine, or adnexal tenderness. Chlamydia trachomatis and Neisseria gonorrhoeae are the most commonly implicated microorganisms; however, other microorganisms may be involved. The spectrum of disease ranges from asymptomatic to life-threatening tubo-ovarian abscess. Patients should be treated empirically, even if they present with few symptoms. Most women can be treated successfully as outpatients with a single dose of a parenteral cephalosporin plus oral doxycycline, with or without oral metronidazole. Delay in treatment may lead to major sequelae, including chronic pelvic pain, ectopic pregnancy, and infertility. Hospitalization and parenteral treatment are recommended if the patient is pregnant, has human immunodeficiency virus infection, does not respond to oral medication, or is severely ill. Strategies for preventing pelvic inflammatory disease include routine screening for chlamydia and patient education. PMID:22534388

  16. Sweet's syndrome as the presenting manifestation of gall bladder adenocarcinoma

    PubMed Central

    Jindal, Rashmi; Jain, Anshu; Mittal, Ankur; Shirazi, Nadia

    2012-01-01

    Sweet's syndrome is a neutrophilic inflammatory dermatosis presenting with sudden onset tender red to purple papules and nodules, fever and neutrophilia. Gastrointestinal and urinary tract infections, pregnancy, inflammatory bowel disease, drugs and malignancy are some of the known aetiological factors. Paraneoplastic Sweet's syndrome accounts for 1520% cases and thus forms an important subset. At times its onset helps in suspecting an underlying malignancy, thus making timely intervention possible. In the present case report Sweet's syndrome was the presenting feature of gall bladder adenocarcinoma; an association that has been rarely reported before. PMID:23076693

  17. Medicinal agents and metabolic syndrome.

    PubMed

    Rubio-Ruiz, M E; El Hafidi, M; Prez-Torres, I; Baos, G; Guarner, V

    2013-01-01

    The definition of the Metabolic Syndrome (MS) has encountered difficulty in reaching a universal consensus although there exists an agreement of its main pathologies which are hypertension, obesity, dyslipidemia, insulin resistance, inflammation and renal damage. The prevalent opinion is that three of those alterations may define the syndrome. The incidence of the MS has increased globally, particularly in the last few years, to the point of being regarded as an epidemic. The treatment of the MS can be approached from different angles, since it may be a multifaceted health problem. A healthy lifestyle, which means the practice of regular exercise is suggested to MS patients. Increasing physical activity has anti-inflammatory effects since there is an inverse association of physical activity and inflammatory biomarker concentrations. An adequate diet is recommended, such as the Mediterranean, which contains fish, tomatoes, garlic, red peppers, olive oil and includes red wine, that is, antioxidants and non-saturated oils. There are also the traditional herbal preparations, used in the alternative medicine. Several therapeutic tools can be used; the most common are the pharmaceutical products to deal with obesity, hypertension, dyslipidemias, diabetes and inflammation. In addition several pharmacological therapies such as non steroidal anti-inflammatory drugs are recommended. Recently new mechanisms of action of statins, fibrates, metformin and thiazolidinediones have demonstrated their anti-inflammatory effect and potential use to treat MS. PMID:23590715

  18. [Fisher syndrome and Bickerstaff brainstem encephalitis].

    PubMed

    Kuwabara, Satoshi

    2013-01-01

    Fisher syndrome has been regarded peculiar inflammatory neuropathy with ophthalmoplegia, ataxia, and areflexia, whereas Bickerstaff brainstem encephalitis has been considered pure central nervous system disease characterized with ophthalmoplegia, ataxia, and consciousness disturbance. Both disorder share common features including preceding infection, albumin-cytological dissociation, and association with Guillain-Barre syndrome. The discovery of anti-GQ1b IgG antibodies further supports the view that the two disorder represent a single disease spectrum. Currently Bickerstaff brainstem encephalitis can be regarded as a variant of Fisher syndrome with central nervous system involvement. PMID:24291973

  19. Inflammatory Signaling and Cellular Senescence

    PubMed Central

    Ren, Jian-Lin; Pan, Jin-Shui; Lu, Ya-Pi; Sun, Peiqing

    2010-01-01

    Inflammation is a double-edged sword in the pathogenesis of cancer. Inflammatory responses play a key role in eliminating the potentially cancerous cells. However, inflammatory microenvironment also promotes the development of cancer. Pro-inflammatory cytokines, the key mediators of inflammation, also play a dual role in oncogenesis. While they can promote neoplastic progression, recent studies have revealed an unexpected function of the inflammatory pathways in inhibiting cancer development. These studies demonstrate that cells undergoing senescence, a cellular program serving as a barrier to cancer development, produce increased amount of inflammatory cytokines. These inflammatory cytokines play an essential role in the initiation and maintenance of cellular senescence, and is responsible for triggering an innate immune response that clears the senescent tumor cells in vivo. The purpose of the present review is to discuss the dual roles of the inflammatory cytokines produced by senescent cells in the pathogenesis of cancer, and the signaling pathway mediating their role in cellular senescence. PMID:18992324

  20. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

    MedlinePLUS

    ... and abnormal sensations. CIDP is closely related to Guillain-Barre syndrome and it is considered the chronic counterpart of ... 776-3903 Related NINDS Publications and Information NINDS Guillain-Barr Syndrome Information Page Guillain-Barre Syndrome information sheet compiled ...

  1. Monogenic Autoinflammatory Syndromes: State of the Art on Genetic, Clinical, and Therapeutic Issues

    PubMed Central

    Costa, Luisa; Atteno, Mariangela; Compagnone, Adele; Caso, Paolo; Frediani, Bruno; Galeazzi, Mauro; Punzi, Leonardo

    2013-01-01

    Monogenic autoinflammatory syndromes (MAISs) are caused by innate immune system dysregulation leading to aberrant inflammasome activation and episodes of fever and involvement of skin, serous membranes, eyes, joints, gastrointestinal tract, and nervous system, predominantly with a childhood onset. To date, there are twelve known MAISs: familial Mediterranean fever, tumor necrosis factor receptor-associated periodic syndrome, familial cold urticaria syndrome, Muckle-Wells syndrome, CINCA syndrome, mevalonate kinase deficiency, NLRP12-associated autoinflammatory disorder, Blau syndrome, early-onset sarcoidosis, PAPA syndrome, Majeed syndrome, and deficiency of the interleukin-1 receptor antagonist. Each of these conditions may manifest itself with more or less severe inflammatory symptoms of variable duration and frequency, associated with findings of increased inflammatory parameters in laboratory investigation. The purpose of this paper is to describe the main genetic, clinical, and therapeutic aspects of MAISs and their most recent classification with the ultimate goal of increasing awareness of autoinflammation among various internal medicine specialists. PMID:24282415

  2. Gorlin syndrome.

    PubMed

    Devi, Basanti; Behera, Binodini; Patro, Sibasish; Pattnaik, Subhransu S; Puhan, Manas R

    2013-05-01

    Gorlin Syndrome, a rare genodermatosis, otherwise known as Nevoid basal cell carcinoma syndrome (NBCCS) is a multisystem disease affecting skin, nervous system, eyes, endocrine glands, and bones. It is characterized by multiple basal cell carcinomas, palmoplantar pits, jaw cysts, and bony deformities like kyphoscoliosis and frontal bossing. We would like to report a case of Gorlin syndrome with classical features, as this is a rare genodermatosis. PMID:23723494

  3. Chronic inflammatory systemic diseases

    PubMed Central

    Straub, Rainer H.; Schradin, Carsten

    2016-01-01

    It has been recognized that during chronic inflammatory systemic diseases (CIDs) maladaptations of the immune, nervous, endocrine and reproductive system occur. Maladaptation leads to disease sequelae in CIDs. The ultimate reason of disease sequelae in CIDs remained unclear because clinicians do not consider bodily energy trade-offs and evolutionary medicine. We review the evolution of physiological supersystems, fitness consequences of genes involved in CIDs during different life-history stages, environmental factors of CIDs, energy trade-offs during inflammatory episodes and the non-specificity of CIDs. Incorporating bodily energy regulation into evolutionary medicine builds a framework to better understand pathophysiology of CIDs by considering that genes and networks used are positively selected if they serve acute, highly energy-consuming inflammation. It is predicted that genes that protect energy stores are positively selected (as immune memory). This could explain why energy-demanding inflammatory episodes like infectious diseases must be terminated within 3–8 weeks to be adaptive, and otherwise become maladaptive. Considering energy regulation as an evolved adaptive trait explains why many known sequelae of different CIDs must be uniform. These are, e.g. sickness behavior/fatigue/depressive symptoms, sleep disturbance, anorexia, malnutrition, muscle wasting—cachexia, cachectic obesity, insulin resistance with hyperinsulinemia, dyslipidemia, alterations of steroid hormone axes, disturbances of the hypothalamic-pituitary-gonadal (HPG) axis, hypertension, bone loss and hypercoagulability. Considering evolved energy trade-offs helps us to understand how an energy imbalance can lead to the disease sequelae of CIDs. In the future, clinicians must translate this knowledge into early diagnosis and symptomatic treatment in CIDs. PMID:26817483

  4. Inflammatory Vulvar Dermatoses.

    PubMed

    Guerrero, Angela; Venkatesan, Aruna

    2015-09-01

    Inflammatory vulvar dermatoses affect many women, but are likely underdiagnosed due to embarrassment and reluctance to visit a health care provider. Although itch and pain are common presenting symptoms, the physical examination can help distinguish between different disease entities. Because many women's health providers have minimal training in the categorization and management of dermatologic disease, definitive diagnosis and management can be difficult. Herein, strategies for diagnosing vulvar lichen sclerosus, lichen planus, contact dermatitis, lichen simplex chronicus, and psoriasis are discussed along with basic management of these diseases, which commonly involves decreasing inflammation through behavioral change, gentle skin care, topical corticosteroids, and systemic therapies. PMID:26125955

  5. Cytokines: potential contributors to arrhythmogenesis in demyelinating syndromes?

    PubMed

    Yalta, Kenan; Yalta, Tulin; Turgut, Okan Onur; Y?lmaz, Mehmet Birhan; Tandogan, Izzet

    2011-01-01

    Neurological disorders including chronic demyelinating syndromes (CDSs) have been known to elicit propensity to cardiac arrhythmias possibly due to autonomic imbalance, myocardial myocytolysis and some psychological conditions (major depression etc.) associated with these syndromes. CDSs are generally characterized by variable degrees of inflammatory response that may corrrelate with clinical disease activity (relapse, progression etc.). In the clinical setting, enhanced inflammatory response as measured with increased levels of inflammatory markers may predispose to cardiac arrhythmias via direct or indirect mechanisms. Therefore, substantial levels of inflammatory markers including pro-inflammatory cytokines associated with CDSs may serve as potential contributors to arrhythmogenesis indicating the possible link between disease activity and arrhythmia risk in patients with CDSs. PMID:20036021

  6. Irritable Bowel Syndrome

    MedlinePLUS

    ... How Can I Help a Friend Who Cuts? Irritable Bowel Syndrome KidsHealth > For Teens > Irritable Bowel Syndrome Print ... intestinal disorder called irritable bowel syndrome. What Is Irritable Bowel Syndrome? Irritable bowel syndrome (IBS) is a common ...

  7. Idiopathic Inflammatory Myopathies

    PubMed Central

    Barohn, Richard J.; Amato, Anthony

    2014-01-01

    The idiopathic inflammatory myopathies (IIM) consist of rare heterogenous autoimmune disorders that present with marked proximal and symmetric muscle weakness, except for distal and asymmetric weakness in inclusion body myositis (IBM). Besides frequent creatine kinase (CK) elevation, the electromyogram confirms the presence of an irritative myopathy. Extramuscular involvement affects a significant number of cases with interstitial lung disease (ILD), cutaneous in dermatomyositis (DM), systemic or joint manifestations and increased risk of malignancy especially in DM. Myositis specific autoantibodies influence phenotype of the IIM. Jo-1 antibodies are frequently associated with ILD and the newly described HMG-CoA reductase antibodies are characteristic of autoimmune necrotizing myopathy (NM). Muscle pathology ranges from inflammatory exudates of variable distribution, to intact muscle fiber invasion, necrosis, phagocytosis and in the case of IBM rimmed vacuoles and protein deposits. Despite many similarities, the IIM are a quite heterogeneous from the histopathological and pathogenetic standpoints in addition to some clinical and treatment-response difference. The field has witnessed significant advances in our understanding of pathophysiology and treatment of these rare disorders. In this review, we focus on DM, polymyositis (PM) and NM and examine current and promising therapies. The reader interested in more details on IBM is referred to the corresponding chapter in this issue. PMID:25037081

  8. Inflammatory Pseudotumor of the Spleen

    PubMed Central

    Georgia, Masafumi; Rady, Kirsty; Prince, Henry Miles

    2015-01-01

    Isolated splenic inflammatory pseudotumors (IPT) are extremely rare, typically benign, inflammatory lesions with varied clinical presentations that pose a diagnostic challenge to clinicians due to their similarity in appearance to neoplasms. We present the case of a young woman diagnosed with a splenic IPT following investigation for persistent anemia, raised inflammatory markers, and polyclonal hypergammaglobulinemia, whose symptoms resolved completely following splenectomy. This case highlights the need to consider this diagnosis when evaluating patients with a splenic mass of unknown etiology. PMID:26331003

  9. Prostatitis Syndromes

    PubMed Central

    Nickel, J. Curtis

    1991-01-01

    The many prostatitis syndromes remain a frustrating enigma to family physicians as well as specialists. An understanding of the etiology and pathophysiology of these syndromes and a rigorous diagnostic plan to properly classify the patients at first presentation are essential to a successful treatment outcome. ImagesFigure 1 PMID:21229071

  10. HELLP Syndrome

    MedlinePLUS

    ... get HELLP syndrome if you're white and older than 25 years of age. You are also more likely to get it if you have had children before or if you had a problem with a pregnancy in the past. Treatment How is HELLP syndrome ...

  11. Marfan Syndrome

    MedlinePLUS

    ... Connective tissue helps support all parts of your body. It also helps control how your body grows and develops. Marfan syndrome most often affects ... A mutation, or change, in the gene that controls how the body makes fibrillin causes Marfan syndrome. Fibrillin is a ...

  12. Marfan Syndrome

    MedlinePLUS

    ... even exercise — they just have to be a little more careful. Kids should always check with their doctors about what's ... activities during gym class. But other than that, kids with Marfan syndrome are just like everyone else — only a little taller. If you have Marfan syndrome, you probably ...

  13. Bloom's Syndrome

    MedlinePLUS

    ... Niemann-Pick Disease, Type A Spinal Muscular Atrophy Tay-Sachs Disease Usher Syndrome, Type 1F and Type III Walker- ... Niemann-Pick Disease, Type A Spinal Muscular Atrophy Tay-Sachs Disease Usher Syndrome, Type 1F and Type III Walker- ...

  14. Current Proposed Mechanisms of Action of Intravenous Immunoglobulins in Inflammatory Neuropathies

    PubMed Central

    Jacob, Saiju; Rajabally, Yusuf A

    2009-01-01

    Intravenous immunoglobulins (IVIg) have been shown in a number of trials, to be an effective treatment for the three main types of inflammatory neuropathies: Guillain-Barr Syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and multifocal motor neuropathy (MMN). IVIg is thought to exert its immunomodulatory effects by affecting several components of the immune system including B-cells, T-cells, macrophages, complement, cytokines and cellular adhesion molecules. This article reviews the published evidence and the principal postulated mechanisms of action of intravenous immunoglobulins with special emphasis on inflammatory neuropathies. PMID:20514213

  15. Chronic inflammatory stress.

    PubMed

    Harbuz, M S

    1999-12-01

    A major mechanism involved in maintaining homeostasis in response to chronic inflammation is the hypothalamo-pituitary-adrenal (HPA) axis, resulting in the release of anti-inflammatory glucocorticoids from the adrenal cortex. An inadequate HPA axis response may result in the development of a pathology or an increase in susceptibility and/or severity of disease. Other neuroendocrine systems are also implicated. Increasingly considered important are circadian rhythms, not only of hormones, but also of components of the immune system. Recent evidence concerning changes in hypothalamic control of the HPA axis following development of disease, the implication of these for the response to stress and the use of the HPA axis as a predictor of susceptibility to disease will also be considered. Finally, the influence of stress on autoimmune disease will be discussed. This chapter will concentrate principally on rheumatoid arthritis, although other autoimmune diseases and animal models will be discussed. PMID:10903814

  16. Inflammatory bowel disease.

    PubMed Central

    Van Rosendaal, G M

    1989-01-01

    An increasing number of options are available for the treatment of inflammatory bowel disease; the selection depends on the extent and severity of the disease. Experience with sulfasalazine and corticosteroids has led to a proliferation of 5-aminosalicylic acid (5-ASA) compounds and experimentation with alternative corticosteroid preparations. Given rectally 5-ASA is particularly effective in the treatment of distal ulcerative colitis, and experience is accumulating with several oral formulations. Metronidazole is useful in some cases, and immunosuppressive agents have a role in some patients with chronic refractory disease. A variety of measures, such as nutritional therapy, surgery and psychosocial support, are important elements of therapy. Further therapeutic innovations are expected as the etiology and pathogenesis are clarified. PMID:2568163

  17. Inflammatory Bowel Disease

    PubMed Central

    Kaser, Arthur; Zeissig, Sebastian; Blumberg, Richard S.

    2015-01-01

    Insights into inflammatory bowel disease (IBD) are advancing rapidly owing to immunologic investigations of a plethora of animal models of intestinal inflammation, ground-breaking advances in the interrogation of diseases that are inherited as complex genetic traits, and the development of culture-independent methods to define the composition of the intestinal microbiota. These advances are bringing a deeper understanding to the genetically determined interplay between the commensal microbiota, intestinal epithelial cells, and the immune system and the manner in which this interplay might be modified by relevant environmental factors in the pathogenesis of IBD. This review examines these interactions and, where possible, potential lessons from IBD-directed, biologic therapies that may allow for elucidation of pathways that are central to disease pathogenesis in humans. PMID:20192811

  18. Inflammatory Bowel Disease

    PubMed Central

    Nasseri-Moghaddam, Siavosh

    2012-01-01

    Inflammatory bowel disease (IBD) is the term used for a group of diseases with yet unknown etiology, prevalence of which is increasing almost everywhere in the world. The disease was almost non-existent four decades ago in the east, including the middle-east, while now a days it is seen more and more. In addition to the increasing prevalence, our knowledge about its pathogenesis, clinical course, diagnosis, and treatment has changed dramatically over the past couple of decades. This has changed our concept of this group of diseases, their diagnosis, treatment, and treatment goals. Considering the vast literature on the subject, it is timely to review major topics in IBD with a look on the regional progress and knowledge as well. This essay is aimed to cover this task. PMID:24829639

  19. Histiocytoid Sweet’s syndrome in a patient with myelodsyplastic syndrome: report and review of the literature

    PubMed Central

    Shalaby, Michael M.; Riahi, Ryan R.; Rosen, Les B.; Soine, Erik J.

    2016-01-01

    The neutrophilic dermatoses are a group of disorders characterized by skin lesions for which histological examination reveals intense epidermal and/or dermal inflammatory infiltrates composed primarily of neutrophils without evidence of infection. The myelodysplastic syndromes consist of a heterogeneous group of malignant hematopoietic stem cell disorders characterized by dysplastic and inadequate blood cell production with a variable risk of transformation to acute leukemia. Rarely, histiocytoid Sweet’s syndrome occurring in patients with myelodysplastic syndrome has been described. We present a case of a 66-year-old woman with a history of myelodysplastic syndrome who developed histiocytoid Sweet’s syndrome. We also review the literature and characterize patients with myelodysplastic syndrome who have developed histiocytoid Sweet’s syndrome. PMID:26937301

  20. Cushing's Syndrome

    MedlinePLUS

    ... cortisol can occur from long-term use of synthetic glucocorticoid hormones to treat inflammatory illnesses. Pituitary adenomas ( ... Fax: 805-480-0633 Prepared by: Office of Communications and Public Liaison National Institute of Neurological Disorders ...

  1. Kounis syndrome.

    PubMed

    Ntuli, P M; Makambwa, E

    2015-10-01

    Kounis syndrome is characterised by a group of symptoms that manifest as unstable vasospastic or non-vasospastic angina secondary to a hypersensitivity reaction. It was first described by Kounis and Zavras in 1991 as the concurrence of an allergic response with an anaphylactoid or anaphylactic reaction and coronary artery spasm or even myocardial infarction. Since then, this condition has evolved to include a number of mast cell activation disorders associated with acute coronary syndrome. There are many triggering factors, including reactions to multiple medications, exposure to radiological contrast media, poison ivy, bee stings, shellfish and coronary stents. In addition to coronary arterial involvement, Kounis syndrome comprises other arterial systems with similar physiologies, such as mesenteric and cerebral circulation resulting in ischaemia/infarction of the vital organs. The incidence of this condition is difficult to establish owing to the number of potential instigating factors and its relatively infrequent documentation in the literature.We report the case of an HIV-negative 39-year-old man with no coronary risk factors or family history of premature coronary artery disease, who developed Kounis syndrome after the administration of fluoroquinolone for dysuria. However, to the best of our knowledge,no data on the incidence and prevalence of Kounis syndrome in South Africa have ever been reported in the literature. The recent understanding of Kounis syndrome has led to the condition being classified into three syndrome variants. PMID:26636160

  2. [HELLP syndrome].

    PubMed

    Vigil-De Gracia, Paulino

    2015-01-01

    Hypertensive disorders of pregnancy are one of the most common complications of pregnancy, but one of the most serious expressions of this pathology is HELLP syndrome. The HELLP syndrome is characterized by the presence of hypertension disorder more a triad: microangiopathic hemolysis, elevated liver enzymes and low platelet count. Patient with HELLP syndrome is associated with increased maternal risk complications such as: cerebral hemorrhage, retinal detachment, hematoma/ hepatic rupture, acute renal failure, disseminated intravascular coagulation, placental abruption and therefore a maternal death. For all these reasons it is recommended to search for findings of HELLP syndrome in patients with hypertensive disorder of pregnancy. The main clinical confusion of HELLP syndrome is acute fatty liver of pregnancy, however there are parameters that help correct identification. The presence of HELLP syndrome involves a rapid termination of pregnancy and the administration of corticosteroids does not improve maternal morbidity and mortality but may help raise the platelet count, thus decreasing the need for transfusion and shorten hospital stay. Much of the decline in maternal morbidity and mortality associated with hypertensive disorders of pregnancy is in proper diagnosis and effective management of HELLP syndrome. PMID:26016316

  3. Hormonal control of inflammatory responses

    PubMed Central

    Farsky, Sandra P.

    1993-01-01

    Almost any stage of inflammatory and immunological responses is affected by hormone actions. This provides the basis for the suggestion that hormones act as modulators of the host reaction against trauma and infection. Specific hormone receptors are detected in the reactive structures in inflamed areas and binding of hormone molecules to such receptors results in the generation of signals that influence cell functions relevant for the development of inflammatory responses. Diversity of hormonal functions accounts for recognized pro- and anti-inflammatory effects exerted by these substances. Most hormone systems are capable of influencing inflammatory events. Insulin and glucocorticoids, however, exert direct regulatory effects at concentrations usually found in plasma. Insulin is endowed with facilitatory actions on vascular reactivity to inflammatory mediators and inflammatory cell functions. Increased concentrations of circulating glucocorticoids at the early stages of inflammation results in downregulation of inflammatory responses. Oestrogens markedly reduce the response to injury in a variety of experimental models. Glucagon and thyroid hormones exert indirect anti-inflammatory effects mediated by the activity of the adrenal cortex. Accordingly, inflammation is not only merely a local response, but a hormone-controlled process. PMID:18475521

  4. Vitamin D in inflammatory diseases

    PubMed Central

    Wöbke, Thea K.; Sorg, Bernd L.; Steinhilber, Dieter

    2014-01-01

    Changes in vitamin D serum levels have been associated with inflammatory diseases, such as inflammatory bowel disease (IBD), rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis (MS), atherosclerosis, or asthma. Genome- and transcriptome-wide studies indicate that vitamin D signaling modulates many inflammatory responses on several levels. This includes (i) the regulation of the expression of genes which generate pro-inflammatory mediators, such as cyclooxygenases or 5-lipoxygenase, (ii) the interference with transcription factors, such as NF-κB, which regulate the expression of inflammatory genes and (iii) the activation of signaling cascades, such as MAP kinases which mediate inflammatory responses. Vitamin D targets various tissues and cell types, a number of which belong to the immune system, such as monocytes/macrophages, dendritic cells (DCs) as well as B- and T cells, leading to individual responses of each cell type. One hallmark of these specific vitamin D effects is the cell-type specific regulation of genes involved in the regulation of inflammatory processes and the interplay between vitamin D signaling and other signaling cascades involved in inflammation. An important task in the near future will be the elucidation of the regulatory mechanisms that are involved in the regulation of inflammatory responses by vitamin D on the molecular level by the use of techniques such as chromatin immunoprecipitation (ChIP), ChIP-seq, and FAIRE-seq. PMID:25071589

  5. Neuroacanthocytosis Syndromes

    PubMed Central

    2011-01-01

    Neuroacanthocytosis (NA) syndromes are a group of genetically defined diseases characterized by the association of red blood cell acanthocytosis and progressive degeneration of the basal ganglia. NA syndromes are exceptionally rare with an estimated prevalence of less than 1 to 5 per 1'000'000 inhabitants for each disorder. The core NA syndromes include autosomal recessive chorea-acanthocytosis and X-linked McLeod syndrome which have a Huntingtons disease-like phenotype consisting of a choreatic movement disorder, psychiatric manifestations and cognitive decline, and additional multi-system features including myopathy and axonal neuropathy. In addition, cardiomyopathy may occur in McLeod syndrome. Acanthocytes are also found in a proportion of patients with autosomal dominant Huntington's disease-like 2, autosomal recessive pantothenate kinase-associated neurodegeneration and several inherited disorders of lipoprotein metabolism, namely abetalipoproteinemia (Bassen-Kornzweig syndrome) and hypobetalipoproteinemia leading to vitamin E malabsorption. The latter disorders are characterized by a peripheral neuropathy and sensory ataxia due to dorsal column degeneration, but movement disorders and cognitive impairment are not present. NA syndromes are caused by disease-specific genetic mutations. The mechanism by which these mutations cause neurodegeneration is not known. The association of the acanthocytic membrane abnormality with selective degeneration of the basal ganglia, however, suggests a common pathogenetic pathway. Laboratory tests include blood smears to detect acanthocytosis and determination of serum creatine kinase. Cerebral magnetic resonance imaging may demonstrate striatal atrophy. Kell and Kx blood group antigens are reduced or absent in McLeod syndrome. Western blot for chorein demonstrates absence of this protein in red blood cells of chorea-acanthocytosis patients. Specific genetic testing is possible in all NA syndromes. Differential diagnoses include Huntington disease and other causes of progressive hyperkinetic movement disorders. There are no curative therapies for NA syndromes. Regular cardiologic studies and avoidance of transfusion complications are mandatory in McLeod syndrome. The hyperkinetic movement disorder may be treated as in Huntington disease. Other symptoms including psychiatric manifestations should be managed in a symptom-oriented manner. NA syndromes have a relentlessly progressive course usually over two to three decades. PMID:22027213

  6. LEOPARD Syndrome.

    PubMed

    Ghosh, Sudip Kumar; Majumdar, Biswajit; Rudra, Olympia; Chakraborty, Sougat

    2015-01-01

    LEOPARD syndrome (LS) is an autosomal dominantly inherited or sporadic disorder of variable penetrance and expressivity. The acronym LEOPARD stands for its cardinal clinical features including Lentigines, Electrocardiographic conduction abnormalities, Ocular hypertelorism, Pulmonary stenosis, Abnormalities of genitalia, Retardation of growth, and Deafness. We present herein a patient with LEOPARD syndrome and distinctive features. It was noteworthy that our patient presented with the concern of generalized lentiginosis and subsequent evaluation revealed that the patient had LEOPARD syndrome. In this report we would like to highlight the importance of detailed clinical examination and appropriate imaging in patients with multiple lentigines. PMID:26632807

  7. Syndrome designations.

    PubMed Central

    Cohen, M M

    1976-01-01

    Because syndrome designations permit the collection of data, they are much more than just lables. As new syndromes become delineated, their names connote (1) their phenotypic spectra, (2) their natural histories, and (3) their modes of inheritance or risk of recurrence. Various methods for designating new syndromes are reviewed, including naming them after (1) the basic defect, (2) an eponym, (3) one or more striking features, (4) an acronym, (5) a numeral, (6) a geographic term, and (7) some combination of the above. None of these systems of nomenclature is without fault. The advantages and disadvantages of each are discussed. PMID:957375

  8. Velocardiofacial syndrome.

    PubMed Central

    Pike, A. C.; Super, M.

    1997-01-01

    Velocardiofacial syndrome is a syndrome of multiple anomalies that include cleft palate, cardiac defects, learning difficulties, speech disorder and characteristic facial features. It has an estimated incidence of 1 in 5000. The majority of cases have a microdeletion of chromosome 22q11.2. The phenotype of this condition shows considerable variation, not all the principal features are present in each case. Identification of the syndrome can be difficult as many of the anomalies are minor and present in the general population. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 PMID:9497944

  9. Lipid Bodies in Inflammatory Cells

    PubMed Central

    Melo, Rossana C. N.; DAvila, Heloisa; Wan, Hsiao-Ching; Bozza, Patrcia T.; Dvorak, Ann M.; Weller, Peter F.

    2011-01-01

    Lipid bodies (LBs), also known as lipid droplets, have increasingly been recognized as functionally active organelles linked to diverse biological functions and human diseases. These organelles are actively formed in vivo within cells from the immune system, such as macrophages, neutrophils, and eosinophils, in response to different inflammatory conditions and are sites for synthesis and storage of inflammatory mediators. In this review, the authors discuss structural and functional aspects of LBs and current imaging techniques to visualize these organelles in cells engaged in inflammatory processes, including infectious diseases. The dynamic morphological aspects of LBs in leukocytes as inducible, newly formable organelles, elicitable in response to stimuli that lead to cellular activation, contribute to the evolving understanding of LBs as organelles that are critical regulators of different inflammatory diseases, key markers of leukocyte activation, and attractive targets for novel anti-inflammatory therapies. PMID:21430261

  10. Acute respiratory distress syndrome.

    PubMed

    Wyncoll, D L; Evans, T W

    1999-08-01

    Outcome in acute respiratory distress syndrome (ARDS) is influenced by a number of factors, including the nature of the precipitating condition and the extent to which multiorgan failure ensues. Most studies of potential therapeutic interventions have been unsuccessful due to the enrollment of limited numbers of patients with a wide variety of pathologies of varying severity. Moreover, the value of initiating single-agent interventions at varying time points in what is an evolving and complex inflammatory process must be questioned. Mortality may therefore represent an inappropriate end-point for clinical trials, which are increasingly focusing on ventilator-free days. Despite these uncertainties, survival appears to be improving, possibly due to the application of supportive techniques in a protocol-driven fashion to patients in whom the underlying condition has been rigorously treated. PMID:10465189

  11. Charcot foot syndrome.

    PubMed

    Jeffcoate, W J

    2015-06-01

    Charcot foot syndrome is an uncommon complication of diabetes but is potentially devastating in its consequences. Outcome is made worse by widespread professional ignorance leading to delayed diagnosis, but it is also hampered by lack of understanding of its causes and lack of treatments with proven effectiveness, other than offloading. There remains a desperate need for studies into its causes as well as comparative audit and trials designed to determine the best treatment for this difficult condition. Such work can probably only be effectively carried out through the establishment of multicentre networks. Nevertheless, improved understanding in recent years of the likely role of inflammatory pathways has raised awareness of the multiple ways in which the effects of neuropathy may be manifest in the development of the Charcot foot. This awareness is also leading to the realization that similar processes may conceivably contribute to the refractoriness of other foot diseases in diabetes, including both chronic unhealing ulcers and osteomyelitis. PMID:25818542

  12. Attenuated Age-Impact on Systemic Inflammatory Markers in the Presence of a Metabolic Burden

    PubMed Central

    Anuurad, Erdembileg; Mirsoian, Annie; Enkhmaa, Byambaa; Zhang, Wei; Beckett, Laurel A.; Murphy, William J.; Berglund, Lars F.

    2015-01-01

    Background The overall burden of chronic disease, inflammation and cardiovascular risk increases with age. Whether the relationship between age and inflammation is impacted by presence of an adverse metabolic burden is not known. Methods We determined inflammatory markers in humans (336 Caucasians and 224 African Americans) and in mice, representing a spectrum of age, weight and metabolic burden. Results In humans, levels of inflammatory markers increased significantly with age in subjects without the metabolic syndrome, (P=0.009 and P=0.037 for C-reactive protein, P<0.001 and P=0.001 for fibrinogen, P<0.001 and P=0.005 for serum amyloid-A, for Caucasians and African Americans, respectively). In contrast, trend patterns of inflammatory markers did not change significantly with age in subjects with metabolic syndrome in either ethnic group, except for fibrinogen in Caucasians. A composite z-score for systemic inflammation increased significantly with age in subjects without metabolic syndrome (P=0.004 and P<0.006 for Caucasians and African Americans, respectively) but not in subjects with metabolic syndrome (P=0.009 for difference in age trend between metabolic syndrome and non-metabolic syndrome). In contrast, no similar age trend was found in vascular inflammation. The findings in humans were paralleled by results in mice as serum amyloid-A levels increased across age (range 2-15 months, P<0.01) and were higher in ob/ob mice compared to control mice (P<0.001). Conclusions Presence of a metabolic challenge in mice and humans influences levels of inflammatory markers over a wide age range. Our results underscore that already at a young age, presence of a metabolic burden enhances inflammation to a level that appears to be similar to that of decades older people without metabolic syndrome. PMID:25815855

  13. Maladaptive immune and inflammatory pathways lead to cardiovascular insulin resistance

    PubMed Central

    Aroor, Annayya R.; McKarns, Susan; DeMarco, Vincent G.; Guanghong, Jia; Sowers, James R.

    2013-01-01

    Insulin resistance is a hallmark of obesity, the cardiorenal metabolic syndrome and type 2 diabetes mellitus (T2DM). The progression of insulin resistance increases the risk for cardiovascular disease (CVD). The significance of insulin resistance is underscored by the alarming rise in the prevalence of obesity and its associated comorbidities in the Unites States and worldwide over the last 40-50 years. The incidence of obesity is also on the rise in adolescents. Furthermore, premenopausal women have lower CVD risk compared to men, but this protection is lost in the setting of obesity and insulin resistance. Although systemic and cardiovascular insulin resistance are associated with impaired insulin metabolic signaling and cardiovascular dysfunction, the mechanisms underlying insulin resistance and cardiovascular dysfunction remain poorly understood. Recent studies show that insulin resistance in obesity and diabetes is linked to a metabolic inflammatory response, a state of systemic and tissue specific chronic low grade inflammation. Evidence is also emerging that there is polarization of macrophages and lymphocytes towards a pro-inflammatory phenotype that contribute to progression of insulin resistance in obesity, cardiorenal metabolic syndrome and diabetes. In this review, we provide new insights into factors, such as, the renin-angiotensin-aldosterone system, sympathetic activation and incretin modulators (e.g., DPP-4) and immune responses that mediate this inflammatory state in obesity and other conditions characterized by insulin resistance. PMID:23932846

  14. Maladaptive immune and inflammatory pathways lead to cardiovascular insulin resistance.

    PubMed

    Aroor, Annayya R; McKarns, Susan; Demarco, Vincent G; Jia, Guanghong; Sowers, James R

    2013-11-01

    Insulin resistance is a hallmark of obesity, the cardiorenal metabolic syndrome and type 2 diabetes mellitus (T2DM). The progression of insulin resistance increases the risk for cardiovascular disease (CVD). The significance of insulin resistance is underscored by the alarming rise in the prevalence of obesity and its associated comorbidities in the Unites States and worldwide over the last 40-50 years. The incidence of obesity is also on the rise in adolescents. Furthermore, premenopausal women have lower CVD risk compared to men, but this protection is lost in the setting of obesity and insulin resistance. Although systemic and cardiovascular insulin resistance is associated with impaired insulin metabolic signaling and cardiovascular dysfunction, the mechanisms underlying insulin resistance and cardiovascular dysfunction remain poorly understood. Recent studies show that insulin resistance in obesity and diabetes is linked to a metabolic inflammatory response, a state of systemic and tissue specific chronic low grade inflammation. Evidence is also emerging that there is polarization of macrophages and lymphocytes towards a pro-inflammatory phenotype that contributes to progression of insulin resistance in obesity, cardiorenal metabolic syndrome and diabetes. In this review, we provide new insights into factors, such as, the renin-angiotensin-aldosterone system, sympathetic activation and incretin modulators (e.g., DPP-4) and immune responses that mediate this inflammatory state in obesity and other conditions characterized by insulin resistance. PMID:23932846

  15. Renal systems biology of patients with systemic inflammatory response syndrome.

    PubMed

    Tsalik, Ephraim L; Willig, Laurel K; Rice, Brandon J; van Velkinburgh, Jennifer C; Mohney, Robert P; McDunn, Jonathan E; Dinwiddie, Darrell L; Miller, Neil A; Mayer, Eric S; Glickman, Seth W; Jaehne, Anja K; Glew, Robert H; Sopori, Mohan L; Otero, Ronny M; Harrod, Kevin S; Cairns, Charles B; Fowler, Vance G; Rivers, Emanuel P; Woods, Christopher W; Kingsmore, Stephen F; Langley, Raymond J

    2015-10-01

    A systems biology approach was used to comprehensively examine the impact of renal disease and hemodialysis (HD) on patient response during critical illness. To achieve this, we examined the metabolome, proteome, and transcriptome of 150 patients with critical illness, stratified by renal function. Quantification of plasma metabolites indicated greater change as renal function declined, with the greatest derangements in patients receiving chronic HD. Specifically, 6 uremic retention molecules, 17 other protein catabolites, 7 modified nucleosides, and 7 pentose phosphate sugars increased as renal function declined, consistent with decreased excretion or increased catabolism of amino acids and ribonucleotides. Similarly, the proteome showed increased levels of low-molecular-weight proteins and acute-phase reactants. The transcriptome revealed a broad-based decrease in mRNA levels among patients on HD. Systems integration revealed an unrecognized association between plasma RNASE1 and several RNA catabolites and modified nucleosides. Further, allantoin, N1-methyl-4-pyridone-3-carboxamide, and N-acetylaspartate were inversely correlated with the majority of significantly downregulated genes. Thus, renal function broadly affected the plasma metabolome, proteome, and peripheral blood transcriptome during critical illness; changes were not effectively mitigated by hemodialysis. These studies allude to several novel mechanisms whereby renal dysfunction contributes to critical illness. PMID:25993322

  16. Caplan syndrome

    MedlinePLUS

    ... people with rheumatoid arthritis who have breathed in mining dust that contains coal. This lung disease is ... Caplan syndrome is caused by breathing in coal mining dust. This causes inflammation and can lead to ...

  17. Joubert Syndrome

    MedlinePLUS

    ... NINDS Funding Information Research Programs Training & Career Awards Enhancing Diversity Find People About NINDS NINDS Joubert Syndrome ... Funding | News From NINDS | Find People | Training | Research | Enhancing Diversity Careers@NINDS | FOIA | Accessibility Policy | Contact Us | ...

  18. Aicardi Syndrome

    MedlinePLUS

    ... NINDS Funding Information Research Programs Training & Career Awards Enhancing Diversity Find People About NINDS NINDS Aicardi Syndrome ... Funding | News From NINDS | Find People | Training | Research | Enhancing Diversity Careers@NINDS | FOIA | Accessibility Policy | Contact Us | ...

  19. Behcet's Syndrome

    MedlinePLUS

    Behcet's syndrome is a disease that involves vasculitis, which is inflammation of the blood vessels. It causes problems in many parts of the body. The ... National Institute of Arthritis and Musculoskeletal and Skin Diseases

  20. Turner syndrome

    MedlinePLUS

    ... birth if a chromosome analysis is done during prenatal testing. The doctor will perform a physical exam and look for signs of poor development. Infants with Turner syndrome often have swollen hands ...

  1. Tourette Syndrome

    MedlinePLUS

    ... won't make them less intelligent or need treatment at a hospital or doctor's office. Sometimes a person with Tourette syndrome might have other conditions, like attention deficit hyperactivity ...

  2. Aicardi syndrome

    MedlinePLUS

    ... the two sides of the brain (called the corpus callosum) is partly or completely missing. Nearly all known ... Aicardi syndrome if they meet the following criteria: Corpus callosum that is partly or completely missing Female sex ...

  3. Usher Syndrome

    MedlinePLUS

    ... expand treatment options. Scientists also are developing mouse models that have the same characteristics as the human types of Usher syndrome. Mouse models will make it easier to determine the function ...

  4. Down Syndrome

    MedlinePLUS

    ... chromosome 21. People with Down syndrome can have physical problems, as well as intellectual disabilities. Every person ... can help improve skills. They may include speech, physical, occupational, and/or educational therapy. With support and ...

  5. HELLP syndrome

    MedlinePLUS

    ... early. It is very important to have regular prenatal checkups. You should also let your health care ... prevent HELLP syndrome. All pregnant women should start prenatal care early and continue it through the pregnancy. ...

  6. Proteus Syndrome

    MedlinePLUS

    ... Criteria & FAQs Medical Research Glossary Donate Cash Donation Life Insurance Gift Matching Gift Stock Gift Sunshine Society Contact Privacy Policy Proteus Syndrome Definition Common Signs Diagnostic Criteria (I have a paragraph ...

  7. Menkes syndrome

    MedlinePLUS

    ... Menkes syndrome, cells in the body can absorb copper, but they are unable to release it. It ... makes it hard for the body to distribute copper in food from the intestines into the bloodstream ...

  8. Down Syndrome

    MedlinePLUS

    ... or problems with their heart, stomach or eyes. Intelligence ranges from low normal to very retarded (slow ... a baby who has Down syndrome will be. Intelligence ranges from low normal to very retarded (slow ...

  9. Cushing's Syndrome

    MedlinePLUS

    ... not have abnormally elevated cortisol levels. For example, polycystic ovary syndrome can cause menstrual disturbances, weight gain beginning in ... alcohol, have poorly controlled diabetes, or are severely obese. Pseudo-Cushing’s does not have the same long- ...

  10. Williams syndrome

    MedlinePLUS

    ... condition caused by missing a copy of several genes. Parents may not have any family history of the condition. However, a person with Williams syndrome has a 50% ... 25 missing genes is the gene that produces elastin, a protein ...

  11. Alport syndrome

    MedlinePLUS

    ... Learning new skills such as lip reading or sign language and getting hearing aids may help. Young men with Alport syndrome should use hearing protection in noisy environments. Genetic counseling may be recommended because the disorder is inherited.

  12. Bartter syndrome

    MedlinePLUS

    ... syndrome include: High levels of potassium , calcium, and chloride in the urine High levels of the hormones renin and aldosterone in the blood Low blood chloride Metabolic alkalosis These same signs and symptoms can ...

  13. Sanfilippo syndrome

    MedlinePLUS

    ... recessive trait. Sanfilippo syndrome occurs when the substances (enzymes) needed to break down the heparan sulfate sugar ... The type a person has depends on which enzyme is affected. Sanfilippo type A is the most ...

  14. Beals Syndrome

    MedlinePLUS

    ... have many of the skeletal (bone) and aortic enlargement problems as people with Marfan syndrome, and treatments ... appearance to the top of the ear Aortic enlargement and/or mitral valve regurgitation (occasionally) People with ...

  15. Ohtahara Syndrome

    MedlinePLUS

    ... have primarily tonic seizures, but may also experience partial seizures, and rarely, myoclonic seizures. Ohtahara syndrome is ... a characteristic pattern of high voltage spike wave discharge followed by little activity. This pattern is known ...

  16. Klinefelter syndrome

    MedlinePLUS

    These groups can provide more information: The American Association for Klinefelter Syndrome Information and Support (AAKSIS) -- www.aaksis.org National Institute of Health, National Human Genome Research Institute -- www.genome.gov/19519068

  17. Piriformis syndrome

    MedlinePLUS

    ... sciatica; Hip socket neuropathy; Pelvic outlet syndrome; Low back pain - piriformis ... or numbness in the buttock and along the back of the leg Difficulty sitting Pain from sitting that grows worse as you continue ...

  18. Reye syndrome

    MedlinePLUS

    ... Reye syndrome: Confusion Lethargy Loss of consciousness or coma Mental changes Nausea and vomiting Seizures Unusual placement ... breathing machine may be needed during a deep coma) Fluids by IV to provide electrolytes and glucose ...

  19. [Heptopulmonary syndrome].

    PubMed

    Cuadrado, Antonio; Díaz, Ainhoa; Iruzubieta, Paula; Salcines, José Ramón; Crespo, Javier

    2015-01-01

    Hepatopulmonary syndrome is characterized by the presence of liver disease, pulmonary vascular dilatations, and arterial hypoxemia. It is usually associated with cirrhosis of any origin, but has been described in other liver diseases, both acute and chronic, and not always associated with portal hypertension. The gold standard method to detect pulmonary vascular dilations is contrast enhancement echocardiography with saline and is essential for the diagnosis of hepatopulmonary syndrome. These dilatations reflect changes in the pulmonary microvasculature (vasodilatation, intravascular monocyte accumulation, and angiogenesis) and induce a ventilation/perfusion mismatch, or even true intrapulmonary shunts, which eventually trigger hypoxemia. This syndrome worsens patients' prognosis and impairs their quality of life and may lead to the need for liver transplantation, which is the only effective and definitive treatment. In this article, we review the etiological, pathophysiological, clinical and therapeutic features of this syndrome. PMID:25840463

  20. Sheehan syndrome

    MedlinePLUS

    ... occur in a woman who bleeds severely during childbirth. Sheehan syndrome is a type of hypopituitarism . ... Severe bleeding during childbirth can cause tissue in the pituitary gland to die. This gland does not work properly as a result. The ...

  1. Isaac's Syndrome

    MedlinePLUS

    ... often is caused by an autoimmune condition. Autoimmune-mediated Issacs' syndrome is typically caused by antibodies that ... Espaol sndrome de Isaac Prepared by: Office of Communications and Public Liaison National Institute of Neurological Disorders ...

  2. Klinefelter Syndrome

    MedlinePLUS

    ... Families Recursos en Español Teaching Resources Medical and Science Glossaries More Quick Links Evaluating Health Information Financial ... Links About the National Center for Advancing Translational Sciences (NCATS) GARD Home Diseases Klinefelter syndrome Diseases Genetic ...

  3. Usher Syndrome

    MedlinePLUS

    ... Families Recursos en Español Teaching Resources Medical and Science Glossaries More Quick Links Evaluating Health Information Financial ... Links About the National Center for Advancing Translational Sciences (NCATS) GARD Home Diseases Usher syndrome Diseases Genetic ...

  4. Branchiootorenal Syndrome

    MedlinePLUS

    ... Families Recursos en Español Teaching Resources Medical and Science Glossaries More Quick Links Evaluating Health Information Financial ... Links About the National Center for Advancing Translational Sciences (NCATS) GARD Home Diseases Branchiootorenal syndrome Diseases Genetic ...

  5. Troyer Syndrome

    MedlinePLUS

    ... Troyer syndrome is one of more than 40 genetically-distinct neurological disorders known collectively as the hereditary ... the NINDS or the NIH is appreciated. Last Modified January 3, 2012 National Institute of Neurological Disorders ...

  6. Metabolic Syndrome

    MedlinePLUS

    ... cause of metabolic syndrome. The cause might be insulin resistance. Insulin is a hormone your body produces to help ... into energy for your body. If you are insulin resistant, too much sugar builds up in your ...

  7. Tourette Syndrome

    MedlinePLUS

    ... shouts unexpectedly or blinks his eyes hard. These tics are symptoms of Luke's Tourette syndrome. But to ... looks like he's in pain or needs help. Tics are sudden, repetitive movements or sounds that some ...

  8. Down syndrome

    MedlinePLUS

    There is no specific treatment for Down syndrome. A child born with a gastrointestinal blockage may need major surgery immediately after birth. Certain heart defects may also require surgery. When breast-feeding, ...

  9. Cushing Syndrome

    MedlinePLUS

    ... The syndrome is named after a brain surgeon, Harvey Cushing, who identified the condition in 1932. 2 ... Shlomo, M., Polonsky, K.S, Larsen, P.R., eds. Williams. Textbook of Endocrinology. 12th ed. Philadelphia, Pa: Saunders ...

  10. Reye Syndrome

    MedlinePLUS

    ... are recovering from a viral infection, such as chicken pox or the flu. It usually develops a week ... after common viral infections such as influenza or chickenpox. Reye syndrome can also develop after an ordinary ...

  11. Metabolic Syndrome

    MedlinePLUS

    ... Web version Metabolic Syndrome Overview What is insulin resistance? Your body changes most of the food you ... insulin. Doctors refer to this condition as insulin resistance. If you have insulin resistance, your body will ...

  12. Hunter syndrome

    MedlinePLUS

    Hunter syndrome is a disease in which long chains of sugar molecules (glycosaminoglycans, formerly called mucopolysaccharides ) are ... of the enzyme iduronate sulfatase. Without this enzyme, chains of sugar molecules build up in various body ...

  13. Marfan Syndrome

    MedlinePLUS

    Marfan syndrome is a disorder that affects connective tissue. Connective tissues are proteins that support skin, bones, blood vessels, and other organs. One of these proteins is fibrillin. A problem with the ...

  14. Rett Syndrome

    MedlinePLUS

    ... features include reduced mobility, curvature of the spine (scoliosis) and muscle weakness, rigidity, spasticity, and increased muscle ... does not have Rett syndrome. Supportive criteria include scoliosis. teeth-grinding, small cold hands and feet in ...

  15. Aarskog syndrome

    MedlinePLUS

    ... the face. Inherited means that it is passed down through families. ... Seek genetic counseling if you have a family history of Aarskog syndrome. Contact a genetic specialist if your doctor thinks ...

  16. Inflammatory bowel disease.

    PubMed

    Vatn, Morten H; Sandvik, Arne K

    2015-06-01

    Scandinavian researchers have contributed to the present understanding of inflammatory bowel disease (IBD). Important epidemiological data and family risk factors have been reported from all the Nordic countries, original twin studies mainly from Denmark and Sweden, and relationships to cancer and surgery mostly from Sweden. In collaboration with the industry, development of medical compounds was for a long time in the front line of international research, and the Scandinavian countries participated in the clinical breakthrough of biologic treatment. At present, many Nordic centers are working in the forefront of IBD research. An increasing number of young investigators have entered the scene along with the extended distribution of University clinics and research laboratories in these countries. This presentation of IBD gives a brief overview in the fields of clinical epidemiology and molecular biology. Many areas are covered by International collaborations with partners from Nordic centers. IBD was a topic focused by the founders of Scandinavian Journal of Gastroenterology. After 50 years one may state that the journal's history reflects important pieces of scientific knowledge within these diseases. The early scope of Johannes Myren for IBD was shown through his work in the original World Association of Gastroenterology (OMG), and after 50 years we can clearly support the view that global perspectives in IBD are increasingly important. PMID:25855003

  17. Noonan syndrome

    PubMed Central

    Roberts, Amy E; Allanson, Judith E; Tartaglia, Marco; Gelb, Bruce D

    2014-01-01

    Noonan syndrome is a genetic multisystem disorder characterised by distinctive facial features, developmental delay, learning difficulties, short stature, congenital heart disease, renal anomalies, lymphatic malformations, and bleeding difficulties. Mutations that cause Noonan syndrome alter genes encoding proteins with roles in the RASMAPK pathway, leading to pathway dysregulation. Management guidelines have been developed. Several clinically relevant genotypephenotype correlations aid risk assessment and patient management. Increased understanding of the pathophysiology of the disease could help development of pharmacogenetic treatments. PMID:23312968

  18. The anit-inflammatory protein tristetraprolin is phosphorylated at multiple sites by multiple protein kinases

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Transgenic mice without tristetraprolin (TTP) protein develop a profound inflammatory syndrome with erosive arthritis, autoimmunity, and myeloid hyperplasia. TTP is a hyperphosphorylated zinc finger protein that binds to AU-rich elements within certain mRNAs such as tumor necrosis factor mRNA and ca...

  19. Grisel's Syndrome Induced by Mycobacterium tuberculosis

    PubMed Central

    Lee, Jun Ki; Oh, Chang Hyun; Park, Hyung-Chun

    2015-01-01

    Grisel's syndrome is a non-traumatic subluxation of the atlantoaxial joints, which is caused by an inflammatory process in the upper neck. It is rare to find literary reports of Grisel's syndrome with an evident pathogen in a lesion. For the first time in Korea, we report a 36-year-old female with Grisel's syndrome having an atlantoaxial subluxation, which was caused by a retropharyngeal abscess secondary to pulmonary Mycobacterium tuberculosis. The patient was treated with an anti-tuberculosis regimen and was prescribed a Philadelphia collar for the control of torticollis. The result of magnetic resonance imaging (MRI) showed an improved atlantoaxial alignment, after drug treatment and immobilization. This patient was neurologically intact and free from symptomatic complaints at follow-up visit. Dynamic cervical radiograph confirmed that the atlantoaxial joints had been stable. The pathophysiology of Grisel's syndrome, along with anatomical attributes, was explained on the basis of the patient's clinical course. PMID:26217388

  20. [Fisher Syndrome and Bickerstaff Brainstem Encephalitis].

    PubMed

    Kuwabara, Satoshi

    2015-11-01

    Fisher syndrome has been regarded as a peculiar inflammatory neuropathy with ophthalmoplegia, ataxia, and areflexia, whereas Bickerstaff brainstem encephalitis has been considered a pure central nervous system disease characterized by ophthalmoplegia, ataxia, and consciousness disturbance. Both disorders share common features including preceding infection, albumin-cytological dissociation, and association with Guillain-Barr syndrome. The discovery of anti-GQ1b IgG antibodies further supports the view that the two disorders represent a single disease spectrum. The lesions in Fisher syndrome and Bickerstaff brainstem encephalitis are presumably determined by the expression of ganglioside GQ1b in the human peripheral and central nervous systems. Bickerstaff brainstem encephalitis is likely to represent a variant of Fisher syndrome with central nervous system involvement. PMID:26560952

  1. Neonatal Sepsis and Inflammatory Mediators

    PubMed Central

    Reis Machado, Juliana; Soave, Danilo Figueiredo; da Silva, Marcos Vincius; de Menezes, Liliana Borges; Etchebehere, Renata Margarida; Monteiro, Maria Luiza Gonalves dos Reis; Antnia dos Reis, Marlene; Corra, Rosana Rosa Miranda; Celes, Mara Rbia Nunes

    2014-01-01

    Neonatal sepsis is a major cause of morbidity and mortality and its signs and symptoms are nonspecific, which makes the diagnosis difficult. The routinely used laboratory tests are not effective methods of analysis, as they are extremely nonspecific and often cause inappropriate use of antibiotics. Sepsis is the result of an infection associated with a systemic inflammatory response with production and release of a wide range of inflammatory mediators. Cytokines are potent inflammatory mediators and their serum levels are increased during infections, so changes from other inflammatory effector molecules may occur. Although proinflammatory and anti-inflammatory cytokines have been identified as probable markers of neonatal infection, in order to characterize the inflammatory response during sepsis, it is necessary to analyze a panel of cytokines and not only the measurement of individual cytokines. Measurements of inflammatory mediators bring new options for diagnosing and following up neonatal sepsis, thus enabling early treatment and, as a result, increased neonatal survival. By taking into account the magnitude of neonatal sepsis, the aim of this review is to address the role of cytokines in the pathogenesis of neonatal sepsis and its value as a diagnostic criterion. PMID:25614712

  2. Eicosanoids in Metabolic Syndrome

    PubMed Central

    Hardwick, James P.; Eckman, Katie; Lee, Yoon Kwang; Abdelmegeed, Mohamed A.; Esterle, Andrew; Chilian, William M.; Chiang, John Y.; Song, Byoung-Joon

    2013-01-01

    Chronic persistent inflammation plays a significant role in disease pathology of cancer, cardiovascular disease, and metabolic syndrome (MetS). MetS is a constellation of diseases that include obesity, diabetes, hypertension, dyslipidemia, hypertriglyceridemia, and hypercholesterolemia. Nonalcoholic fatty liver disease (NAFLD) is associated with many of the MetS diseases. These metabolic derangements trigger a persistent inflammatory cascade, which includes production of lipid autacoids (eicosanoids) that recruit immune cells to the site of injury and subsequent expression of cytokines and chemokines that amplify the inflammatory response. In acute inflammation, the transcellular synthesis of antiinflammatory eicosanoids resolve inflammation, while persistent activation of the autacoid-cytokine-chemokine cascade in metabolic disease leads to chronic inflammation and accompanying tissue pathology. Many drugs targeting the eicosanoid pathways have been shown to be effective in the treatment of MetS, suggesting a common linkage between inflammation, MetS and drug metabolism.The cross-talk between inflammation and MetS seems apparent because of the growing evidence linking immune cell activation and metabolic disorders such as insulin resistance, dyslipidemia, and hypertriglyceridemia. Thus modulation of lipid metabolism through either dietary adjustment or selective drugs may become a new paradigm in the treatment of metabolic disorders. This review focuses on the mechanisms linking eicosanoid metabolism to persistent inflammation and altered lipid and carbohydrate metabolism in MetS. PMID:23433458

  3. Learning about WAGR Syndrome

    MedlinePLUS

    ... children who have WAGR syndrome may have normal intelligence. Other symptoms of WAGR syndrome may also include: ... mild. Some individuals with WAGR syndrome have normal intelligence. Children with WAGR syndrome should be referred for ...

  4. Complex Regional Pain Syndrome

    MedlinePLUS

    ... Diversity Find People About NINDS NINDS Complex Regional Pain Syndrome Information Page Synonym(s): Reflex Sympathetic Dystrophy Syndrome, ... Additional resources from MedlinePlus What is Complex Regional Pain Syndrome? Complex regional pain syndrome (CRPS) is a ...

  5. Miller Fisher Syndrome

    MedlinePLUS

    ... Enhancing Diversity Find People About NINDS NINDS Miller Fisher Syndrome Information Page Synonym(s): Fisher Syndrome Table of Contents ( ... and Information Publicaciones en Espaol What is Miller Fisher Syndrome? Miller Fisher syndrome is a rare, acquired nerve ...

  6. Androgen insensitivity syndrome

    MedlinePLUS

    ... at the tip Reifenstein syndrome (also known as Gilbert-Dreyfus syndrome or Lubs syndrome) Infertile male syndrome ... F, Leveno KJ, Bloom SL, et al., eds. Williams Obstetrics . 23rd ed. New York, NY: McGraw-Hill, ...

  7. Down Syndrome (For Parents)

    MedlinePLUS

    ... Allergy Emergency Cerebral Palsy: Caring for Your Child Down Syndrome KidsHealth > For Parents > Down Syndrome Print A A ... Help en espaol El sndrome de Down About Down Syndrome Down syndrome (DS), also called Trisomy 21, is ...

  8. Hyperimmunoglobulin E syndrome

    MedlinePLUS

    Job syndrome; Hyper IgE syndrome ... Hyperimmunoglobulin E syndrome is also called Job syndrome, after the biblical character Job whose faithfulness was tested by an affliction with draining skin sores and pustules . People with this ...

  9. Irritable Bowel Syndrome

    MedlinePLUS

    ... Sledding, Skiing, Snowboarding, Skating Crushes What's a Booger? Irritable Bowel Syndrome KidsHealth > For Kids > Irritable Bowel Syndrome Print ... to minimize or prevent these symptoms. What Is Irritable Bowel Syndrome? Irritable bowel syndrome (IBS) is a fairly ...

  10. Proteus Syndrome Foundation

    MedlinePLUS

    ... Gift Stock Gift Sunshine Society Contact Privacy Policy Proteus Syndrome Foundation The Proteus Syndrome Foundation , a 501c3 ... Phase 1 Clinical Trail Patient Enrollment Has Begun Proteus Syndrome Patient Registry The Proteus Syndrome Foundation Contact ...

  11. What Is Usher Syndrome?

    MedlinePLUS

    ... You are here Home › Retinal Diseases Listen What is Usher Syndrome? What is Usher syndrome? How is ... are available? Are there any related diseases? What is Usher Syndrome? Usher syndrome is an inherited condition ...

  12. Carpal Tunnel Syndrome

    MedlinePLUS

    ... Enhancing Diversity Find People About NINDS NINDS Carpal Tunnel Syndrome Information Page Condensed from Carpal Tunnel Syndrome ... Español Additional resources from MedlinePlus What is Carpal Tunnel Syndrome? Carpal tunnel syndrome (CTS) occurs when the ...

  13. Somatostatin in inflammatory bowel disease

    PubMed Central

    Wilson, J. H. P.

    1997-01-01

    Intestinal inflammation is controlled by various immunomodulating cells, interacting by molecular mediators. Neuropeptides, released by enteric nerve cells and neuroendocrine mucosa cells, are able to affect several aspects of the general and intestinal immune system, with both pro- as well as anti-inflammatory activities. In inflammatory bowel disease (IBD) there is both morphological as well as experimental evidence for involvement of neuropeptides in the pathogenesis. Somatostatin is the main inhibitory peptide in inflammatory processes, and its possible role in IBD is discussed. PMID:18472863

  14. Microalbuminuria in inflammatory bowel disease.

    PubMed Central

    Mahmud, N; Stinson, J; O'Connell, M A; Mantle, T J; Keeling, P W; Feely, J; Weir, D G; Kelleher, D

    1994-01-01

    Microalbuminuria independently predicts the development of nephropathy and increased cardiovascular morbidity and mortality in diabetic patients, but it may be an indicator of the acute phase response. This study examined microalbuminuria as a marker of the acute phase response in patients with inflammatory bowel disease and correlated it with the disease activity in 95 patients with inflammatory bowel disease (ulcerative colitis (n = 52), Crohn's disease (n = 43)) determined by the simple index of Harvey and Bradshaw. Fifty patients were in complete clinical remission and 45 patients had active disease. Microalbuminuria was detected in all patients with inflammatory bowel disease (147 (17) v 18 (2) microgram/min, inflammatory bowel disease v controls mean (SEM), p < 0.007). Patients with active inflammatory bowel disease had higher concentrations of microalbuminuria compared with patients in remission (206 (19) v 65 (8) microgram/min, mean (SEM), p < 0.0001). Eight patients with active inflammatory bowel disease who were sequentially followed up with measurements of microalbuminuria had significantly lower values, when the disease was inactive (active inflammatory bowel disease 192 (44) v inactive inflammatory bowel disease 64 (14) microgram/min, p < 0.03). There was a significant correlation with the simple index of Harvey and Bradshaw (r = 0.818, p < 0.0001). Microalbuminuria values were significantly lower in inflammatory bowel disease patients in remission, maintained with olsalazine compared with those patients maintained with mesalazine and salazopyrine, but no significant difference was seen in values of microalbuminuria in active inflammatory bowel disease patients receiving different salicylates. This study also measured serum amyloid-A as an indicator of the acute phase response in the same patients. Serum amyloid-A was significantly increased in active disease compared with inactive disease (151 (43) v 33 (7) or controls 11 (2) micrograms/ml, p < 0.05). In conclusion microalbuminuria is present in abnormal amounts in all patients with active inflammatory bowel disease, and values fall when the disease is quiescent. Microalbuminuria is probably a consequence of an acute phase response and provides a simple, rapid, and inexpensive test, which has the potential to monitor inflammatory bowel disease activity and response to treatment. PMID:7828980

  15. The inflammasomes and autoinflammatory syndromes.

    PubMed

    Broderick, Lori; De Nardo, Dominic; Franklin, Bernardo S; Hoffman, Hal M; Latz, Eicke

    2015-01-01

    Inflammation, a vital response of the immune system to infection and damage to tissues, can be initiated by various germline-encoded innate immune-signaling receptors. Among these, the inflammasomes are critical for activation of the potent proinflammatory interleukin-1 cytokine family. Additionally, inflammasomes can trigger and maintain inflammatory responses aimed toward excess nutrients and the numerous danger signals that appear in a variety of chronic inflammatory diseases. We discuss our understanding of how inflammasomes assemble to trigger caspase-1 activation and subsequent cytokine release, describe how genetic mutations in inflammasome-related genes lead to autoinflammatory syndromes, and review the contribution of inflammasome activation to various pathologies arising from metabolic dysfunction. Insights into the mechanisms that govern inflammasome activation will help in the development of novel therapeutic strategies, not only for managing genetic diseases associated with overactive inflammasomes, but also for treating common metabolic diseases for which effective therapies are currently lacking. PMID:25423351

  16. Alport Syndrome Diagnosis

    MedlinePLUS

    ... Meet Jessi Patient to Patient - John Connect on Twitter Tweets by @AlportSyndFndn Alport Syndrome Diagnosis Early and ... Alport Syndrome YouTube Alport Syndrome LinkedIn Alport Syndrome Twitter Alport Syndrome Flickr Alport Syndrome Instagram Follow @twitterapi ...

  17. [Autoimmune hemolytic anemia in a patient with TAFRO syndrome].

    PubMed

    Edahiro, Yoko; Ichikawa, Kunimoto; Sunami, Yoshitaka; Koike, Michiaki; Komatsu, Norio

    2015-11-01

    TAFRO syndrome is a systemic inflammatory disorder characterized by low platelet counts, anasarca, fever, reticulin fibrosis, renal dysfunction, and organomegaly. Patients with TAFRO syndrome occasionally have courses complicated by immunological diseases. Herein, we describe a case of TAFRO syndrome associated with autoimmune hemolytic anemia (AIHA). The patient was admitted because of menorrhagia. She had thrombocytopenia, pleural effusion and ascites, hepatomegaly, and multiple lymphadenopathies. Her symptoms worsened, especially fever, pleural effusion and ascites, and she developed AIHA. Steroid pulse therapy followed by 45 mg of prednisolone (PSL) improved not only the symptoms of TAFRO syndrome but also those of AIHA. There have been no reports, to our knowledge, of AIHA associated with TAFRO syndrome, and detailed studies on this syndrome are needed. PMID:26666723

  18. Macrophage Polarization in Inflammatory Diseases

    PubMed Central

    Liu, Yan-Cun; Zou, Xian-Biao; Chai, Yan-Fen; Yao, Yong-Ming

    2014-01-01

    Diversity and plasticity are two hallmarks of macrophages. M1 macrophages (classically activated macrophages) are pro-inflammatory and have a central role in host defense against infection, while M2 macrophages (alternatively activated macrophages) are associated with responses to anti-inflammatory reactions and tissue remodeling, and they represent two terminals of the full spectrum of macrophage activation. Transformation of different phenotypes of macrophages regulates the initiation, development, and cessation of inflammatory diseases. Here we reviewed the characters and functions of macrophage polarization in infection, atherosclerosis, obesity, tumor, asthma, and sepsis, and proposed that targeting macrophage polarization and skewing their phenotype to adapt to the microenvironment might hold great promise for the treatment of inflammatory diseases. PMID:24910531

  19. THE INFLAMMATORY RESPONSE IN STROKE

    PubMed Central

    Wang, Qing; Tang, Xian Nan; Yenari, Midori A.

    2007-01-01

    Recent work in the area of stroke and brain ischemia has demonstrated the significance of the inflammatory response accompanying necrotic brain injury. Acutely, this response appears to contribute to ischemic pathology, and anti-inflammatory strategies have become popular. This chapter will discuss the current knowledge of the contribution of systemic and local inflammation in experimental stroke. It will review the role of specific cell types including leukocytes, endothelium, glia, microglia, the extracellular matrix and neurons. Intracellular inflammatory signaling pathways such as nuclear factor kappa beta and mitogen-activated protein kinases, and mediators produced by inflammatory cells such as cytokines, chemokines, reactive oxygen species and arachidonic acid metabolites will be reviewed as well as the potential for therapy in stroke and hypoxic-ischemic injury. PMID:17188755

  20. Pelvic Inflammatory Disease (PID) Statistics

    MedlinePLUS

    ... Years, United States, 2004–2013 Click for larger image Source : 2014 STD Surveillance Report STDs Home Page Bacterial Vaginosis (BV) Chlamydia Genital Herpes Gonorrhea Hepatitis HIV/AIDS & STDs Human Papillomavirus (HPV) Pelvic Inflammatory ...

  1. Develop Anti-Inflammatory Nanotherapies to Treat Cardiovascular Disease

    NASA Astrophysics Data System (ADS)

    Tang, Jun

    Cardiovascular disease (CVD) is the leading cause of disease-related death in the world, accounting for 30 % global mortality. The majority of CVD is caused by atherosclerosis, a chronic inflammatory disease of major arteries featured by the deposition of lipids and cholesterol. Inflammation of atherosclerosis is mainly promoted by the pathological macrophages and monocytes, and modulating their functions has been proposed as a promising therapeutic target. This dissertation first presents the development of a novel simvastatin-loaded high-density lipoprotein (HDL) based nanoparticle ([S]-rHDL), which was able to deliver anti-inflammatory simvastatin preferentially to inflammatory monocytes in the blood and to macrophages in advanced atherosclerotic plaques, leading to the reduced inflammation in the tissue. Second, extensive in vivo characterization of [S]-rHDL in a mouse atherosclerosis model revealed that the anti-inflammatory capability of [S]-rHDL derived from its effects on blood monocytes, endothelial layer, monocyte recruitment, and plaque macrophage function. Third, a translational study that integrated the use of [S]-rHDL into oral statin treatment demonstrated a great potential for this nanomedicine as an attractive addition to the current high-dose oral statin standard-of-care for acute coronary syndrome. Finally, preliminary results suggested potential applications of the rHDL platform to other macrophage-implicated diseases.

  2. Osteoarthritis as an inflammatory disease (osteoarthritis is not osteoarthrosis!).

    PubMed

    Berenbaum, F

    2013-01-01

    Osteoarthritis (OA) has long been considered a "wear and tear" disease leading to loss of cartilage. OA used to be considered the sole consequence of any process leading to increased pressure on one particular joint or fragility of cartilage matrix. Progress in molecular biology in the 1990s has profoundly modified this paradigm. The discovery that many soluble mediators such as cytokines or prostaglandins can increase the production of matrix metalloproteinases by chondrocytes led to the first steps of an "inflammatory" theory. However, it took a decade before synovitis was accepted as a critical feature of OA, and some studies are now opening the way to consider the condition a driver of the OA process. Recent experimental data have shown that subchondral bone may have a substantial role in the OA process, as a mechanical damper, as well as a source of inflammatory mediators implicated in the OA pain process and in the degradation of the deep layer of cartilage. Thus, initially considered cartilage driven, OA is a much more complex disease with inflammatory mediators released by cartilage, bone and synovium. Low-grade inflammation induced by the metabolic syndrome, innate immunity and inflammaging are some of the more recent arguments in favor of the inflammatory theory of OA and highlighted in this review. PMID:23194896

  3. Dengue infection associated hemophagocytic syndrome: Therapeutic interventions and outcome.

    PubMed

    Wan Jamaludin, Wan Fariza; Periyasamy, Petrick; Wan Mat, Wan Rahiza; Abdul Wahid, S Fadilah

    2015-08-01

    Infection associated hemophagocytic syndrome is increasingly recognized as a potentially fatal complication of dengue fever. It should be suspected with prolonged fever beyond seven days associated with hepatosplenomegaly, hyperferritinemia, worsening cytopenias and development of multiorgan dysfunction. Surge of similar pro-inflammatory cytokines observed in dengue associated hemophagocytic syndrome and multiorgan dysfunction may indicate they are part of related inflammatory spectrum. A proportion of patients recovered with supportive therapy, however most required interventions with corticosteroids, intravenous immunoglobulin or chemotherapy. We report three cases of dengue associated IAHS with good outcome following early recognition and treatment with dexamethasone and intravenous immunoglobulin. PMID:26209387

  4. Inflammatory bowel disease in pregnancy.

    PubMed

    Beaulieu, Dawn B; Kane, Sunanda

    2011-06-01

    Crohn disease and ulcerative colitis commonly affect women in their childbearing years. Fortunately, advances in the field of inflammatory bowel disease have made successful pregnancy outcomes a reality for many women. These advances have led to family planning as a common discussion between gastroenterologists and inflammatory bowel disease patients. Common discussion topics are fertility, conception, medication safety, pregnancy, delivery, and breastfeeding although there are limited available data. Education and patient awareness have become vital factors in successful pregnancy outcomes. PMID:21601787

  5. [Anticonvulsant Hypersensitivity Syndrome: A Case Report].

    PubMed

    Valderrama Escudero, Felipe; Montoya González, Laura Elisa

    2014-01-01

    DRESS syndrome (skin reaction with eosinophilia and systemic symptoms) is an idiosyncratic drug reaction characterized by rash, fever, lymphadenopathy, and internal organ dysfunction. This case report is on a patient with bipolar affective disorder who presented with a systemic inflammatory response associated with the use of valproic acid, and an important activation of symptoms when used with other drugs with a different pharmacological action mechanism. The diagnosis of DRESS syndrome is primarily by exclusion, and its detection may be difficult, which could potentially become fatal for the patient. PMID:26574080

  6. Nephrotic syndrome.

    PubMed

    Andolino, Tecile Prince; Reid-Adam, Jessica

    2015-03-01

    On the basis of observational studies, the most common cause of nephrotic syndrome in school-aged children is minimal change disease. On the basis of research evidence and consensus, corticosteroids are considered first-line therapy for treatment of nephrotic syndrome. On the basis of consensus, prednisone therapy should be initiated at doses of 60 mg/m2 per day (2 mg/kg per day) administered for 4 to 6 weeks, followed by 40 mg/m2 per dose (1.5 mg/kg) every other day for at least 6 to 8 weeks. On the basis of consensus and expert opinion, it is important to recognize and manage the complications that can arise in patients with nephrotic syndrome, such as dyslipidemia, infection, and thrombosis. On the basis of research evidence, consensus, and expert opinion, several alternative therapies have been observed to have variable efficacy in children with both corticosteroid-dependent and corticosteroid-resistant nephrotic syndrome, although caution must be exercised in the administration of these corticosteroid-sparing medications secondary to toxic adverse effects. On the basis of observational studies, the course of nephrotic syndrome in most patients is that of relapse and remission. PMID:25733763

  7. Preexcitation Syndromes.

    PubMed

    Bhatia, Atul; Sra, Jasbir; Akhtar, Masood

    2016-03-01

    The classic electrocardiogram in Wolff-Parkinson-White (WPW) syndrome is characterized by a short PR interval and prolonged QRS duration in the presence of sinus rhythm with initial slurring. The clinical syndrome associated with above electrocardiogram finding and the history of paroxysmal supraventricular tachycardia is referred to as Wolff-Parkinson-White syndrome. Various eponyms describing accessory or anomalous conduction pathways in addition to the normal pathway are collectively referred to as preexcitation syndromes. The latter form and associated eponyms are frequently used in literature despite controversy and disagreements over their actual anatomical existence and electrophysiological significance. This communication highlights inherent deficiencies in the knowledge that has existed since the use of such eponyms began. With the advent of curative ablation, initially surgical, and then catheter based, the knowledge gaps have been mostly filled with better delineation of the anatomic and electrophysiological properties of anomalous atrioventricular pathways. It seems reasonable, therefore, to revisit the clinical and electrophysiologic role of preexcitation syndromes in current practice. PMID:26897561

  8. Nutrition in inflammatory bowel disease.

    PubMed

    Gassull, M A; Cabré, E

    2001-11-01

    Nutritional derangements are frequent in inflammatory bowel disease. In the past year significant work has been published examining the mechanisms of impaired food intake in animal models of inflammatory bowel disease, which allow a better understanding of these processes. Data from the same laboratory have shed further light on the relative role of underfeeding and inflammation on the growth retardation associated with intestinal inflammation. Other studies have provided further data on the risk factors and predictive biomarkers of bone loss in patients with inflammatory bowel disease. The potential role of enteral nutrition as primary therapy for Crohn's disease is particularly addressed in this review. Recent contributions to the field emphasized the special importance of this modality of therapy in paediatric patients. The possible mechanisms for such a therapeutic action are not well understood. Other nutrients may have a therapeutic potential in inflammatory bowel disease. In particular, recent data on the in-vivo anti-inflammatory actions of butyrate merit special mention. Finally, novel nutritional therapeutic strategies for inflammatory bowel disease, such as transforming growth factor-beta2-enriched enteral feeding, or hydrothermally processed cereals have recently been explored. PMID:11706295

  9. IL-1 Blockade in Autoinflammatory Syndromes1

    PubMed Central

    Jesus, Adriana A.; Goldbach-Mansky, Raphaela

    2014-01-01

    Monogenic autoinflammatory syndromes present with excessive systemic inflammation including fever, rashes, arthritis, and organ-specific inflammation and are caused by defects in single genes encoding proteins that regulate innate inflammatory pathways. Pathogenic variants in two interleukin-1 (IL-1)regulating genes, NLRP3 and IL1RN, cause two severe and early-onset autoinflammatory syndromes, CAPS (cryopyrin associated periodic syndromes) and DIRA (deficiency of IL-1 receptor antagonist). The discovery of the mutations that cause CAPS and DIRA led to clinical and basic research that uncovered the key role of IL-1 in an extended spectrum of immune dysregulatory conditions. NLRP3 encodes cryopyrin, an intracellular molecular sensor that forms a multimolecular platform, the NLRP3 inflammasome, which links danger recognition to the activation of the proinflammatory cytokine IL-1?. The success and safety profile of drugs targeting IL-1 in the treatment of CAPS and DIRA have encouraged their wider use in other autoinflammatory syndromes including the classic hereditary periodic fever syndromes (familial Mediterranean fever, TNF receptorassociated periodic syndrome, and hyperimmunoglobulinemia D with periodic fever syndrome) and additional immune dysregulatory conditions that are not genetically well defined, including Stills, Behcets, and Schnitzler diseases. The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1?-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease. PMID:24422572

  10. Inflammatory and immunomodulatory mechanisms in the carotid body.

    PubMed

    Porzionato, Andrea; Macchi, Veronica; De Caro, Raffaele; Di Giulio, Camillo

    2013-06-01

    Evidence is available about the role of inflammatory/immunological factors in the physiology and plasticity of the carotid body, with potential clinical implications in obstructive sleep apnea syndrome and sudden infant death syndrome. In humans, lymphomonocytic aggregations (chronic carotid glomitis) have been reported in aging and opiate addiction. Glomus cells produce prostaglandin E2 and the cytokines interleukin 1β, interleukin 6 and TNF-α, with corresponding receptors. These factors modulate glomus cell excitability, catecholamine release and/or chemoreceptor discharge. The above cytokines are up-regulated in chronic sustained or intermittent hypoxia, and prevention of these changes, with ibuprofen or dexamethasone, may modulate hypoxia-induced changes in carotid body chemosensitivity. The main transcription factors considered to be involved are NF-kB and HIFs. Circulating immunogens (lipopolysaccharide) and cytokines may also affect peripheral arterial chemoreception, with the carotid body exerting an immunosensing function. PMID:23485800

  11. [Vulvar lichen sclerosus in a girl with Turner syndrome].

    PubMed

    Ocampo, Dolores; Gonzlez, Vernica

    2014-08-01

    Dermatological complications in Turner syndrome are infrequent but occasionally cause significant morbidity. Lichen sclerosus (LS) is a chronic inflammatory mucocutaneous affection characterized by pruritus in the anogenital area. It is yet not clear its pathophysiology but it's linked with genetic factors and autoimmunity. This is a case report of a girl with Turner syndrome with growth hormone treatment that started with vulvar pruritus and was diagnosed as lichen sclerosus. PMID:24955917

  12. [Kallmann syndrome].

    PubMed

    Mokosch, A; Bernecker, C; Willenberg, H S; Neumann, N J

    2011-10-01

    The Kallmann syndrome is a very rare congenital association of gonadotropin-releasing hormone deficiency and hyposmia or anosmia. Clinically it is characterized by low serum concentrations of testosterone and inadequate low levels of luteinizing hormone and follicle-stimulating hormone as well as incomplete sexual maturation, lack of secondary sexual features (facial and body hair growth, deepening of the voice), micropenis and sometimes even cryptorchidism. The reduced or absent sense of smell is typical for the Kallmann syndrome and distinguishes this syndrome from other causes of hypogonadotropic hypogonadism. Additional findings may include synkinesia, hearing loss, unilateral renal aplasia, brachy- or syndactyly, agenesis of corpus callosum, cleft palate and dental agenesis. A 19-year-old man presented to our male infertility clinic with delayed sexual maturation, eunuchoid habitus, micropenis, cryptorchidism, erectile dysfunction and absence of ejaculation, anemia and osteoporosis as well as low serum concentrations of luteinizing hormone, follicle-stimulating hormone and testosterone in combination with hyposmia. PMID:21918848

  13. Compartment syndromes

    NASA Technical Reports Server (NTRS)

    Mubarak, S. J.; Pedowitz, R. A.; Hargens, A. R.

    1989-01-01

    The compartment syndrome is defined as a condition in which high pressure within a closed fascial space (muscle compartment) reduces capillary blood perfusion below the level necessary for tissue viability'. This condition occurs in acute and chronic (exertional) forms, and may be secondary to a variety of causes. The end-result of an extended period of elevated intramuscular pressure may be the development of irreversible tissue injury and Volkmann's contracture. The goal of treatment of the compartment syndrome is the reduction of intracompartmental pressure thus facilitating reperfusion of ischaemic tissue and this goal may be achieved by decompressive fasciotomy. Controversy exists regarding the critical pressure-time thresholds for surgical decompression and the optimal diagnostic methods of measuring intracompartmental pressures. This paper will update and review some current knowledge regarding the pathophysiology, aetiology, diagnosis, and treatment of the acute compartment syndrome.

  14. Flammer syndrome

    PubMed Central

    2014-01-01

    The new term Flammer syndrome describes a phenotype characterized by the presence of primary vascular dysregulation together with a cluster of symptoms and signs that may occur in healthy people as well as people with disease. Typically, the blood vessels of the subjects with Flammer syndrome react differently to a number of stimuli, such as cold and physical or emotional stress. Nearly all organs, particularly the eye, can be involved. Although the syndrome has some advantages, such as protection against the development of atherosclerosis, Flammer syndrome also contributes to certain diseases, such as normal tension glaucoma. The syndrome occurs more often in women than in men, in slender people than in obese subjects, in people with indoor rather than outdoor jobs, and in academics than in blue collar workers. Affected subjects tend to have cold extremities, low blood pressure, prolonged sleep onset time, shifted circadian rhythm, reduced feeling of thirst, altered drug sensitivity, and increased general sensitivity, including pain sensitivity. The plasma level of endothelin-1 is slightly increased, and the gene expression in lymphocytes is changed. In the eye, the retinal vessels are stiffer and their spatial variability larger; the autoregulation of ocular blood flow is decreased. Glaucoma patients with Flammer syndrome have an increased frequency of the following: optic disc hemorrhages, activated retinal astrocytes, elevated retinal venous pressure, optic nerve compartmentalization, fluctuating diffuse visual field defects, and elevated oxidative stress. Further research should lead to a more concise definition, a precise diagnosis, and tools for recognizing people at risk. This may ultimately lead to more efficient and more personalized treatment. PMID:25075228

  15. Flammer syndrome.

    PubMed

    Konieczka, Katarzyna; Ritch, Robert; Traverso, Carlo Enrico; Kim, Dong Myung; Kook, Michael Scott; Gallino, Augusto; Golubnitschaja, Olga; Erb, Carl; Reitsamer, Herbert A; Kida, Teruyo; Kurysheva, Natalia; Yao, Ke

    2014-01-01

    The new term Flammer syndrome describes a phenotype characterized by the presence of primary vascular dysregulation together with a cluster of symptoms and signs that may occur in healthy people as well as people with disease. Typically, the blood vessels of the subjects with Flammer syndrome react differently to a number of stimuli, such as cold and physical or emotional stress. Nearly all organs, particularly the eye, can be involved. Although the syndrome has some advantages, such as protection against the development of atherosclerosis, Flammer syndrome also contributes to certain diseases, such as normal tension glaucoma. The syndrome occurs more often in women than in men, in slender people than in obese subjects, in people with indoor rather than outdoor jobs, and in academics than in blue collar workers. Affected subjects tend to have cold extremities, low blood pressure, prolonged sleep onset time, shifted circadian rhythm, reduced feeling of thirst, altered drug sensitivity, and increased general sensitivity, including pain sensitivity. The plasma level of endothelin-1 is slightly increased, and the gene expression in lymphocytes is changed. In the eye, the retinal vessels are stiffer and their spatial variability larger; the autoregulation of ocular blood flow is decreased. Glaucoma patients with Flammer syndrome have an increased frequency of the following: optic disc hemorrhages, activated retinal astrocytes, elevated retinal venous pressure, optic nerve compartmentalization, fluctuating diffuse visual field defects, and elevated oxidative stress. Further research should lead to a more concise definition, a precise diagnosis, and tools for recognizing people at risk. This may ultimately lead to more efficient and more personalized treatment. PMID:25075228

  16. Pseudoexfoliation Syndrome

    PubMed Central

    Nivean, M; Utkarsha, P

    2013-01-01

    ABSTRACT Pseudoexfoliation (PXF) syndrome is a well-recognized clinical entity of considerable clinical significance. It is associated with poor mydriasis, cataracts with weak zonular support, secondary glaucoma and possibly with biochemical abnormalities, such as elevated homocysteine and systemic diseases involving the cardiovascular and central nervous system. There have also been some recent studies identifying mutations in genes which are associated with PXF. How to cite this article: Ariga M, Nivean M, Utkarsha P. Pseudoexfoliation Syndrome. J Current Glau Prac 2013;7(3): 118-120.

  17. Eagle syndrome.

    PubMed

    Ferreira, Pedro Costa; Mendanha, Mário; Frada, Tiago; Carvalho, Jorge; Silva, Alvaro; Amarante, José

    2014-01-01

    Eagle syndrome, also known as elongated styloid process, is a condition first described by Watt Eagle in 1937. It occurs when an elongated styloid process or calcified stylohyoid ligament causes recurrent throat pain or foreign body sensation, dysphagia, or facial pain. Additional symptoms may include neck or throat pain with radiation to the ipsilateral ear. It is usually hard to diagnose because the symptoms related to this condition can be confused with those attributed to a wide variety of facial neuralgias. In this article, a case of Eagle syndrome exhibiting unilateral symptoms with bilateral elongation of styloid process is reported. PMID:24406612

  18. A Rare Case of Azathioprine-Induced Sweet's Syndrome in a Patient with Crohn's Disease.

    PubMed

    Ben Salem, Chaker; Salem, Chaker B; Larif, Sofiene; Fathallah, Neila; Slim, Raoudha; Aounallah, Amina; Sakhri, Jaballah; Hmouda, Houssem

    2015-01-01

    Sweet's syndrome has been reported in association with inflammatory diseases such as Crohn's disease. It has also been reported in association with several drugs. Here, we report a rare case of Sweet's syndrome induced by azathioprine in a patient with Crohn's disease. PMID:26219289

  19. Occipital Condyle Syndrome in a Young Male: A Rare Presentation of Cranio-Vertebral Tuberculosis

    PubMed Central

    Yogesh, Patidar; Vinod, Puri; A, Khwaja Geeta

    2014-01-01

    Occipital condyle syndrome (OCS) is a rare syndrome characterized by severe, unilateral, occipital headache and ipsilateral 12th nerve palsy. Tumors are a common cause of OCS. Inflammatory lesions causing OCS is however rare. We describe a young male with OCS as the only manifestation of cranio-vertebral tuberculosis. PMID:25664279

  20. Hemophagocytic syndrome: a dilemma chasing the intensivists.

    PubMed

    Queiroz, Adriana Faanha; Benevides, Gabriel Nuncio; Fernandes, Iracema de Cassia Oliveira Ferreira; Goes, Patricia de Freitas; Bousso, Albert; Ferreira, Cristiane Rubia

    2015-01-01

    Hemophagocytic lymphohistiocytosis or hemophagocytic syndrome is represented by an uncontrolled inflammatory response characterized by marked histiocyte activation and a cytokine storm. The entity may present a primary or genetic type, and the secondary type is usually triggered by infectious diseases of any kind, autoimmune disease, or neoplasia. This entity, although well described and with definite diagnostic criteria, still remains misdiagnosed because of the overlap presentation with other inflammatory processes. The authors present the case of a 13-year-old girl who was submitted to an appendicectomy complicated with a pericolic abscess, which required a second operation in order to be drained surgically. During the postoperative period of this second surgical procedure, the patient remained febrile, developing cytopenias, and multiple organ failure. Unfortunately, she died despite the efforts of the intensive care staff. The autopsy findings were characteristic of hemophagocytic syndrome. The authors report the case to call attention to this diagnosis whenever unexpected outcomes of infections are experienced. PMID:26484319

  1. Familial hepatopulmonary syndrome in common variable immunodeficiency.

    PubMed

    Holmes, S N; Condliffe, A; Griffiths, W; Baxendale, H; Kumararatne, D S

    2015-04-01

    Common Variable Immunodeficiency (CVID) comprises a heterogeneous group of primary antibody deficiencies which lead to a range of complications, including infectious, neoplastic and inflammatory disorders. This report describes monozygotic twin brothers with CVID who developed cryptogenic liver disease and subsequently hepatopulmonary syndrome (HPS). This is the second report of the association of HPS and CVID. Its occurrence in two identical twins implicates a genetic basis. PMID:25708586

  2. Theories of schizophrenia: a genetic-inflammatory-vascular synthesis

    PubMed Central

    Hanson, Daniel R; Gottesman, Irving I

    2005-01-01

    Background Schizophrenia, a relatively common psychiatric syndrome, affects virtually all brain functions yet has eluded explanation for more than 100 years. Whether by developmental and/or degenerative processes, abnormalities of neurons and their synaptic connections have been the recent focus of attention. However, our inability to fathom the pathophysiology of schizophrenia forces us to challenge our theoretical models and beliefs. A search for a more satisfying model to explain aspects of schizophrenia uncovers clues pointing to genetically mediated CNS microvascular inflammatory disease. Discussion A vascular component to a theory of schizophrenia posits that the physiologic abnormalities leading to illness involve disruption of the exquisitely precise regulation of the delivery of energy and oxygen required for normal brain function. The theory further proposes that abnormalities of CNS metabolism arise because genetically modulated inflammatory reactions damage the microvascular system of the brain in reaction to environmental agents, including infections, hypoxia, and physical trauma. Damage may accumulate with repeated exposure to triggering agents resulting in exacerbation and deterioration, or healing with their removal. There are clear examples of genetic polymorphisms in inflammatory regulators leading to exaggerated inflammatory responses. There is also ample evidence that inflammatory vascular disease of the brain can lead to psychosis, often waxing and waning, and exhibiting a fluctuating course, as seen in schizophrenia. Disturbances of CNS blood flow have repeatedly been observed in people with schizophrenia using old and new technologies. To account for the myriad of behavioral and other curious findings in schizophrenia such as minor physical anomalies, or reported decreased rates of rheumatoid arthritis and highly visible nail fold capillaries, we would have to evoke a process that is systemic such as the vascular and immune/inflammatory systems. Summary A vascular-inflammatory theory of schizophrenia brings together environmental and genetic factors in a way that can explain the diversity of symptoms and outcomes observed. If these ideas are confirmed, they would lead in new directions for treatments or preventions by avoiding inducers of inflammation or by way of inflammatory modulating agents, thus preventing exaggerated inflammation and consequent triggering of a psychotic episode in genetically predisposed persons. PMID:15707482

  3. Metabolic Syndrome

    MedlinePLUS

    ... Metabolic Syndrome? Changing Your Course en espaol El sndrome metablico Choices. Life is full of them. And many choices affect our health: Will you choose pizza at that post-game dinner or salad with grilled chicken? Do you flop down in front of the TV after school or ...

  4. Reye's Syndrome

    MedlinePLUS

    ... U.S. Department of Health and Human Services 5600 Fishers Lane, CDER-HFD-240 Rockville, MD 20857 http://www.fda.gov Tel: 301-827-4573 888-INFO-FDA (463-6332) National Reye's Syndrome Foundation P.O. Box 829 426 North Lewis ...

  5. Alport Syndrome

    MedlinePLUS

    ... older the risk of kidney failure increases. All boys and girls with the autosomal recessive type of Alport Syndrome ... with this disease have the X-linked type. Boys with this type are severely ... in their lives. Girls with this type usually have milder symptoms than ...

  6. Rett Syndrome.

    ERIC Educational Resources Information Center

    Culbert, Linda A.

    This pamphlet reviews the historical process involved in initially recognizing Rett Syndrome as a specific disorder in girls. Its etiology is unknown, but studies have considered factors as hyperammonemia, a two-step mutation, a fragile X chromosome, metabolic disorder, environmental causation, dopamine deficiency, and an inactive X chromosome.

  7. Compartment syndrome

    MedlinePLUS

    ... affected area (for example, a person with compartment syndrome in the foot or lower leg will have severe pain when moving the toes up and down) Swelling in the area To confirm the diagnosis, the doctor or nurse may need to directly ...

  8. Tourette Syndrome

    MedlinePLUS

    ... hyperactivity disorder (ADHD) Obsessive-compulsive disorder (OCD) Anxiety Depression The cause of Tourette syndrome is unknown. It is more common in boys than girls. The tics usually start in childhood and may be worst in the early teens. Many people eventually outgrow them. No treatment is ...

  9. Satoyoshi syndrome.

    PubMed

    Mukhopadhyay, Debadatta; Ghosh, Apurba; Mukhopadhyay, Maya

    2011-09-01

    Satoyoshi syndrome is a rare autoimmune disease characterized by alopecia, painful muscle spasms, diarrhea and secondary skeletal changes. We report a 11 year old girl presenting with the typical features of alopecia totalis, severe muscle spasm and skeletal deformities. PMID:21992906

  10. Metabolic Syndrome

    MedlinePLUS

    ... levels, and it’s closely linked to overweight and obesity. Genetics (ethnicity and family history) and older age are other factors that may play a role in causing metabolic ... due to a rise in obesity rates among adults. In the future, metabolic syndrome ...

  11. Rett Syndrome.

    ERIC Educational Resources Information Center

    Culbert, Linda A.

    This pamphlet reviews the historical process involved in initially recognizing Rett Syndrome as a specific disorder in girls. Its etiology is unknown, but studies have considered factors as hyperammonemia, a two-step mutation, a fragile X chromosome, metabolic disorder, environmental causation, dopamine deficiency, and an inactive X chromosome.…

  12. Postthrombotic Syndrome

    MedlinePLUS

    ... syndrome. Blood . 2009 ; 114 : 4624 –4631. Abstract / FREE Full Text ↵ Vazquez SR, Freeman A, VanWoerkom RC, Rondina MT. ... CIRCULATIONAHA.109.925651 Extract Free Figures Only Free » Full Text Free PDF Free PPT Slides of All Figures ...

  13. Systemic Inflammatory Response during Laparotomy

    PubMed Central

    Mahamid, Ahmad; Jabarin, Basel; Almogy, Gidon

    2014-01-01

    Background. The aim of this study was to analyze the influence of laparotomy on the systemic inflammatory response in human patients suffering from secondary peritonitis. Study Design. A prospective study investigating the levels of white blood cells, C-reactive protein, platelets, interleukin-six, and tumor necrosis factor-alpha during laparotomy in five patients who suffered from secondary peritonitis. Six venous blood samples were collected perioperatively from each patient. The data were summarized by descriptive statistics and presented in a box plot. The hypothesis was that laparotomy increases the systemic inflammatory response, as has been described in animal models in previous studies. Results. The median age of the patients in this study was 84 years, the male to female ratio was 2 : 3, and the mortality rate was 80%. The most common cause of generalized peritonitis was ischemia of the colon. Analysis of the data showed no significant changes in the level of plasma inflammatory mediators during the surgical procedure, except for the platelet count which showed a significant decrease (P = 0.001). Conclusions. In contrast to experience with animal models, laparotomy in human patients with secondary peritonitis did not significantly increase the systemic inflammatory response. Furthermore, it contributed in significantly decreasing some of the systemic inflammatory mediators. PMID:25161799

  14. Cronkhite- Canada syndrome; a case report and review of the literature

    PubMed Central

    Safari, Mohammad Taghi; Shahrokh, Shabnam; Ebadi, Shahram; Sadeghi, Amir

    2016-01-01

    Cronkhite- Canada syndrome (CCS) considered as a rare and non-hereditary disorder. Gastrointestinal polyposis and diarrhea along with some extra signs and symptoms such as hypoproteinemia, and epidermal manifestations are recognized in this syndrome. The pathophysiology of this syndrome is not completely understood and it seems that inflammatory processes may be involved. We present a 50 year-old man with hamartomatous polyps throughout the colon and long-lasting diarrhea not responding to typical therapies during three years. PMID:26744616

  15. Inflammatory Bowel Disease in the Obese Patient

    PubMed Central

    Boutros, Marylise; Maron, David

    2011-01-01

    Obesity is becoming increasingly more common among patients with inflammatory bowel disease. In this review, we will explore the epidemiological trends of inflammatory bowel disease, the complex interplay between the proinflammatory state of obesity and inflammatory bowel disease, outcomes of surgery for inflammatory bowel disease in obese as compared with non-obese patients, and technical concerns pertaining to restorative proctocolectomy and ileoanal pouch reservoir, stoma creation and laparoscopic surgery for inflammatory bowel disease in obese patients. PMID:23204939

  16. Guillain-Barr syndrome

    MedlinePLUS

    ... Acute inflammatory polyneuropathy; Acute inflammatory demyelinating polyneuropathy; Ascending paralysis ... This nerve damage causes tingling, muscle weakness , and paralysis . GBS most often affects the nerve covering ( myelin ...

  17. Biomarkers in management of inflammatory bowel disease

    PubMed Central

    Moniuszko, Andrzej; Wiśniewska, Anna

    2013-01-01

    In recent years the use of faecal and serologic biomarkers has been evaluated in the diagnosis and management of inflammatory bowel disease (IBD). Faecal calprotectin (FC) has been proposed as a surrogate marker for intestinal inflammation; elevated concentrations in IBD patients have been confirmed in numerous studies. Already available rapid calprotectin tests help to differentiate between IBD and irritable bowel syndrome. Faecal calprotectin greatly correlates with endoscopic activity scales and reflects the mucosal healing; thus in patients in clinical remission high levels of it correlate with increased risk of disease relapse in the following 12 months. Adapting the calprotectin assay as a screening test before colonoscopy enables a significant reduction in endoscopic procedures. ANCA/ASCA antibodies have been used in IBD diagnosis and to distinguish CD from ulcerative colitis (UC). Lactoferrin and S100A12 protein were also used to assess the disease activity. This review aims to present the actual potential of biomarker assays for faster diagnosis of IBD and their ability to monitor the disease course, predict exacerbations and improve the way IBD is managed. PMID:24868269

  18. Marine Bioactives: Pharmacological Properties and Potential Applications against Inflammatory Diseases

    PubMed Central

    D’Orazio, Nicolantonio; Gammone, Maria Alessandra; Gemello, Eugenio; De Girolamo, Massimo; Cusenza, Salvatore; Riccioni, Graziano

    2012-01-01

    Inflammation is a hot topic in medical research, because it plays a key role in inflammatory diseases: rheumatoid arthritis (RA) and other forms of arthritis, diabetes, heart diseases, irritable bowel syndrome, Alzheimer’s disease, Parkinson’s disease, allergies, asthma, even cancer and many others. Over the past few decades, it was realized that the process of inflammation is virtually the same in different disorders, and a better understanding of inflammation may lead to better treatments for numerous diseases. Inflammation is the activation of the immune system in response to infection, irritation, or injury, with an influx of white blood cells, redness, heat, swelling, pain, and dysfunction of the organs involved. Although the pathophysiological basis of these conditions is not yet fully understood, reactive oxygen species (ROS) have often been implicated in their pathogenesis. In fact, in inflammatory diseases the antioxidant defense system is compromised, as evidenced by increased markers of oxidative stress, and decreased levels of protective antioxidant enzymes in patients with rheumatoid arthritis (RA). An enriched diet containing antioxidants, such as vitamin E, vitamin C, β-carotene and phenolic substances, has been suggested to improve symptoms by reducing disease-related oxidative stress. In this respect, the marine world represents a largely untapped reserve of bioactive ingredients, and considerable potential exists for exploitation of these bioactives as functional food ingredients. Substances such as n-3 oils, carotenoids, vitamins, minerals and peptides provide a myriad of health benefits, including reduction of cardiovascular diseases, anticarcinogenic and anti-inflammatory activities. New marine bioactives are recently gaining attention, since they could be helpful in combating chronic inflammatory degenerative conditions. The aim of this review is to examine the published studies concerning the potential pharmacological properties and application of many marine bioactives against inflammatory diseases. PMID:22690145

  19. Inflammatory Cytokines in Diabetic Nephropathy

    PubMed Central

    Donate-Correa, Javier; Martn-Nez, Ernesto; Muros-de-Fuentes, Mercedes; Mora-Fernndez, Carmen; Navarro-Gonzlez, Juan F.

    2015-01-01

    Probably, the most paradigmatic example of diabetic complication is diabetic nephropathy, which is the largest single cause of end-stage renal disease and a medical catastrophe of worldwide dimensions. Metabolic and hemodynamic alterations have been considered as the classical factors involved in the development of renal injury in patients with diabetes mellitus. However, the exact pathogenic mechanisms and the molecular events of diabetic nephropathy remain incompletely understood. Nowadays, there are convincing data that relate the diabetes inflammatory component with the development of renal disease. This review is focused on the inflammatory processes that develop diabetic nephropathy and on the new therapeutic approaches with anti-inflammatory effects for the treatment of chronic kidney disease in the setting of diabetic nephropathy. PMID:25785280

  20. Dobrin syndrome: A case report and review of the literature

    PubMed Central

    Al Qumaizi, K. I.; Halim, K.; Brekeit, K. A.

    2016-01-01

    Dobrin syndrome or tubulointerstitial nephritis and uveitis syndrome is a rare disease with excellent prognosis. We report a 60-year-old male of Indian origin who presented with acute interstitial nephritis (AIN) and unilateral anterior immune-mediated uveitis. The syndrome has been reported sporadically. This is only the third case from a patient of Indian origin. We highlight this case and evaluate the long-term use of nonsteroidal anti-inflammatory drug-induced AIN and uveitis as a potential causative factor. PMID:26937077

  1. Neural Circuitry Engaged by Prostaglandins during the Sickness Syndrome

    PubMed Central

    Saper, Clifford B.; Romanovsky, Andrej A.; Scammell, Thomas E.

    2013-01-01

    During illnesses caused by infectious disease or other sources of inflammation, a suite of brain-mediated responses called the sickness syndrome occurs, including fever, anorexia, sleepiness, hyperalgesia, and elevated corticosteroid secretion. Much of the sickness syndrome is mediated by prostaglandins acting on the brain, and can be prevented by non-steroidal anti-inflammatory drugs, such as aspirin or ibuprofen, that block prostaglandin synthesis. By examining which prostaglandins are produced at which sites and how they interact with the nervous system, researchers have identified specific neural circuits that underlie the sickness syndrome. PMID:22837039

  2. Sweet's syndrome associated with cellulitis - a challenging diagnosis*

    PubMed Central

    Resende, Cristina; Santos, Rui; Pereira, Teresa; Brito, Celeste

    2016-01-01

    Sweet's syndrome is a neutrophilic dermatosis with worldwide distribution that has been associated with inflammatory autoimmune diseases, infections, malignancies, drugs, and pregnancy. The disease is idiopathic in up to 50% of patients. A 64-year-old woman, diagnosed with right limb cellulitis (4 days of evolution), was seen at our department, due to persistent cellulitis and progressive appearance of painful nodules and plaques in both shins and the right forearm (2 days of evolution). Taken together, clinical, laboratory and pathological data suggested the diagnosis of Sweet's syndrome, probably secondary to cellulitis of the right inferior limb. We suggest that cellulitis may be associated with Sweet's syndrome, a rare association in the literature.

  3. Systemic Inflammation in Older Adults With Asthma-COPD Overlap Syndrome

    PubMed Central

    Fu, Juan-juan; McDonald, Vanessa M.; Gibson, Peter G.

    2014-01-01

    Purpose The role of systemic inflammation on asthma-COPD overlap syndrome is unknown. This study aimed to examine systemic inflammation in asthma-COPD overlap syndrome, and to identify associations between clinical characteristics and inflammatory mediators in asthma-COPD overlap syndrome. Methods In 108 adults older than 55 years comprising healthy controls (n=29), asthma (n=16), COPD (n=21) and asthma-COPD overlap syndrome (n=42), serum high sensitivity C-reactive protein and Interleukin 6 (IL-6) were assayed. Spirometry, induced sputum, quality of life, comorbidities and medications were assessed, and their associations with asthma-COPD overlap syndrome were analyzed using logistic regression. Associations between systemic inflammatory mediators and clinical characteristics were tested in multivariate linear regression models. Results Patients with asthma-COPD overlap syndrome had significantly elevated IL-6 levels compared with healthy controls and asthmatics. Age, comorbidity index and IL-6 level were independently associated with asthma-COPD overlap syndrome. FEV1% predicted was inversely associated with IL-6 level, and cardiovascular disease was associated with an increased IL-6 level. Systemic markers were not associated with airway inflammation. Conclusions Systemic inflammation is commonly present in asthma-COPD overlap syndrome, and asthma-COPD overlap syndrome resembled COPD in terms of systemic inflammation. IL-6 is a pivotal inflammatory mediator that may be involved in airflow obstruction and cardiovascular disease and may be an independent treatment target. PMID:24991455

  4. Sphingolipid metabolites in inflammatory disease

    PubMed Central

    Maceyka, Michael; Spiegel, Sarah

    2015-01-01

    Sphingolipids are ubiquitous building blocks of eukaryotic cell membranes. Progress in our understanding of sphingolipid metabolism, state-of-the-art sphingolipidomic approaches and animal models have generated a large body of evidence demonstrating that sphingolipid metabolites, particularly ceramide and sphingosine-1-phosphate, are signalling molecules that regulate a diverse range of cellular processes that are important in immunity, inflammation and inflammatory disorders. Recent insights into the molecular mechanisms of action of sphingolipid metabolites and new perspectives on their roles in regulating chronic inflammation have been reported. The knowledge gained in this emerging field will aid in the development of new therapeutic options for inflammatory disorders. PMID:24899305

  5. Biomarkers of Inflammatory Bowel Disease

    PubMed Central

    Fengming, Yi; Jianbing, Wu

    2014-01-01

    Inflammatory bowel disease (IBD) is a chronic disease mostly involved with intestine with unknown etiology. Diagnosis, evaluation of severity, and prognosis are still present as challenges for physicians. An ideal biomarker with the characters such as simple, easy to perform, noninvasive or microinvasive, cheap, rapid, and reproducible is helpful for patients and clinicians. Currently biomarkers applied in clinic include CRP, ESR, pANCA, ASCA, and fecal calprotectin. However, they are far from ideal. Lots of studies are focused on seeking for ideal biomarker for IBD. Herein, the paper reviewed recent researches on biomarkers of IBD to get advances of biomarkers in inflammatory bowel disease. PMID:24963213

  6. The Source for Syndromes.

    ERIC Educational Resources Information Center

    Richard, Gail J.; Hoge, Debra Reichert

    Designed for practicing speech-language pathologists, this book discusses different syndrome disabilities, pertinent speech-language characteristics, and goals and strategies to begin intervention efforts at a preschool level. Chapters address: (1) Angelman syndrome; (2) Asperger syndrome; (3) Down syndrome; (4) fetal alcohol syndrome; (5) fetal

  7. The Source for Syndromes.

    ERIC Educational Resources Information Center

    Richard, Gail J.; Hoge, Debra Reichert

    Designed for practicing speech-language pathologists, this book discusses different syndrome disabilities, pertinent speech-language characteristics, and goals and strategies to begin intervention efforts at a preschool level. Chapters address: (1) Angelman syndrome; (2) Asperger syndrome; (3) Down syndrome; (4) fetal alcohol syndrome; (5) fetal…

  8. Local inflammatory response induced by scorpionfish Scorpaena plumieri venom in mice.

    PubMed

    Menezes, Thiago N; Carnielli, Juliana B T; Gomes, Helena L; Pereira, Fausto E L; Lemos, Elenice M; Bissoli, Nazar S; Lopes-Ferreira, Mnica; Andrich, Filipe; Figueiredo, Suely G

    2012-07-01

    The Scorpaena plumieri fish venom induces a severe pain and edema, observed both clinically and experimentally. In order to understand more about the envenomation syndrome, the present study characterized experimentally the local acute inflammatory response induced by S. plumieri venom (SpV) in a mouse model of tissue injury. Our results demonstrated that the local inflammatory response provoked after 2h of SpV injection in footpad of mice is characterized by release of pivotal pro-inflammatory mediators (TNF, IL-6 and MCP-1). These mediators could be associated with histopathological changes observed into paw tissue, characterized by cellular infiltration, mainly neutrophils. Additionally, an investigation of edema formation pathways involved in inflammatory response was performed. SpV-induced edema was reduced significantly by previous administration of aprotinin or icatibant (HOE-140). However, the pre-treatment with diclofenac sodium and promethazine had less effect on this response. These results demonstrate that the kallikrein-kinin system (KKS) plays a major role in the edema formation. Despite the whole venom hydrolyzed the kallikrein synthetic substrate S-2302 (Pro-Phe-Arg-pNA), its main pro-inflammatory fraction was devoid of kininogenase activity. Our results demonstrate that SpV evokes a complex inflammatory reaction stimulating a secretion of TNF, IL-6, MCP-1 and leukocytes recruitment at the site of venom injection. In addition provide clear evidence of the involvement of the KKS in inflammatory response induced by S. plumieri venom. PMID:22453065

  9. Pro-/Anti-inflammatory Dysregulation in Patients With First Episode of Psychosis: Toward an Integrative Inflammatory Hypothesis of Schizophrenia

    PubMed Central

    García-Bueno, Borja; Bioque, Miquel; Mac-Dowell, Karina S.; Barcones, M. Fe; Leza, Juan C.

    2014-01-01

    Background: Schizophrenia is a chronic syndrome of unknown etiology, predominantly defined by signs of psychosis. The onset of the disorder occurs typically in late adolescence or early adulthood. Efforts to study pathophysiological mechanisms in early stages of the disease are crucial in order to prompt intervention. Methods: Case-control study of first-episode psychotic (FEP) patients and matched controls. We recruited 117 patients during the first year after their FEP according to the DSM-IV criteria and recruited 106 gender-, race-, and age-matched controls between September 2010 and June 2011. Results: Biochemical studies carried out in peripheral mononuclear blood cells (PMBC) and plasma evidence a significant increase in intracellular components of a main proinflammatory pathway, along with a significant decrease in the anti-inflammatory ones. Multivariate logistic regression analyses identified the expression of inducible isoforms of nitric oxide synthase and cyclooxygenase in PMBC and homocysteine plasma levels as the most reliable potential risk factors and the inhibitor of the inflammatory transcription factor NFκB, IκBα, and the anti-inflammatory prostaglandin 15d-PGJ2 as potential protection factors. Discussion: Taken as a whole, the results of this study indicate robust phenotypical differences at the cellular machinery level in PMBC of patients with FEP. Although more scientific evidence is needed, the determination of multiple components of pro- and anti-inflammatory cellular pathways including the activity of nuclear receptors has interesting potential as biological markers and potential risk/protective factors for FEP. Due to its soluble nature, a notable finding in this study is that the anti-inflammatory mediator 15d-PGJ2 might be used as plasmatic biomarker for first episodes of psychosis. PMID:23486748

  10. Olmsted syndrome: exploration of the immunological phenotype

    PubMed Central

    2013-01-01

    Background Olmsted syndrome is a rare congenital skin disorder presenting with periorifical hyperkeratotic lesions and mutilating palmoplantar keratoderma, which is often associated with infections of the keratotic area. A recent study identified de novo mutations causing constitutive activation of TRPV3 as a cause of the keratotic manifestations of Olmsted syndrome. Methods Genetic, clinical and immunological profiling was performed on a case study patient with the clinical diagnosis of Olmsted syndrome. Results The patient was found to harbour a previously undescribed 1718G-C transversion in TRPV3, causing a G573A point mutation. In depth clinical and immunological analysis found multiple indicators of immune dysregulation, including frequent dermal infections, inflammatory infiltrate in the affected skin, hyper IgE production and elevated follicular T cells and eosinophils in the peripheral blood. Conclusions These results provide the first comprehensive assessment of the immunological features of Olmsted syndrome. The systemic phenotype of hyper IgE and persistent eosinophilia suggest a primary or secondary role of immunological processes in the pathogenesis of Olmsted syndrome, and have important clinical consequences with regard to the treatment of Olmsted syndrome patients. PMID:23692804

  11. Exacerbation of chronic inflammatory diseases by infectious agents: Fact or fiction?

    PubMed Central

    Wang, Cheng-Ming; Kaltenboeck, Bernhard

    2010-01-01

    Chronic inflammatory diseases caused by obesity represent critical public health concerns worldwide. In these diseases such as metabolic syndrome, diabetes and atherosclerosis, adipose tissue acts as an endocrine organ that releases large quantities of inflammatory mediators into circulation. Besides classically recognized effectors on the development of obesity and resultant conditions, infection has attracted attention as an enhancer of chronic inflammatory diseases. Infectious diseases have long been associated with obesity, metabolic syndrome, diabetes and atherosclerosis. However, the infectious hypothesis for chronic inflammatory diseases has been challenged by inconclusive clinical trials. Nevertheless, the large body of evidence accumulated over decades on the association of infectious diseases with obesity, diabetes and cardiovascular disease should not be disregarded. Instead, re-formulation of hypotheses of the mechanisms by which microbes affect obesity-associated diseases may be required with an emphasis on the early events in the progression of such diseases and the multifactorial nature of pathogen-host interactions. This review focuses on pathogens that directly promote obesity and on pathogens that cause chronic infections and thereby enhance metabolic diseases in obese patients. A new perspective on the interaction between infections and obesity-related diseases may improve management of chronic inflammatory diseases that rank high among global threats to human health. PMID:21537425

  12. Azathioprine hypersensitivity syndrome: a case report.

    PubMed

    Fenaux, S; Tintillier, M; Cuvelier, Ch; Migali, G; Pochet, J M

    2013-01-01

    We report here the case of a 51-year-old man presenting to the Emergency Department with a febrile cutaneous eruption with diffuse arthralgia 10 days after the onset of azathioprine therapy. The clinical examination did not reveal any inflammatory syndrome and the results of all bacteriological tests were negative. A skin biopsy was performed, which revealed a granulocytary pustula with superficial dermal oedema and a neutrophil infiltration without sign of vasculitis. A side effect of azathioprine was suspected, and treatment was discontinued. Fortunately, the patient recovered within a few days. Azathioprine hypersensitivity syndrome is a rare side effect of azathioprine. Hypersensitivity syndrome is an idiosyncratic, non-IgE-mediated reaction that appears to be unrelated to thiopurine methyltransferase levels. Diagnosis is mainly clinical and requires an exclusion of other processes. The only treatment option available is to stop azathioprine intake. PMID:24156226

  13. Paraneoplastic syndromes

    SciTech Connect

    Weller, R.E.

    1994-03-01

    Paraneoplastic syndromes (PNS) comprise a diverse group of disorders that are associated with cancer but unrelated to the size, location, metastases, or physiologic activities of the mature tissue of origin. They are remote effects of tumors that may appear as signs, symptoms, or syndromes which can mimic other disease conditions encountered in veterinary medicine. Recognition of PNS is valuable for several reasons: the observed abnormalities may represent tumor cell markers and facilitate early diagnosis of the tumor; they may allow assessment of premalignant states; they may aid in the search metastases; they may help quantify and monitor response to therapy; and, they may provide insight into the study of malignant transformation and oncogene expression. This review will concentrate on the pathophysiology, diagnosis, and treatment of some of the common PNS encountered in veterinary medicine.

  14. Cushing's syndrome.

    PubMed

    Lacroix, Andr; Feelders, Richard A; Stratakis, Constantine A; Nieman, Lynnette K

    2015-08-29

    Chronic exposure to excess glucorticoids results in diverse manifestations of Cushing's syndrome, including debilitating morbidities and increased mortality. Genetic and molecular mechanisms responsible for excess cortisol secretion by primary adrenal lesions and adrenocorticotropic hormone (ACTH) secretion from corticotroph or ectopic tumours have been identified. New biochemical and imaging diagnostic approaches and progress in surgical and radiotherapy techniques have improved the management of patients. The therapeutic goal is to normalise tissue exposure to cortisol to reverse increased morbidity and mortality. Optimum treatment consisting of selective and complete resection of the causative tumour is necessay to allow eventual normalisation of the hypothalamic-pituitary-adrenal axis, maintenance of pituitary function, and avoidance of tumour recurrence. The development of new drugs offers clinicians several choices to treat patients with residual cortisol excess. However, for patients affected by this challenging syndrome, the long-term effects and comorbidities associated with hypercortisolism need ongoing care. PMID:26004339

  15. Overtraining Syndrome

    PubMed Central

    Kreher, Jeffrey B.; Schwartz, Jennifer B.

    2012-01-01

    Context: Fatigue and underperformance are common in athletes. Understanding overtraining syndrome (OTS) is helpful in the evaluation, management, and education of athletes. Evidence Acquisition: Relevant articles in English were searched with OVID (1948-2011) and PubMed using the following keywords: overtraining syndrome, overtraining, overreaching, unexplained underperformance, staleness, pathophysiology, management, treatment, evaluation. Bibliographies were reviewed for additional resources. Results: OTS appears to be a maladapted response to excessive exercise without adequate rest, resulting in perturbations of multiple body systems (neurologic, endocrinologic, immunologic) coupled with mood changes. Many hypotheses of OTS pathogenesis are reviewed, and a clinical approach to athletes with possible OTS (including history, testing, and prevention) is presented. Conclusions: OTS remains a clinical diagnosis with arbitrary definitions per the European College of Sports Science’s position statement. History and, in most situations, limited serologies are helpful. However, much remains to be learned given that most past research has been on athletes with overreaching rather than OTS. PMID:23016079

  16. Kartagener syndrome.

    PubMed

    Skeik, Nedaa; Jabr, Fadi I

    2011-01-01

    Kartagener syndrome is a rare, ciliopathic, autosomal recessive genetic disorder that causes a defect in the action of the cilia lining the respiratory tract and fallopian tube. Patients usually present with chronic recurrent rhinosinusitis, otitis media, pneumonia, and bronchiectasis caused by pseudomonal infection. Situs inversus can be seen in about 50% of cases. Diagnosis can be made by tests to prove impaired cilia function, biopsy, and genetic studies. Treatment is supportive. In severe cases, the prognosis can be fatal if bilateral lung transplantation is delayed. We present a case of a 66-year-old woman with chronic recurrent upper respiratory infections, pseudomonal pneumonia, and chronic bronchiectasis who presented with acute respiratory failure. She was diagnosed with Kartagener syndrome based on her clinical presentation and genetic studies. She expired on ventilator with refractory respiratory and multiorgan failure. PMID:21403791

  17. [Hepatorenal syndrome].

    PubMed

    Pillebout, Evangline

    2014-02-01

    Hepatorenal syndrome is a severe complication of end-stage liver disease. The pathophysiological hallmark is severe renal vasoconstriction, resulting from peripheral and splanchnic vasodilation as well as activation of renal vasoconstrictor molecules, which induce the effective arterial volume reduction and the functional renal failure. The diagnosis of hepatorenal syndrome is currently based on the exclusion of other causes of renal failure (especially prerenal). Spontaneous bacterial peritonitis is one of the triggering factors and should be sought in all patients with severe liver disease and acute renal failure. Quickly treating patients with parental antibiotics and albumin infusion significantly decreases the risk. The combined use of intravenous albumin, splanchnic and peripheral vasoconstrictor and/or renal replacement therapy sometimes enables a delay until liver transplantation (or combined liver-kidney in selected patients). Transplantation is in fact the only way to improve the long-term prognosis. PMID:24388293

  18. Metabolic syndrome.

    PubMed

    Denke, Margo A

    2002-11-01

    The metabolic syndrome is like an elephant, and any literary review of its importance is shamefully reduced to an examination of tusks, trunk, and tail. Evidence continues to mount that this diminutive approach is an incorrect management strategy for such a large problem. Diet and lifestyle are effective strategies, but they must effectively compete with behaviors that have instant gratification. Our society has turned its focus away from the long-term rewards of good sustainable behaviors and has instead focused on short-term rewards of unsustainable behaviors. To tame the behaviors that promote the metabolic syndrome, simple answers from diet and drug therapy will require support from society to be effective. PMID:12361491

  19. Bruck syndrome.

    PubMed

    Datta, Vikram; Sinha, Aditi; Saili, Arvind; Nangia, Sushma

    2005-05-01

    The combination of arthrogryposis multiplex congenita and osteogenesis imperfecta is extremely rare. This combination is named Bruck syndrome. A 34 week male baby weighing 1.7 kg at birth was noted to have multiple flexion contractures and pterygia at elbows, wrists and knees, in addition to right foot talipes equinovarus deformity. Postnatally the child developed multiple swellings involving both the upper and lower limbs. A plain radiograph revealed the presence of fractures involving the long bones of the upper and lower limbs. A diagnosis of osteogenesis imperfecta with arthrogryposis multiplex congenita was made, and the patient was labeled as a case of Bruck Syndrome. The aim of this report is to make the readers aware regarding this rare entity and to specifically look for presence of features suggestive of osteogenesis imperfecta when encountered with a neonate born with arthrogryposis multiplex congenita. PMID:15973030

  20. [Fibromyalgia syndrome].

    PubMed

    Naranjo Hernndez, A; Rodrguez Lozano, C; Ojeda Bruno, S

    1992-02-01

    The Fibromialgia Syndrome (FS) is a common clinical entity which may produce symtoms and signs related to multiple fields of Medicine. Typical clinical characteristics of FS include extensive pain, presence of sensitive points during exploration, morning stiffness, asthenia and non-refresing sleep. Frequently, associated rheumatologic diseases are observed, as rheumatoid arthritis, osteoarthrosis and vertebral disorders. In FS, complementary tests are usually normal. The most widely accepted hypothesis suggests that this is a disorder affecting modulation of pain sensitivity. PMID:1576317

  1. Lemierre's syndrome and genetic polymorphisms: a case report

    PubMed Central

    Constantin, Jean-Michel; Mira, Jean-Paul; Guerin, Renaud; Cayot-Constantin, Sophie; Lesens, Olivier; Gourdon, Florence; Romaszko, Jean-Pierre; Linval, Philippe; Laurichesse, Henri; Bazin, Jean-Etienne

    2006-01-01

    Background Lemierre's syndrome presents a classic clinical picture, the pathophysiology of which remains obscure. Attempts have been made to trace genetic predispositions that modify the host detection of pathogen or the resultant systemic reaction. Case presentation A 17-year old female, with no previous medical history, was admitted to the intensive care unit for septic shock, acute respiratory distress syndrome and Lemierre's syndrome. Her DNA was assayed for single nucleotide polymorphisms previously incriminated in the detection of the pathogen, the inflammatory response and the coagulation cascade. We observed functional variations in her Toll like 5 receptor (TLR 5) gene and two coagulation variations (Tissue Factor (TF) 603 and Plasminogen-Activator-Inhibitor-1 (PAI-1) 4G-4G homozygosity) associated with thrombotic events. Conclusion The innate immune response and the prothrombogenic mutations could explain, at least in part, the symptoms of Lemierre's syndrome. Genomic study of several patients with Lemierre's syndrome may reveal its pathophysiology. PMID:16846490

  2. Fluency Disorders in Genetic Syndromes

    ERIC Educational Resources Information Center

    Van Borsel, John; Tetnowski, John A.

    2007-01-01

    The characteristics of various genetic syndromes have included "stuttering" as a primary symptom associated with that syndrome. Specifically, Down syndrome, fragile X syndrome, Prader-Willi syndrome, Tourette syndrome, Neurofibromatosis type I, and Turner syndrome all list "stuttering" as a characteristic of that syndrome. An extensive review of…

  3. Fluency Disorders in Genetic Syndromes

    ERIC Educational Resources Information Center

    Van Borsel, John; Tetnowski, John A.

    2007-01-01

    The characteristics of various genetic syndromes have included "stuttering" as a primary symptom associated with that syndrome. Specifically, Down syndrome, fragile X syndrome, Prader-Willi syndrome, Tourette syndrome, Neurofibromatosis type I, and Turner syndrome all list "stuttering" as a characteristic of that syndrome. An extensive review of

  4. Cathelicidin impact on inflammatory cells.

    PubMed

    Agier, Justyna; Efenberger, Magdalena; Brzezińska-Błaszczyk, Ewa

    2015-01-01

    Cathelicidins, like other antimicrobial peptides, exhibit direct antimicrobial activities against a broad spectrum of microbes, including both Gram-positive and Gram-negative bacteria, enveloped viruses, and fungi. These host-derived peptides kill the invaded pathogens by perturbing their cell membranes and can neutralize biological activities of endotoxin. Nowadays, more and more data indicate that these peptides, in addition to their antimicrobial properties, possess various immunomodulatory activities. Cathelicidins have the potential to influence and modulate, both directly and indirectly, the activity of various cell populations involved in inflammatory processes and in host defense against invading pathogens. They induce migration of neutrophils, monocytes/macrophages, eosinophils, and mast cells and prolong the lifespan of neutrophils. These peptides directly activate inflammatory cells to production and release of different pro-inflammatory and immunoregulatory mediators, cytokines, and chemokines, however cathelicidins might mediate the generation of anti-inflammatory cytokines as well. Cathelicidins also modulate epithelial cell/keratinocyte responses to infecting pathogens. What is more, they affect activity of monocytes, dendritic cells, keratinocytes, or epithelial cells acting in synergy with cytokines or β-defensins. In addition, these peptides indirectly balance TLR-mediated responses of monocytes, macrophages, dendritic cells, epithelial cells, and keratinocytes. This review discusses the role and significance of cathelicidins in inflammation and innate immunity against pathogens. PMID:26557038

  5. Inflammatory response in islet transplantation.

    PubMed

    Kanak, Mazhar A; Takita, Morihito; Kunnathodi, Faisal; Lawrence, Michael C; Levy, Marlon F; Naziruddin, Bashoo

    2014-01-01

    Islet cell transplantation is a promising beta cell replacement therapy for patients with brittle type 1 diabetes as well as refractory chronic pancreatitis. Despite the vast advancements made in this field, challenges still remain in achieving high frequency and long-term successful transplant outcomes. Here we review recent advances in understanding the role of inflammation in islet transplantation and development of strategies to prevent damage to islets from inflammation. The inflammatory response associated with islets has been recognized as the primary cause of early damage to islets and graft loss after transplantation. Details on cell signaling pathways in islets triggered by cytokines and harmful inflammatory events during pancreas procurement, pancreas preservation, islet isolation, and islet infusion are presented. Robust control of pre- and peritransplant islet inflammation could improve posttransplant islet survival and in turn enhance the benefits of islet cell transplantation for patients who are insulin dependent. We discuss several potent anti-inflammatory strategies that show promise for improving islet engraftment. Further understanding of molecular mechanisms involved in the inflammatory response will provide the basis for developing potent therapeutic strategies for enhancing the quality and success of islet transplantation. PMID:24883060

  6. Chlamydophila abortus Pelvic Inflammatory Disease

    PubMed Central

    Meusburger, Herwig; Hotzel, Helmut; Oehme, Albrecht; Neunteufel, Walter; Dierich, Manfred P.; Wrzner, Reinhard

    2003-01-01

    We report the first documented case of an extragestational infection with Chlamydophila abortus in humans. The pathogen was identified in a patient with severe pelvic inflammatory disease (PID) by sequence analysis of the ompA gene. Our findings raise the possibility that Chlamydiaceae other than Chlamydia trachomatis are involved in PID. PMID:14720414

  7. Cathelicidin impact on inflammatory cells

    PubMed Central

    Efenberger, Magdalena; Brzezińska-Błaszczyk, Ewa

    2015-01-01

    Cathelicidins, like other antimicrobial peptides, exhibit direct antimicrobial activities against a broad spectrum of microbes, including both Gram-positive and Gram-negative bacteria, enveloped viruses, and fungi. These host-derived peptides kill the invaded pathogens by perturbing their cell membranes and can neutralize biological activities of endotoxin. Nowadays, more and more data indicate that these peptides, in addition to their antimicrobial properties, possess various immunomodulatory activities. Cathelicidins have the potential to influence and modulate, both directly and indirectly, the activity of various cell populations involved in inflammatory processes and in host defense against invading pathogens. They induce migration of neutrophils, monocytes/macrophages, eosinophils, and mast cells and prolong the lifespan of neutrophils. These peptides directly activate inflammatory cells to production and release of different pro-inflammatory and immunoregulatory mediators, cytokines, and chemokines, however cathelicidins might mediate the generation of anti-inflammatory cytokines as well. Cathelicidins also modulate epithelial cell/keratinocyte responses to infecting pathogens. What is more, they affect activity of monocytes, dendritic cells, keratinocytes, or epithelial cells acting in synergy with cytokines or β-defensins. In addition, these peptides indirectly balance TLR-mediated responses of monocytes, macrophages, dendritic cells, epithelial cells, and keratinocytes. This review discusses the role and significance of cathelicidins in inflammation and innate immunity against pathogens. PMID:26557038

  8. Preclinical Assessment of Inflammatory Pain.

    PubMed

    Muley, Milind M; Krustev, Eugene; McDougall, Jason J

    2016-02-01

    While acute inflammation is a natural physiological response to tissue injury or infection, chronic inflammation is maladaptive and engenders a considerable amount of adverse pain. The chemical mediators responsible for tissue inflammation act on nociceptive nerve endings to lower neuronal excitation threshold and sensitize afferent firing rate leading to the development of allodynia and hyperalgesia, respectively. Animal models have aided in our understanding of the pathophysiological mechanisms responsible for the generation of chronic inflammatory pain and allowed us to identify and validate numerous analgesic drug candidates. Here we review some of the commonly used models of skin, joint, and gut inflammatory pain along with their relative benefits and limitations. In addition, we describe and discuss several behavioral and electrophysiological approaches used to assess the inflammatory pain in these preclinical models. Despite significant advances having been made in this area, a gap still exists between fundamental research and the implementation of these findings into a clinical setting. As such we need to characterize inherent pathophysiological pathways and develop new endpoints in these animal models to improve their predictive value of human inflammatory diseases in order to design safer and more effective analgesics. PMID:26663896

  9. Inflammatory process in Alzheimer's Disease

    PubMed Central

    Meraz-Ros, Marco A.; Toral-Rios, Danira; Franco-Bocanegra, Diana; Villeda-Hernndez, Juana; Campos-Pea, Victoria

    2013-01-01

    Alzheimer Disease (AD) is a neurodegenerative disorder and the most common form of dementia. Histopathologically is characterized by the presence of two major hallmarks, the intracellular neurofibrillary tangles (NFTs) and extracellular neuritic plaques (NPs) surrounded by activated astrocytes and microglia. NFTs consist of paired helical filaments of truncated tau protein that is abnormally hyperphosphorylated. The main component in the NP is the amyloid-? peptide (A?), a small fragment of 4042 amino acids with a molecular weight of 4 kD. It has been proposed that the amyloid aggregates and microglia activation are able to favor the neurodegenerative process observed in AD patients. However, the role of inflammation in AD is controversial, because in early stages the inflammation could have a beneficial role in the pathology, since it has been thought that the microglia and astrocytes activated could be involved in A? clearance. Nevertheless the chronic activation of the microglia has been related with an increase of A? and possibly with tau phosphorylation. Studies in AD brains have shown an upregulation of complement molecules, pro-inflammatory cytokines, acute phase reactants and other inflammatory mediators that could contribute with the neurodegenerative process. Clinical trials and animal models with non-steroidal anti-inflammatory drugs (NSAIDs) indicate that these drugs may decrease the risk of developing AD and apparently reduce A? deposition. Finally, further studies are needed to determine whether treatment with anti-inflammatory strategies, may decrease the neurodegenerative process that affects these patients. PMID:23964211

  10. Inflammatory Response in Islet Transplantation

    PubMed Central

    Kanak, Mazhar A.; Kunnathodi, Faisal; Lawrence, Michael C.; Levy, Marlon F.

    2014-01-01

    Islet cell transplantation is a promising beta cell replacement therapy for patients with brittle type 1 diabetes as well as refractory chronic pancreatitis. Despite the vast advancements made in this field, challenges still remain in achieving high frequency and long-term successful transplant outcomes. Here we review recent advances in understanding the role of inflammation in islet transplantation and development of strategies to prevent damage to islets from inflammation. The inflammatory response associated with islets has been recognized as the primary cause of early damage to islets and graft loss after transplantation. Details on cell signaling pathways in islets triggered by cytokines and harmful inflammatory events during pancreas procurement, pancreas preservation, islet isolation, and islet infusion are presented. Robust control of pre- and peritransplant islet inflammation could improve posttransplant islet survival and in turn enhance the benefits of islet cell transplantation for patients who are insulin dependent. We discuss several potent anti-inflammatory strategies that show promise for improving islet engraftment. Further understanding of molecular mechanisms involved in the inflammatory response will provide the basis for developing potent therapeutic strategies for enhancing the quality and success of islet transplantation. PMID:24883060

  11. Surgery for inflammatory bowel disease

    PubMed Central

    Hwang, John M; Varma, Madhulika G

    2008-01-01

    Despite the new and ever expanding array of medications for the treatment of inflammatory bowel disease (IBD), there are still clear indications for operative management of IBD and its complications. We present an overview of indications, procedures, considerations, and controversies in the surgical therapy of IBD. PMID:18461653

  12. Acrodysostosis syndromes.

    PubMed

    Silve, C; Le-Stunff, C; Motte, E; Gunes, Y; Linglart, A; Clauser, E

    2012-01-01

    Acrodysostosis (ADO) refers to a heterogeneous group of rare skeletal dysplasia that share characteristic features including severe brachydactyly, facial dysostosis and nasal hypoplasia. The literature describing acrodysostosis cases has been confusing because some reported patients may have had other phenotypically related diseases presenting with Albright Hereditary Osteodystrophy (AHO) such as pseudohypoparathyroidism type 1a (PHP1a) or pseudopseudohypoparathyroidism (PPHP). A question has been whether patients display or not abnormal mineral metabolism associated with resistance to PTH and/or resistance to other hormones that bind G-protein coupled receptors (GPCR) linked to Gsα, as observed in PHP1a. The recent identification in patients affected with acrodysostosis of defects in two genes, PRKAR1A and PDE4D, both important players in the GPCR-Gsα-cAMP-PKA signaling, has helped clarify some issues regarding the heterogeneity of acrodysostosis, in particular the presence of hormonal resistance. Two different genetic and phenotypic syndromes are now identified, both with a similar bone dysplasia: ADOHR, due to PRKAR1A defects, and ADOP4 (our denomination), due to PDE4D defects. The existence of GPCR-hormone resistance is typical of the ADOHR syndrome. We review here the PRKAR1A and PDE4D gene defects and phenotypes identified in acrodysostosis syndromes, and discuss them in view of phenotypically related diseases caused by defects in the same signaling pathway. PMID:24363928

  13. Acrodysostosis syndromes

    PubMed Central

    Silve, C; Le-Stunff, C; Motte, E; Gunes, Y; Linglart, A; Clauser, E

    2012-01-01

    Acrodysostosis (ADO) refers to a heterogeneous group of rare skeletal dysplasia that share characteristic features including severe brachydactyly, facial dysostosis and nasal hypoplasia. The literature describing acrodysostosis cases has been confusing because some reported patients may have had other phenotypically related diseases presenting with Albright Hereditary Osteodystrophy (AHO) such as pseudohypoparathyroidism type 1a (PHP1a) or pseudopseudohypoparathyroidism (PPHP). A question has been whether patients display or not abnormal mineral metabolism associated with resistance to PTH and/or resistance to other hormones that bind G-protein coupled receptors (GPCR) linked to Gsα, as observed in PHP1a. The recent identification in patients affected with acrodysostosis of defects in two genes, PRKAR1A and PDE4D, both important players in the GPCR–Gsα–cAMP–PKA signaling, has helped clarify some issues regarding the heterogeneity of acrodysostosis, in particular the presence of hormonal resistance. Two different genetic and phenotypic syndromes are now identified, both with a similar bone dysplasia: ADOHR, due to PRKAR1A defects, and ADOP4 (our denomination), due to PDE4D defects. The existence of GPCR-hormone resistance is typical of the ADOHR syndrome. We review here the PRKAR1A and PDE4D gene defects and phenotypes identified in acrodysostosis syndromes, and discuss them in view of phenotypically related diseases caused by defects in the same signaling pathway. PMID:24363928

  14. CUSHING'S SYNDROME

    PubMed Central

    Wilkinson, Allan B.

    1961-01-01

    Sixteen cases of verified Cushing's syndrome, and twelve cases of probable Cushing's syndrome were reviewed and data on them were compared with various reports on Cushing's syndrome in the literature. The diagnosis hinges upon a high index of suspicion, and one or several of the major criteria may be lacking. Ultimate establishment of correct diagnosis should be based largely on the clinical features, although stimulation and suppression tests may help to confirm a clinical diagnosis. In well-established clinical cases, with borderline laboratory confirmation, exploration may be justified, especially if tests fail to identify a specific cause. In cases of adrenal cortical tumor, all pathological tissue should be removed if possible, with great care to support and stimulate the remaining atrophic adrenal gland during and following operation. In cases of bilateral adrenal cortical hyperplasia, the problem is one of how much to remove. At present most investigators advocate radical subtotal resection, leaving less than 10 per cent of one side. ImagesFigure 1.Figure 2.Figure 3.Figure 4.Figure 5.Figure 6. PMID:13785315

  15. Hepatorenal syndrome.

    PubMed

    Lata, Jan

    2012-09-28

    Hepatorenal syndrome (HRS) is defined as a functional renal failure in patients with liver disease with portal hypertension and it constitutes the climax of systemic circulatory changes associated with portal hypertension. This term refers to a precisely specified syndrome featuring in particular morphologically intact kidneys, where regulatory mechanisms have minimised glomerular filtration and maximised tubular resorption and urine concentration, which ultimately results in uraemia. The syndrome occurs almost exclusively in patients with ascites. Type 1 HRS develops as a consequence of a severe reduction of effective circulating volume due to both an extreme splanchnic arterial vasodilatation and a reduction of cardiac output. Type 2 HRS is characterised by a stable or slowly progressive renal failure so that its main clinical consequence is not acute renal failure, but refractory ascites, and its impact on prognosis is less negative. Liver transplantation is the most appropriate therapeutic method, nevertheless, only a few patients can receive it. The most suitable "bridge treatments" or treatment for patients ineligible for a liver transplant include terlipressin plus albumin. Terlipressin is at an initial dose of 0.5-1 mg every 4 h by intravenous bolus to 3 mg every 4 h in cases when there is no response. Renal function recovery can be achieved in less than 50% of patients and a considerable decrease in renal function may reoccur even in patients who have been responding to therapy over the short term. Transjugular intrahepatic portosystemic shunt plays only a marginal role in the treatment of HRS. PMID:23049205

  16. Brugada Syndrome

    PubMed Central

    ANTZELEVITCH, CHARLES

    2007-01-01

    First introduced as a new clinical entity in 1992, the Brugada syndrome is associated with a relatively high risk of sudden death in young adults, and occasionally in children and infants. Recent years have witnessed a striking proliferation of papers dealing with the clinical and basic aspects of the disease. Characterized by a coved-type ST-segment elevation in the right precordial leads of the electrocardiogram (ECG), the Brugada syndrome has a genetic basis that thus far has been linked only to mutations in SCN5A, the gene that encodes the ?-subunit of the sodium channel. The Brugada ECG is often concealed, but can be unmasked or modulated by a number of drugs and pathophysiological states including sodium channel blockers, a febrile state, vagotonic agents, tricyclic antidepressants, as well as cocaine and propranolol intoxication. Average age at the time of initial diagnosis or sudden death is 40 22, with the youngest patient diagnosed at 2 days of age and the oldest at 84 years. This review provides an overview of the clinical, genetic, molecular, and cellular aspects of the Brugada syndrome, incorporating the results of two recent consensus conferences. Controversies with regard to risk stratification and newly proposed pharmacologic strategies are discussed. PMID:17038146

  17. [Crush syndrome].

    PubMed

    Scapellato, S; Maria, S; Castorina, G; Sciuto, G

    2007-08-01

    Crush injuries and crush syndrome are common after natural (e.g. earthquake, land-slide, tornadoes, tsunami) or man-made catastrophes (e.g. wars, terrorist attacks), in fact the history of this disease is well reported both in earthquake rescue reviews and in military literature. However, there are instances due to conventional causes, such as building collapses, road traffic accident, accident at work or altered level of consciousness after stroke or drug overdose. These situations of ''big or small'' catastrophes can occur at any time and anywhere, for this reason every clinician should be prepared to address issues of crush syndrome quickly and aggressively. The treatment has to manage and to predict clinical conditions before they present themselves. In particular, acute renal failure is one of the few life-threatening complications that can be reversed. This article reviews the various evidences and summarizes the treatment strategies available. Fundamental targets in crush syndrome management are early aggressive hydration, urine alkalinization and, when possible, forced diuresis. Since electrolyte imbalance may be fatal due to arrhythmias secondary to hyperkalemia (especially associated with hypocalcemia), it's necessary to correct these abnormalities using insulin-glucose solution and/or potassium binders, and if nevertheless serum potassium levels remain high this serious disease will necessitate dialysis, which is often a vital procedure. PMID:17641588

  18. [Evaluation of anti-inflammatory activity of extracts from Siberian plants].

    PubMed

    Nesterova, Iu V; Povet'eva, T N; Aksinenko, S G; Suslov, N I; Ga?damovich, N N; Nagorniak, Iu G; Popova, E V; Kravtsova, S S; Andreeva, T I

    2009-01-01

    Experimental investigations have shown that water-alcohol extracts from plants containing alkaloids (Aconitum baikalense, Aconitum septentrionale, Delphinium elatum L., Conium maculatum) and salicylic acid (Filipendula ulmaria, Salix viminalis, Fragaria vesca, Rubus idaeus) inhibited the development of main symptoms of inflammation, viz. exudation, pain, fever, to the same extent as non-steroidal anti-inflammatory agents. The substances studied in this work may be used to develop new efficient pharmacological preparations for the treatment of different inflammatory conditions associated with severe pain syndrome. PMID:20017405

  19. Acidic Mammalian Chitinase and the Eye: Implications for Ocular Inflammatory Diseases

    PubMed Central

    Bucolo, Claudio; Musumeci, Maria; Musumeci, Salvatore; Drago, Filippo

    2011-01-01

    Chitinases have an important role in the defense of organisms against chitin-containing parasites. An acidic mammalian chitinase (AMCase) has been detected in epithelial cells in lung tissue samples taken from patients with asthma as well as in conjunctival epithelium of patients with inflammatory ocular diseases. Particularly, elevated AMCase activity has been observed in ocular tissues of patients with vernal keratoconjunctivitis, seasonal allergic conjunctivitis, and in patients affected by dry eye syndrome. This enzyme is induced via a TH2-specific, IL-13-dependent pathway. AMCase may thus be a key mediator of IL-13-induced responses in TH2-driven inflammatory ocular diseases. PMID:21811466

  20. Kearns-Sayre Syndrome

    MedlinePLUS

    ... Awards Enhancing Diversity Find People About NINDS NINDS Kearns-Sayre Syndrome Information Page Table of Contents (click to ... is being done? Clinical Trials Organizations What is Kearns-Sayre Syndrome? Kearns-Sayre syndrome (KSS) is a rare ...