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1

[Hemolytic anemias due to enzymopathies].  

PubMed

The most inherited enzymopathies associated with hemolytic anaemias are due to enzyme deficiencies (as a consequence of either synthesis reduction or impairement of the enzyme function). Such deficiencies can disturb some metabolism of the red cells. The most of enzyme deficiencies are involved in glycolysis that represents the main source of energy for this cell. Generally the genetic transmission of these enzymopathies is recessive autosomal with the exception of two cases (glucose 6-phosphate dehydrogenase and phosphoglycerate kinase) which are X-chromosome-linked. It stands to reason that the only treatment of these enzymopathies is dependent on gene therapy, a fine future method. Nevertheless prenatal diagnosis can be considered in some cases that display particularly severe symptoms. PMID:8235390

Rosa, R

1993-06-01

2

Hemolytic Anemia  

MedlinePLUS

... from the NHLBI on Twitter. What Is Hemolytic Anemia? Hemolytic anemia (HEE-moh-lit-ick uh-NEE-me-uh) ... blood cells to replace them. However, in hemolytic anemia, the bone marrow can't make red blood ...

3

Hemolytic anemia  

MedlinePLUS

Anemia - hemolytic ... Hemolytic anemia occurs when the bone marrow is unable to replace the red blood cells that are being destroyed. Immune hemolytic anemia occurs when the immune system mistakenly sees your ...

4

Coomb's Positive Hemolytic Anemia Due To Insect Bite  

PubMed Central

Hemolytic anemia has occasionally been described in association with insect bites. The venom of certain spiders, bees and wasps, and some snakes can rarely cause intravascular hemolysis. We report here a case of Coombs positive hemolytic anemia due to an insect bite. These bites often pose diagnostic challenges and when associated with systemic manifestations necessitate early intervention. This communication reviews the clinico- hematologic spectrum in these cases and also emphasizes the need to capture the insect as identification would help in early diagnosis and management. PMID:22400097

2007-01-01

5

Types of Hemolytic Anemia  

MedlinePLUS

... from the NHLBI on Twitter. Types of Hemolytic Anemia There are many types of hemolytic anemia. The ... the condition, but you develop it. Inherited Hemolytic Anemias With inherited hemolytic anemias, one or more of ...

6

HEMOLYTIC ANEMIA Erythrocytes premature  

E-print Network

LABORATORY FINDINGS · M:E ratio decreased · Increased Reticulocytes · Nucleated RBC in peripheral blood, Venous Thrombosis, Infection, and Bone Marrow Hyperplasia · Ham Test #12;9/16/2013 6 HEMOLYTIC ANEMIA · Normocytic, Normochromic Anemia · Jaundice · Gallstones · Transfusions, Splenectomy #12;9/16/2013 7 IMMUNE

7

Drug-induced immune hemolytic anemia  

MedlinePLUS

Immune hemolytic anemia secondary to drugs; Anemia - immune hemolytic - secondary to drugs ... Drugs that can cause this type of hemolytic anemia include: Cephalosporins (a class of antibiotics) -- most common ...

8

Treatment of autoimmune hemolytic anemias.  

PubMed

Autoimmune hemolytic anemia (AIHA) is a relatively uncommon disorder caused by autoantibodies directed against self red blood cells. It can be idiopathic or secondary, and classified as warm, cold (cold hemagglutinin disease (CAD) and paroxysmal cold hemoglobinuria) or mixed, according to the thermal range of the autoantibody. AIHA may develop gradually, or have a fulminant onset with life-threatening anemia. The treatment of AIHA is still not evidence-based. The first-line therapy for warm AIHA are corticosteroids, which are effective in 70-85% of patients and should be slowly tapered over a time period of 6-12 months. For refractory/relapsed cases, the current sequence of second-line therapy is splenectomy (effective approx. in 2 out of 3 cases but with a presumed cure rate of up to 20%), rituximab (effective in approx. 80-90% of cases), and thereafter any of the immunosuppressive drugs (azathioprine, cyclophosphamide, cyclosporin, mycophenolate mofetil). Additional therapies are intravenous immunoglobulins, danazol, plasma-exchange, and alemtuzumab and high-dose cyclophosphamide as last resort option. As the experience with rituximab evolves, it is likely that this drug will be located at an earlier point in therapy of warm AIHA, before more toxic immunosuppressants, and in place of splenectomy in some cases. In CAD, rituximab is now recommended as first-line treatment. PMID:25271314

Zanella, Alberto; Barcellini, Wilma

2014-10-01

9

Treatment of autoimmune hemolytic anemias  

PubMed Central

Autoimmune hemolytic anemia (AIHA) is a relatively uncommon disorder caused by autoantibodies directed against self red blood cells. It can be idiopathic or secondary, and classified as warm, cold (cold hemagglutinin disease (CAD) and paroxysmal cold hemoglobinuria) or mixed, according to the thermal range of the autoantibody. AIHA may develop gradually, or have a fulminant onset with life-threatening anemia. The treatment of AIHA is still not evidence-based. The first-line therapy for warm AIHA are corticosteroids, which are effective in 7085% of patients and should be slowly tapered over a time period of 612 months. For refractory/relapsed cases, the current sequence of second-line therapy is splenectomy (effective approx. in 2 out of 3 cases but with a presumed cure rate of up to 20%), rituximab (effective in approx. 8090% of cases), and thereafter any of the immunosuppressive drugs (azathioprine, cyclophosphamide, cyclosporin, mycophenolate mofetil). Additional therapies are intravenous immunoglobulins, danazol, plasma-exchange, and alemtuzumab and high-dose cyclophosphamide as last resort option. As the experience with rituximab evolves, it is likely that this drug will be located at an earlier point in therapy of warm AIHA, before more toxic immunosuppressants, and in place of splenectomy in some cases. In CAD, rituximab is now recommended as first-line treatment. PMID:25271314

Zanella, Alberto; Barcellini, Wilma

2014-01-01

10

Hemolytic anemias and erythrocyte enzymopathies.  

PubMed

The human erythrocyte generates high-energy adenosine triphosphate by anaerobic glycolysis and cycles oxidized and reduced nicotinamide adenine dinucleotide phosphate by the aerobic pentose phosphate shunt pathway. Certain enzymopathies of the pentose phosphate shunt are associated with hemolysis resulting from oxidative denaturation of hemoglobin. Glucose-6-phosphate dehydrogenase deficiency, an X-chromosome-linked disorder, is the prototype of these diseases and is genetically and clinically polymorphic. Six enzymopathies of anaerobic glycolysis cause hemolytic anemia; lactate dehydrogenase deficiency does not. In 2,3-diphosphoglycerate mutase deficiency, 2,3-diphosphoglycerate is greatly reduced and asymptomatic polycythemia is noted. Pyrimidine-5'-nucleotidase deficiency, an enzymopathy of nucleotide metabolism, is characterized by intracellular accumulations of pyrimidine-containing nucleotides, marked basophilic stippling on the stained blood film, splenomegaly, and hemolysis. Lead inhibits the nucleotidase and an identical syndrome occurs during severe lead poisoning. Hemolysis also accompanies an unusual enzymopathy characterized by a 40- to 70-fold increase (not decrease) in adenosine deaminase activity. PMID:2990276

Valentine, W N; Tanaka, K R; Paglia, D E

1985-08-01

11

Hemolytic disease of the fetus and newborn with late-onset anemia due to anti-M: a case report and review of the Japanese literature.  

PubMed

Hemolytic disease of the fetus and newborn (HDFN) attributed to M/N-incompatibility varies from asymptomatic to lethally hydropic. Case reports are rare, and the clinical significance of anti-M is not completely understood. A challenging case of HDFN due to anti-M prompted an investigation of the Japanese literature, in order to characterize the clinical spectrum of M/N-incompatibility pregnancies in Japan and report results to English-language readers. Japanese reports of HDFN attributed to M/N incompatibility were compiled. Abstracted data include maternal antibody titers at delivery, fetal direct antiglobulin test, hemoglobin, total bilirubin, reticulocyte count at birth, and therapeutic interventions. We investigated characteristics of HDFN due to M/N-incompatible pregnancies in Japan after encountering a case of severe HDFN along with late-onset anemia in an infant born to a woman carrying IgG anti-M with a titer of 1. In total, thirty-three babies with HDFN due to anti-M and one due to anti-N have been reported in Japan since 1975. The median maternal antibody titer was 64 at delivery and was 16 or less in 10 of 34 women (29%). Five of 34 babies (15%) were stillborn or died as neonates. Twenty-one of 29 survivors (72%) had severe hemolytic anemia and/or hydrops fetalis. The reticulocyte count of neonates with anemia stayed below the reference interval. Sixteen (55%) developed late-onset anemia and 14 (48%) were transfused with M-negative RBCs. Significant positive correlation (P < .05) between the hemoglobin value and the reticulocyte count within 4 days of birth was obtained in 16 babies with anti-M HDFN. In the Japanese population, 21 of 34 cases of M/N-incompatible HDFN (72%) have manifested as severe hemolytic anemia and/or hydrops fetalis. Low reticulocyte count in neonates with late-onset anemia is consistent with suppressed erythropoiesis due to anti-M. PMID:24262303

Yasuda, Hiroyasu; Ohto, Hitoshi; Nollet, Kenneth E; Kawabata, Kinuyo; Saito, Shunnichi; Yagi, Yoshihito; Negishi, Yutaka; Ishida, Atsushi

2014-01-01

12

Acute nonimmune hemolytic anemia without fulminant hepatitis in Wilson disease.  

PubMed

Owing to the insidious course and variable presentation, Wilson disease is often diagnosed months to years after the initial symptoms. Although fulminant hepatitis with nonimmune hemolytic anemia is frequently reported, chronic mild hepatitis can occur with bouts of transient hemolytic anemia. We report a 16-year-old female who presented with fatigue, dizziness, and new onset jaundice. She had a hemolytic anemia, although diagnosis of Wilson disease was initially confounded by a family history of autoimmunity with a high erythrocyte sedimentation rate and only mildly elevated bilirubin and aspartate aminotransferase. Macrocytosis, poor liver synthetic function, and low serum alkaline phosphatase led to the diagnosis. PMID:21516016

Agrawal, Anurag K; Haddad, Fadi G; Matsunaga, Alison

2011-05-01

13

Autoimmune hemolytic anemia in chronic mucocutaneous candidiasis.  

PubMed Central

Chronic mucocutaneous candidiasis is an immunodeficiency disease characterized by T-cell dysregulation and chronic superficial candidal infections. We report on three patients with chronic mucocutaneous candidiasis who developed autoantibodies to erythrocytes. Our first patient, a 19-year-old female, developed autoimmune hemolytic anemia (AIHA) that required multiple courses of treatment, including corticosteroids, intravenous immunoglobulin, and danazol. During the last exacerbation of AIHA, intensive treatment with corticosteroids and intravenous immunoglobulin failed and yet the patient responded to plasmapheresis. Our second patient, a 21-year-old male, developed AIHA which responded to oral corticosteroid therapy. Our third patient, a 6-year-old female without evidence of hemolysis, was found to have erythrocyte autoantibodies on routine screening. These three patients had positive direct antiglobulin tests, and the first patient had both immunoglobulin G (IgG) and IgM erythrocyte autoantibodies, while the remaining two patients had only IgG autoantibody. This is the first report of the association of AIHA with chronic mucocutaneous candidiasis. We suggest that all patients with chronic mucocutaneous candidiasis be screened periodically for erythrocyte autoantibodies. Plasmapheresis, a safe ancillary procedure in the management of AIHA, may be life-saving in some cases. The occurrence of erythrocyte autoantibodies in mucocutaneous candidiasis may be related to immunoregulatory disorders in this disease. PMID:7496919

Oyefara, B I; Kim, H C; Danziger, R N; Carroll, M; Greene, J M; Douglas, S D

1994-01-01

14

Impairment of Bone Health in Pediatric Patients with Hemolytic Anemia  

PubMed Central

Introduction Sickle cell anemia and thalassemia result in impaired bone health in both adults and youths. Children with other types of chronic hemolytic anemia may also display impaired bone health. Study Design To assess bone health in pediatric patients with chronic hemolytic anemia, a cross-sectional study was conducted involving 45 patients with different forms of hemolytic anemia (i.e., 17 homozygous sickle cell disease and 14 hereditary spherocytosis patients). Biochemical, radiographic and anamnestic parameters of bone health were assessed. Results Vitamin D deficiency with 25 OH-vitamin D serum levels below 20 ng/ml was a common finding (80.5%) in this cohort. Bone pain was present in 31% of patients. Analysis of RANKL, osteoprotegerin (OPG) and osteocalcin levels indicated an alteration in bone modeling with significantly elevated RANKL/OPG ratios (control: 0.08+0.07; patients: 0.26+0.2, P?=?0.0007). Osteocalcin levels were found to be lower in patients compared with healthy controls (68.5+39.0 ng/ml vs. 118.0+36.6 ng/ml, P?=?0.0001). Multiple stepwise regression analysis revealed a significant (P<0.025) influence of LDH (partial r2?=?0.29), diagnosis of hemolytic anemia (partial r2?=?0.05) and age (partial r2?=?0.03) on osteocalcin levels. Patients with homozygous sickle cell anemia were more frequently and more severely affected by impaired bone health than patients with hereditary spherocytosis. Conclusion Bone health is impaired in pediatric patients with hemolytic anemia. In addition to endocrine alterations, an imbalance in the RANKL/OPG system and low levels of osteocalcin may contribute to this impairment. PMID:25299063

Schundeln, Michael M.; Goretzki, Sarah C.; Hauffa, Pia K.; Wieland, Regina; Bauer, Jens; Baeder, Lena; Eggert, Angelika; Hauffa, Berthold P.; Grasemann, Corinna

2014-01-01

15

Congenital Nonspherocytic Hemolytic Anemia With an Unstable Hexokinase Variant  

Microsoft Academic Search

We report a family with a new hexokinase mal reaction kinetics, and normal dee- variant that gives rise to nonspherocytic trophoretic properties, but has reduced hemolytic anemia in one apparently activity and is apparently inactivated homozygous family member. The variant rapidly as the affected erythrocytes age. enzyme has a normal pH optimum, nor- B ECAUSE ERYTHROCYTE HEXOKINASE (HK) has a

P. G. Board; R. Trueworthy; J. E. Smith; Kateri Moore

1978-01-01

16

Hemolytic anemia associated with heterograft replacement of the mitral valve.  

PubMed

The first case of overt hemolytic anemia following mitral valve replacement with a porcine heterograft is reported. Cardiac catheterization failed to reveal a paravalvular leak or valvular incompetence to account for the hemolysis. Red cell traumatization by the Dacron-covered Stellite ring and stent is suggested as the cause of hemolysis with the porcine heterograft. PMID:567264

Myers, T J; Hild, D H; Rinaldi, M J

1978-08-01

17

Auto-immune hemolytic anemia in two horses.  

PubMed

Two cases of Auto-immune hemolytic anemia (AHA) in the horse are described. The pathogenesis of AHA in man is related to the findings in the horses. Besides from routine hematological and biochemical investigations specific data were obtained from the erythrocyte osmotic fragility test, the Coombs test, the serum haptoglobulin level and the cold agglutinin test. The first patient, a six month old Dutch standardbred colt, probably suffered from an acute attack of cold-induced hemoglobinuria with severe anemia and acronecrosis of the tops of both ears and of several parts of the skin that had been in close contact with the cold floor. The second patient, a nine years old Friesian mare, showed a type of AHA resembling the acute hemolyte type of cold agglutinin disease in man. This patient had a clear septicemic picture, extensive bacteriological examination, however, was negative. PMID:1162684

Lokhorst, H M; Breukink, H J

1975-07-15

18

Hematologic characterization and chromosomal localization of the novel dominantly inherited mouse hemolytic anemia, neonatal anemia (Nan).  

PubMed

One of the most commonly inherited anemias in man is Hereditary Spherocytosis (HS) with an incidence of 1 in 2000 for persons of Northern European descent. Mouse models of HS include spontaneous inherited hemolytic anemias and those generated by gene targeting. The Neonatal anemia (Nan) mouse is a novel model of HS generated by N-ethyl-N-nitrosurea mutagenesis and suffers from a severe neonatal anemia. Adult Nan mice have a lifelong hemolytic anemia with decreased red blood cell numbers, hematocrit, and hemoglobin, but elevated zinc protoporphyrin levels. Blood smears taken from Nan mice show a hypochromic anemia characterized by poikilocytosis, anisocytosis and polychromasia. The Nan phenotype can be transferred by bone marrow transplantation indicating that the defect is intrinsic to bone marrow. The hemolytic anemia in adult Nan mice can be identified by osmotic fragility testing. Examination of the erythrocyte membrane skeleton proteins (EMS) reveals a global deficiency of these proteins with protein 4.1a being completely absent. The Nan locus maps to mouse Chromosome 8 and does not co-localize with any known EMS genes. The identification of the Nan gene will likely uncover a novel protein that contributes to the stability of the EMS and may identify a new mutation for HS. PMID:19409822

White, Robert A; Sokolovsky, Inna V; Britt, Margaret I; Nsumu, Ndona N; Logsdon, Derek P; McNulty, Steven G; Wilmes, Leigh A; Brewer, Brandon P; Wirtz, Eric; Joyce, Heather R; Fegley, Barbara; Smith, Ann; Heruth, Daniel P

2009-01-01

19

Molecular basis of erythroenzymopathies associated with hereditary hemolytic anemia: tabulation of mutant enzymes.  

PubMed

Molecular abnormalities of erythroenzymopathies associated with hereditary hemolytic anemia have been determined by means of molecular biology. Pyruvate kinase (PK) deficiency is the most common and well-characterized enzyme deficiency in the glycolytic pathway, and it causes hereditary hemolytic anemia. To date, 47 gene mutations have been identified. We identified one base deletion, one splicing mutation, and six distinct missense mutations in 12 unrelated families with a homozygous PK deficiency. Mutations located near the substrate or fructose-1,6- diphosphate binding site may change the conformation of the active site, resulting in a drastic loss of activity and severe clinical symptoms. Glucose-6-phosphate dehydrogenase (G6PD)deficiency is the most common metabolic disorder, and it is associated with chronic hemolytic anemia and/or drug- or infection-induced acute hemolytic attack. An estimated 400 million people are affected worldwide. The mutations responsible for about 78 variants have been determined. Some have polymorphic frequencies in different populations. Most variants are produced by one or two nucleotide substitutions. Molecular studies have disclosed that most of the class 1 G6PD variants associated with chronic hemolysis have the mutations surrounding either the substrate or the NADP binding site. Among rare enzymopathies, missense mutations have been determined in deficiencies of glucosephosphate isomerase, (TPI), phosphoglycerate kinase, and adenylate kinase. Compound heterozygosity with missense mutation and base deletion has been determined in deficiencies of hexokinase and diphosphoglyceromutase. Compound heterozygosity with missense and nonsense mutations has been identified in TPI deficiency. One base junction mutations resulting in abnormally spliced PFK-M mRNA have been identified in homozygous PFK deficiency. An exception is hemolytic anemia due to increased adenosine deaminase activity. The basic abnormality appears to result from the overproduction of a structurally normal enzyme. PMID:8579052

Miwa, S; Fujii, H

1996-02-01

20

Pleural solitary fibrous tumor complicated with autoimmune hemolytic anemia.  

PubMed

We herein report a 74-year-old woman who presented with autoimmune hemolytic anemia (AIHA) associated with pleural solitary fibrous tumor (SFT). Her AIHA was initially treated with 1 mg/kg daily of oral prednisolone (PSL) for 2 months, which had a limited effect. However, after surgical tumor resection, the patient showed remarkable improvement of AIHA with normalizations of serum lactate dehydrogenase and bilirubin levels, and we were able to rapidly reduce the PSL dosage. This is the first description of a case of AIHA caused by SFT. PMID:25030571

Takahashi, Hiroshi; Ohkawara, Hiroshi; Ikeda, Kazuhiko; Harada-Shirado, Kayo; Furukawa, Miki; Sukegawa, Masumi; Shichishima-Nakamura, Akiko; Noji, Hideyoshi; Wakamatsu, Saho; Tasaki, Kazuhiro; Suzuki, Hiroyuki; Ogawa, Kazuei; Takeishi, Yasuchika

2014-01-01

21

Molecular aspects of erythroenzymopathies associated with hereditary hemolytic anemia.  

PubMed

Since the discovery of glucose 6-phosphate dehydrogenase (G6PD) and of pyruvate kinase deficiencies, erythroenzymopathies associated with hereditary hemolytic anemia have been extensively investigated. Kinetic and electrophoretic studies have shown that most, if not all, erythroenzymopathies are caused by the production of a mutant enzyme. Except for a few enzymes that are abundant in blood and tissues, it is difficult to obtain enough sample to study the functional and structural abnormalities of mutant enzymes associated with genetic disorders in man. The primary structures of only two normal red cell enzymes which can cause hereditary hemolytic anemia, phosphoglycerate kinase (PGK) and adenylate kinase, have been determined. Single amino acid substitutions of PGK variants have been found, and the identification of the exact molecular abnormalities of such variants has helped us to understand the accompanying functional abnormality. Gene cloning makes possible the identification of the DNA sequence that codes for enzyme proteins. Recently, human complementary DNA (cDNA) for aldolase, PGK, G6PD, and adenosine deaminase (ADA) have been isolated, and the nucleotide sequences for PGK and ADA determined. In the near future, human cDNA sequencing should permit identification of the gene alteration that gives rise to the mutant enzymes. PMID:2990202

Miwa, S; Fujii, H

1985-07-01

22

Hemolytic-Anemia-Associated Pulmonary Hypertension: Sickle-Cell-Disease- and Thalassemia-Associated Pulmonary Hypertension  

Microsoft Academic Search

\\u000a Pulmonary hypertension (PH) is now recognized as a complication of both chronic and acquired hemolytic anemias. The process\\u000a of hemolysis appears to be central to disease pathogenesis. Sickle cell disease (SCD), a congenital hemoglobinopathy affecting\\u000a as many as 30 million individuals worldwide, is the best characterized hemolytic anemia associated with PH. Multiple clinical\\u000a studies have demonstrated a 1030% prevalence of

Elizabeth S. Klings; Mark T. Gladwin

23

Aortic valve replacement for a patient with glucose-6-phosphate dehydrogenase deficiency and autoimmune hemolytic anemia.  

PubMed

Autoimmune hemolytic anemia and deficiency of glucose-6-phosphate deyhdrogenase (G6PD) result in severe hemolysis with different mechanisms. In patients with both pathologies, the effects of cardiopulmonary bypass on red blood cells and thrombocytes demand special care before and after open heart surgery. We evaluated the preoperative management and postoperative care of a patient with severe aortic insufficiency associated with G6PD deficiency and autoimmune hemolytic anemia who underwent aortic valve replacement. PMID:15985145

Tas, Serpil; Donmez, Arzu Antal; Kirali, Kaan; Alp, Mete H; Yakut, Cevat

2005-01-01

24

[Pathophysiology and laboratory tests of hemolytic anemia: with special reference to erythroenzymopathies].  

PubMed

Since the discovery of glucose-6-phosphate dehydrogenase (G6PD) deficiency and pyruvate kinase deficiency, erythroenzymopathies associated with hereditary hemolytic anemia have been extensively investigated. Kinetic and electrophoretic studies have shown that most erythroenzymopathies are caused by the production of a mutant enzyme. Single amino acid substitutions have been determined in G6PD and phosphoglycerate kinase variants by studies of the enzyme. Except for these two enzymes, it has been difficult to purify and to characterize the patient's enzyme because of the low protein contents in red blood cells. Recent advance in recombinant DNA technology has made possible the isolation of normal genomic DNA or cDNA for several enzymes. These results permit us to study the molecular basis of erythroenzymopathies at the nucleotide level. Single base substitutions have been identified in aldolase, triosephosphate isomerase, G6PD and adenylate kinase variants by the cloning and nucleotide sequence of the patients' genes. To date, all of the enzyme-deficient variants which have been investigated are caused by point mutations. An exception is a hemolytic anemia secondary to increased adenosine deaminase (ADA) activity. Red cell ADA activity increases on the order of a hundred-fold in affected individuals. The basic abnormality appears to result from overproduction of structurally normal enzyme due to abnormal translational efficiency. PMID:2693773

Fujii, H; Miwa, S

1989-12-01

25

The Lbw2 locus promotes autoimmune hemolytic anemia.  

PubMed

The lupus-prone New Zealand Black (NZB) strain uniquely develops a genetically imposed severe spontaneous autoimmune hemolytic anemia (AIHA) that is very similar to the corresponding human disease. Previous studies have mapped anti-erythrocyte Ab (AEA)-promoting NZB loci to several chromosomal locations, including chromosome 4; however, none of these have been analyzed with interval congenics. In this study, we used NZB.NZW-Lbw2 congenic (designated Lbw2 congenic) mice containing an introgressed fragment of New Zealand White (NZW) on chromosome 4 encompassing Lbw2, a locus previously linked to survival, glomerulonephritis, and splenomegaly, to investigate its role in AIHA. Lbw2 congenic mice exhibited marked reductions in AEAs and splenomegaly but not in anti-nuclear Abs. Furthermore, Lbw2 congenics had greater numbers of marginal zone B cells and reduced expansion of peritoneal cells, particularly the B-1a cell subset at early ages, but no reduction in B cell response to LPS. Analysis of a panel of subinterval congenic mice showed that the full effect of Lbw2 on AEA production was dependent on three subloci, with splenomegaly mapping to two of the subloci and expansions of peritoneal cell populations, including B-1a cells to one. These results directly demonstrated the presence of AEA-specific promoting genes on NZB chromosome 4, documented a marked influence of background genes on autoimmune phenotypes related to Lbw2, and further refined the locations of the underlying genetic variants. Delineation of the Lbw2 genes should yield new insights into both the pathogenesis of AIHA and the nature of epistatic interactions of lupus-modifying genetic variants. PMID:22371393

Scatizzi, John C; Haraldsson, Maria K; Pollard, K Michael; Theofilopoulos, Argyrios N; Kono, Dwight H

2012-04-01

26

Alpha-methyldopa-induced autoimmune hemolytic anemia in the third trimester of pregnancy.  

PubMed

Alpha-methyldopa has been demonstrated to be safe for use during pregnancy and is now used to treat gestational hypertension. In pregnancy, alpha-methyldopa-induced autoimmune hemolytic anemia does not have typical features and the severity of symptoms ranges from mild fatigue to dyspnea, respiratory failure, and death if left untreated. A case of alpha-methyldopa-induced autoimmune hemolytic anemia in a 36-year-old gravida 2, para 1 woman at 37(+6) weeks of gestation is reported herein along with the differential diagnostic procedure and the potential risks to the mother and the fetus. PMID:24175105

Grigoriadis, Charalampos; Tympa, Aliki; Liapis, Angelos; Hassiakos, Dimitrios; Bakas, Panagiotis

2013-01-01

27

Alpha-Methyldopa-Induced Autoimmune Hemolytic Anemia in the Third Trimester of Pregnancy  

PubMed Central

Alpha-methyldopa has been demonstrated to be safe for use during pregnancy and is now used to treat gestational hypertension. In pregnancy, alpha-methyldopa-induced autoimmune hemolytic anemia does not have typical features and the severity of symptoms ranges from mild fatigue to dyspnea, respiratory failure, and death if left untreated. A case of alpha-methyldopa-induced autoimmune hemolytic anemia in a 36-year-old gravida 2, para 1 woman at 37+6 weeks of gestation is reported herein along with the differential diagnostic procedure and the potential risks to the mother and the fetus. PMID:24175105

Tympa, Aliki; Liapis, Angelos; Hassiakos, Dimitrios; Bakas, Panagiotis

2013-01-01

28

Post-transfusion hypertension and seizure in congenital hemolytic anemia: a case report and literature review.  

PubMed

A rare syndrome of hypertension, seizures and intracranial bleed has been reported among patients with congenital hemolytic anemia who underwent multiple blood transfusions. We report this syndrome in a 12-year-old Malay girl with hemoglobin E-beta-thalassemia, who underwent intensive transfusion and subsequently had headache, visual loss, severe hypertension and seizures. A comprehensive literature review revealed 30 patients with this syndrome, of whom 15 had intracranial bleed and 12 among these 15 died. A less-intensive transfusion regimen among patients with chronic hemolytic anemia and prompt detection and management of hypertension may prevent this potentially fatal syndrome. PMID:24473404

Ngim, Chin Fang; Ng, Chen Siew; Lai, Nai Ming

2014-06-01

29

Case of cytomegalovirus-associated direct anti-globulin test-negative autoimmune hemolytic anemia.  

PubMed

A 1-year-old boy developed autoimmune hemolytic anemia after a negative direct anti-globulin test. The concentration of erythrocyte membrane-associated immunoglobulin G, determined using an immunoradiometric assay, correlated with disease activity. He was positive for cytomegalovirus (CMV) both serologically and by quantitative real-time polymerase chain reaction, indicating that his autoimmune hemolytic anemia was directly caused by CMV infection. Since anti-CMV immunoglobulin G was not absorbed by the patient's erythrocytes, cross-reaction between erythrocyte antigens and CMV was not likely a causative factor for hemolysis. PMID:24330288

Kaneko, Saeko; Sato, Masanori; Sasaki, Goro; Eguchi, Hiroyuki; Oishi, Tsutomu; Kamesaki, Toyomi; Kawaguchi, Hiroyuki

2013-12-01

30

Incompatible blood transfusion: Challenging yet lifesaving in the management of acute severe autoimmune hemolytic anemia  

PubMed Central

Background and Aim: Autoimmune hemolytic anemia (AIHA) is characterized by the production of autoantibodies directed against red cell antigens. Most patients of AIHA arrive in the emergency or out-patient department (OPD) with severe anemia requiring urgent blood transfusion. Here we share our experience of managing these patients with incompatible blood transfusions and suggest the minimal test required to assure patient safety. Materials and Methods: A total of 14 patients admitted with severe anemia, diagnosed with AIHA and requiring blood transfusion urgently were included in the study. A series of immunohematological investigations were performed to confirm the diagnosis and issue best match packed red blood cells (PRBC) to these patients. Results: A total of 167 PRBC units were crossmatched for 14 patients of which 46 units (28%) were found to be best match ones and 26 (56.5%) of these units were transfused. A mean turn around time of 222 min was observed in issuing the best match blood. Severe hemolysis was observed in all patients with a median hemoglobin increment of 0.88 g/dl after each unit PRBC transfusion. Conclusion: Decision to transfuse in AIHA should be based on the clinical condition of the patient. No critical patient should be denied blood transfusion due to serological incompatibility. Minimum investigations such as direct antiglobulin test (DAT), antibody screening and autocontrol should be performed to ensure transfusion safety in patients. All transfusion services should be capable of issuing best match PRBCs in AIHA. PMID:25161349

Das, Sudipta Sekhar; Zaman, Rafiq Uz; Safi, Mohammad

2014-01-01

31

Unexplained hemolytic anemia of pregnancy: Case report with review of related literature  

Microsoft Academic Search

We present a case of a multipara lady who developed hemolytic anemia during pregnancy with spontaneous remission after delivery. She was managed with low dose steroid for hemolysis during pregnancy with good feto-maternal outcome. Despite extensive investigations carried out to determine the cause, they remained in vain. Very few of such cases have been described in the literature, which merits

Paban Sharma; Rekha Sthapit

2008-01-01

32

Deficiencies of glycolytic enzymes as a possible cause of hemolytic anemia.  

PubMed

The critical minimum values of Na,K-ATPase and glycolytic enzyme activities at which the erythrocyte viability is lost were calculated using the mathematical model of the erythrocyte, which included all reactions of glycolysis, adenylate metabolism, ionic balance, and osmotic regulation of erythrocyte volume. The criterion for cell death was an increase in its volume to the level at which it is sequestrated from the circulation or is lysed. In hemolytic anemia associated with hexokinase or pyruvate kinase deficiency, activities of these enzymes measured in patient erythrocytes appeared to be close to the calculated critical values. By contrast, in hemolytic anemia associated with phosphofructokinase, glucosephosphate isomerase, triosephosphate isomerase, or phosphoglycerate kinase deficiency, activities of these enzymes measured in patient erythrocytes were significantly greater than the calculated critical values. In this case, if the deficient enzyme were stable, i.e. its activity in the cell were low, but constant in time, the deficiency observed would not account for the erythrocyte destruction observed and the development of hemolytic anemia. It was shown, however, that in phosphofructokinase, glucosephosphate isomerase, triosephosphate isomerase, or phosphoglycerate kinase deficiency, hemolytic anemia can arise because of the instability of these enzymes in time. PMID:10699493

Martinov, M V; Plotnikov, A G; Vitvitsky, V M; Ataullakhanov, F I

2000-03-01

33

Brown recluse spider (Loxosceles reclusa) envenomation leading to acute hemolytic anemia in six adolescents.  

PubMed

Loxosceles reclusa (brown recluse spider) bites often cause local envenomation reactions; however, acute hemolysis from systemic loxoscelism is rare. To highlight this important diagnostic consideration for unexplained hemolysis in areas endemic for brown recluse spiders, we report on 6 adolescents with acute hemolytic anemia from presumed L reclusa bites. PMID:20006769

McDade, Jenny; Aygun, Banu; Ware, Russell E

2010-01-01

34

A case of primary ovarian lymphoma with autoimmune hemolytic anemia achieving complete response with Rituximab-based combination chemotherapy  

PubMed Central

Ovarian involvement as primary or secondary lymphomatous process is extremely uncommon. In most cases, the diagnosis is usually not suspected initially and is confirmed only after detailed histopathological evaluation. We report a patient with primary ovarian diffuse large B-cell lymphoma (DLBCL) and associated auto-immune hemolytic anemia (AIHA) who achieved complete remission after treatment with Rituximab-cyclophosphamide-doxorubicin-vincristine and prednisolone (R-CHOP) chemotherapy. This patient was a 50 year old female, who presented with fever, abdominal pain, vomiting, weight loss and anemia. Computed tomography scan of the abdomen and pelvis revealed a large left ovarian mass with bilateral hydronephrosis. We performed exploratory laparotomy and partial resection of the mass was done due to the adhesions. Histopathology confirmed the diagnosis of DLBCL. After six R-CHOP chemotherapy cycles, patient achieved complete response with correction of anemia. To our knowledge, this may be the first case report till date of primary ovarian DLBCL with AIHA treated with R-CHOP chemotherapy who achieved complete remission in terms of primary disease as well as hemolytic anemia. PMID:22563154

Ghadyalpatil, N. S.; Chandrasekar, R.; Snehalatha, D.; Reddy, B. M.

2011-01-01

35

Your Guide to Anemia  

MedlinePLUS

... e m i a Treatments for Hemolytic Anemia Treatments for Acquired Hemolytic Anemia Type Possible Treatments Immune hemolytic ... destruction of RBCs in this form of anemia). Treatments for Inherited Hemolytic Anemia Type Possible Treatments Hemoglobin disorders ( ...

36

A Thermolabile Aldolase A Mutant Causes Fever-Induced Recurrent Rhabdomyolysis without Hemolytic Anemia  

PubMed Central

Aldolase A deficiency has been reported as a rare cause of hemolytic anemia occasionally associated with myopathy. We identified a deleterious homozygous mutation in the ALDOA gene in 3 siblings with episodic rhabdomyolysis without hemolytic anemia. Myoglobinuria was always triggered by febrile illnesses. We show that the underlying mechanism involves an exacerbation of aldolase A deficiency at high temperatures that affected myoblasts but not erythrocytes. The aldolase A deficiency was rescued by arginine supplementation in vitro but not by glycerol, betaine or benzylhydantoin, three other known chaperones, suggesting that arginine-mediated rescue operated by a mechanism other than protein chaperoning. Lipid droplets accumulated in patient myoblasts relative to control and this was increased by cytokines, and reduced by dexamethasone. Our results expand the clinical spectrum of aldolase A deficiency to isolated temperature-dependent rhabdomyolysis, and suggest that thermolability may be tissue specific. We also propose a treatment for this severe disease. PMID:25392908

Mamoune, Asmaa; Bahuau, Michel; Hamel, Yamina; Serre, Valrie; Pelosi, Michele; Habarou, Florence; Nguyen Morel, Marie-Ange; Boisson, Bertrand; Vergnaud, Sabrina; Viou, Mai Thao; Nonnenmacher, Luc; Piraud, Monique; Nusbaum, Patrick; Vamecq, Joseph; Romero, Norma; Ottolenghi, Chris; Casanova, Jean-Laurent; de Lonlay, Pascale

2014-01-01

37

Paravertebral Mass in a Patient with Hemolytic Anemia: Computed Tomographic Findings  

PubMed Central

Extramedullary hematopoiesis is characterized by the presence of hematopoietic tissue outside of the bone marrow and is typically associated with chronic hemolytic anemias. Intrathoracic extramedullary hematopoiesis is a rare and usually asymptomatic condition. The authors report a case of a 57-year-old man with intrathoracic extramedullary hematopoiesis and hereditary spherocytosis. Clinical and laboratory evaluation, together with radiological findings, are described. The diagnosis of the disease was confirmed by tissue biopsy. PMID:20368781

Carvalho, Juliana Franca; Marchiori, Edson; Zanetti, Glaucia; Mano, Claudia Mauro; Sarcinelli-Luz, Branca; Vianna, Flavia Gavinho; Assed, Carla; Santos, Isabella Guedes; Santos, Alair Augusto S. M. D.; Vianna, Alberto Domingues

2010-01-01

38

Hemolytic anemia after operation for aortic dissection using teflon felt strips.  

PubMed

We report three cases of hemolytic anemia caused by anastomotic stenosis after surgical treatment for aortic dissection in which internal and external Teflon (DuPont, Wilmington, DE) felt strips were used for reinforcement of the aortic stump. To detect this complication, laboratory findings typical of red cell fragmentation syndrome as well as appropriate imaging modalities are necessary. As a precaution, it is necessary to be meticulous when stitching the internal felt strip. PMID:18442587

Nakamura, Yuki; Ogino, Hitoshi; Matsuda, Hitoshi; Minatoya, Kenji; Sasaki, Hiroaki; Kitamura, Soichiro

2008-05-01

39

Iron-rich drinking water and ascorbic acid supplementation improved hemolytic anemia in experimental Wistar rats.  

PubMed

Abstract Anemia is a frequent problem in both the primary and secondary health care programs. In contrast, most areas of northeast India are vulnerable to iron toxicity. In the present study, we documented the effect of administration of iron rich water on hemolytic anemia in a Wistar rats' animal model. Hemolytic anemia was induced by phenyl hydrazine through intraperitoneal route and diagnosed by the lowering of blood hemoglobin. After inducing the hemolytic anemia, 24 Wistar rats (n?=?6 in four groups) were randomly assigned to 1?mg/l, 5?mg/l, and 10?mg/l ferric oxide iron along with 1?mg/ml ascorbic acid administered through drinking water; a control group was treated with iron-free water. The hematological and biochemical parameters, iron levels in liver, spleen, and kidney were estimated after 30?d of treatment. In the group treated with 5?mg/l iron and ascorbic acid, a significant increase of serum iron and ferritin, and a decrease of TIBC (total iron binding capacity) were observed without changes in other biochemical parameters and histopathological findings. However, in the group treated with 10?mg/l iron and ascorbic acid, hematological changes with significantly higher values for white blood cell count, serum glutamic phospho transaminase, serum glutamic oxaloacetic transaminase, alkaline phosphatase, glucose, splenic, and liver iron content, indicate potential toxicity at this supplementation level. Data suggest that the optimum concentration of iron (5?mg/l) and ascorbic acid solution may improve anemic conditions and may be therapeutically beneficial in the treatment of iron deficiency anemia without any negative impact, while 10?mg/l in drinking water seems to be the threshold for the initiation of toxicity. PMID:24896300

Chaturvedi, Richa; Chattopadhyay, Pronobesh; Banerjee, Saumen; Bhattacharjee, Chira R; Raul, Prasanta; Borah, Kusum; Singh, Lokendra; Veer, Vijay

2014-11-01

40

Heinz-body hemolytic anemia from the ingestion of crude oil: a primary toxic effect in marine birds  

Microsoft Academic Search

Hemolytic anemia developed in young herring gulls and Atlantic puffins given daily oral doses of a Prudhoe Bay crude oil. Anemia developed 4 to 5 days after the initiation of oil ingestion and was accompainied by Heinz-body formation and a strong regenerative response. The data evince a toxic effect on circulating red blood cells involving an oxidative biochemical mechanism and

F. A. Leighton; D. B. Peakall; R. G. Butler

1983-01-01

41

Heinz-Body Hemolytic Anemia from the Ingestion of Crude Oil: A Primary Toxic Effect in Marine Birds  

Microsoft Academic Search

Hemolytic anemia developed in young herring gulls and Atlantic puffins given daily oral doses of a Prudhoe Bay crude oil. Anemia developed 4 to 5 days after the initiation of oil ingestion and was accompanied by Heinz-body formation and a strong regenerative response. The data evince a toxic effect on circulating red blood cells involving an oxidative biochemical mechanism and

Frederick A. Leighton; David B. Peakall; Ronald G. Butler

1983-01-01

42

Erythrocyte volume distribution analysis and hematologic changes in two horses with immune-mediated hemolytic anemia.  

PubMed

Immune-mediated hemolytic anemia was diagnosed in two horses on the basis of regenerative anemia, increased erythrocyte fragility in hypotonic saline, autoagglutination, and a positive direct antiglobulin (Coomb's) test. During steroid therapy partial resolution of the anemia was indicated by rising packed cell volume, macrocytosis, and bone marrow erythroid hyperplasia. Using erythrocyte volume distribution histograms (erythrograms), the regenerative response was characterized by analysis of macrocytic and normocytic erythrocyte subpopulations. In both horses, a gradual net increase of about 2 X 10(6) macrocytes/microliter occurred over a four- to five-week period. Over the same interval there was a gradual decrease in the number of normocytes. We suggest that the macrocytes remained large through this period rather than contributing to normocyte population growth. Erythrograms may provide an additional means of evaluating erythrocyte regeneration in horses. PMID:6623846

Weiser, G; Kohn, C; Vachon, A

1983-07-01

43

Enzymatic diagnosis in non-spherocytic hemolytic anemia.  

PubMed

Blood samples from 722 unrelated patients with anemia and/or reticulocytosis were submitted to our laboratory for red cell enzyme assay during the past 7 years. Among these 722 cases, we found 82 cases of 7 different red cell enzyme deficiencies and 2 of unstable hemoglobin. Abnormalities of pyruvate kinase (PK) were found to cause hemolysis in 55 patients. Although their average PK activity was about 35% of the normal level, 5 showed normal and 2 demonstrated high PK activity. Among 17 patients in whom pyruvate kinase assays or screening tests had been carried out in routine laboratories, the correct diagnoses had been made in only 4. Glucose-6-phosphate dehydrogenase (G6PD) deficiency was found in 15 patients, pyrimidine 5'-nucleotidase deficiency in 5, glucose phosphate isomerase deficiency in 3, adenylate kinase deficiency in 2, phosphoglycerate kinase deficiency in 1, and glutathione synthetase deficiency in 1 patient. Even after we performed a panel of over 20 different red cell enzyme assays, 519 patients still remained undiagnosed. PMID:3352512

Hirono, A; Forman, L; Beutler, E

1988-03-01

44

Anemia  

MedlinePLUS

Anemia is a condition in which the body does not have enough healthy red blood cells. Red ... provide oxygen to body tissues. Other types of anemia include: Anemia due to B12 deficiency Anemia due ...

45

Severe Hemolytic Anemia Associated with Mild Pneumonia Caused by Mycoplasma pneumonia  

PubMed Central

We report a case of M. pneumoniae infection presenting with severe hemolytic anemia in a 4-year-old girl, with a ten-day history of paleness, weakness, and nonproductive cough. She was very pale and tachycardic. However, she was not tachypneic. Chest examination showed normal breath sounds. No rhoncus or whistling was heard. As the erythrocyte sedimentation rate was excessively elevated, the differential diagnosis primarily comprised hematological malignancies. Direct Coombs' test was positive. Diagnosis of M. pneumoniae infection was confirmed by elevated levels of M. pneumoniae IgG and IgM antibodies and a chest X-ray suggestive of atypical pneumonia. The patient was treated with clarithromycin and packed red cell transfusion and showed a favorable recovery within ten days after admission. In conclusion, this case demonstrates that severe hemolytic anemia caused by M. pneumoniae is not always associated with severe pulmonary involvement, even when the respiratory infection is very mild, M. pneumoniae may be the cause of severe anemia. PMID:23049568

Kurugol, Zafer; Onen, Serife Sebnem; Koturoglu, Guldane

2012-01-01

46

Molecular basis of red cell enzymopathies associated with hereditary nonspherocytic hemolytic anemia.  

PubMed

In the past few years, very rapid advances have been made in the field of red cell enzymopathies associated with hereditary nonspherocytic hemolytic anemia, particularly in molecular basis. Nucleotide sequence and amino acid sequence of normal human red cell enzymes have been clarified in phosphofructokinase, aldolase, triosephosphate isomerase, phosphoglycerate kinase, pyruvate kinase, diphosphoglycerate mutase, glucose 6-phosphate dehydrogenase, adenylate kinase and adenosine deaminase. Furthermore, in aldolase-, triosephosphate isomerase-, diphosphoglycerate mutase-, glucose 6-phosphate dehydrogenase-, and adenylate kinase deficiency, single nucleotide changes which cause single amino acid substitutions and finally hemolysis, have been found. PMID:2560452

Miwa, S

1989-01-01

47

[Metastatic breast cancer with microangiopathic hemolytic anemia successfully treated by using eribulin].  

PubMed

A 48-year-old woman was diagnosed with metastatic breast carcinoma and multiple bone metastases as well as a brain metastasis in 2004. Multiple bone metastases and brain metastases were also diagnosed in 2005, 2006, and 2010, but she remained stable with the use of chemotherapy and hormonal therapy for about 8 years. In 2013, severe anemia occurred, and the patient was diagnosed with microangiopathic hemolytic anemia (MHA). She was treated with eribulin(1.4 mg/m), and recovered successfully after treatment. Approximately 8 months have elapsed after initiating the therapy, and there has been no recurrence. MHA associated with breast cancer is very rare, and is regarded as a disease with a poor prognosis. However, eribulin could be a valid treatment for prolonging the survival of patients with MHA associated with breast cancer. PMID:25248898

Morita, Midori; Fukuda, Ken-Ichiro; Konishi, Tomoki; Kiuchi, Jun; Umehara, Seiji; Nakashima, Susumu; Fujiyama, Junshin; Masuyama, Mamoru

2014-09-01

48

Anti-CD20 Treatment of Giant Cell Hepatitis With Autoimmune Hemolytic Anemia.  

PubMed

Giant cell hepatitis with autoimmune hemolytic anemia (GCH-AHA) is a rare autoimmune disease of infancy characterized by severe liver disease associated with Coombs-positive hemolytic anemia. We recently showed that GCH-AHA is probably caused by a humoral immune mechanism. Such data support the use of rituximab, an anti-CD-20 monoclonal antibody specifically targeting B lymphocytes, as a treatment for GCH-AHA. We describe here the detailed clinical evolution of 4 children with GCH-AHA who showed a complete response to rituximab. All patients shared a severe course of the disease with poor control on standard and aggressive immunosuppression. Rituximab was well tolerated, and no side effects or infections were registered. Several doses were needed to induce remission, and 5 to 11 additional maintenance injections were necessary in the 2 more severe cases. Weaning from corticosteroids was achieved in all subjects. A steroid-sparing effect was noted in the 3 children who started rituximab early in the course of the disease. Overall, we show here that there is a strong rationale for treating GCH-AHA with rituximab. Early treatment could reduce the use of corticosteroids. Nevertheless, short-term steroids should be initially associated with rituximab to account for autoantibodies' half-life. Repeated injections are needed to treat and prevent relapses, but the best frequency and duration of treatment remain to be defined. PMID:25201797

Paganelli, Massimiliano; Patey, Natacha; Bass, Lee M; Alvarez, Fernando

2014-10-01

49

Gingival overgrowth in a dog that received long-term cyclosporine for immune-mediated hemolytic anemia  

PubMed Central

Gingival mass lesions developed when cyclosporine was administered for 600 days to a female, 7-year-old, longhaired dachshund diagnosed with intractable immune-mediated hemolytic anemia (IMHA). Histopathology indicated hyperplastic suppurative gingivitis. As the anemia improved, the dosage of cyclosporine A (CsA) was markedly decreased, and the mass lesions decreased in size and disappeared, thus suggesting that the mass lesions were an adverse reaction to CsA. PMID:22753966

Namikawa, Kazuhiko; Maruo, Takuya; Honda, Mayumi; Hirata, Hitomi; Lynch, Jonathan; Madarame, Hiroo

2012-01-01

50

Hereditary hemolytic anemia in Korea from 2007 to 2011: A study by the Korean Hereditary Hemolytic Anemia Working Party of the Korean Society of Hematology  

PubMed Central

Background The number of patients diagnosed with hereditary hemolytic anemia (HHA) has increased since the advent of novel diagnostic techniques that accurately identify this disorder. Here, we report data from a survey on the prevalence and characteristics of patients diagnosed with HHA in Korea from 2007 to 2011. Methods Information on patients diagnosed with HHA in Korea and their clinical and laboratory results were collected using a survey questionnaire. Globin gene and red blood cell (RBC) enzyme analyses were performed. In addition, we analyzed data collected by pediatricians. Results In total, 195 cases of HHA were identified. Etiologies identified for HHA were RBC membranopathies, hemoglobinopathies, and RBC enzymopathies, which accounted for 127 (64%), 39 (19.9%), and 26 (13.3%) cases, respectively. Of the 39 patients with hemoglobinopathies, 26 were confirmed by globin gene analysis, including 20 patients with ?-thalassemia minor, 5 patients with ?-thalassemia minor, and 1 patient with unstable hemoglobin disease. Conclusion The number of patients diagnosed with hemoglobinopathies and RBC enzymopathies has increased considerably since the previous survey on HHA in Korea, dated from 1997 to 2006. This is likely the result of improved diagnostic techniques. Nevertheless, there is still a need for more sensitive diagnostic tests utilizing flow cytometry and for better standardization of test results to improve the accuracy of diagnosis of RBC membranopathies in Korea. Additionally, more accurate assays for the identification of RBC enzymopathies are warranted. PMID:24086942

Park, Eun Sil; Jung, Hye Lim; Kim, Hee-Jin; Park, Sung Sup; Bae, Soon Hwan; Shin, Hee Young; Song, Sang Hoon; Koh, Kyung-Nam; Lyu, Chuhl Joo; Lim, Young Tak; Han, Dong Kyun

2013-01-01

51

A case of autoimmune hemolytic anemia with anti-D specificity in a one-year-old  

PubMed Central

While antibodies to antigens in the Rh group are common causes of warm autoimmune hemolytic anemia, specificity for only the D-antigen is rare in autoimmune hemolysis in pediatric patients. This case reports an anti-D associated with severe hemolytic anemia (Hb = 2.1 g/dL) in a previously healthy 14-month-old who presented with a three-day history of low-grade fevers and vomiting. Because of his severe anemia, on admission to the hospital he was found to have altered mental status, metabolic acidosis, abnormal liver function tests, and a severe coagulopathy. He was successfully resuscitated with uncrossmatched units of Group O, Rh-negative blood, and following corticosteroid therapy he had complete resolution of his anti-D-mediated hemolysis. PMID:24046918

Bercovitz, Rachel S.; Macy, Margaret; Ambruso, Daniel R.

2014-01-01

52

T cell deficiency in patients with autoimmune hemolytic anemia ('warm type').  

PubMed

19 patients with chronic 'warm type' autoimmune hemolytic anemia were studied for abnormalities of cellular immune reactions. Evidence was obtained for a reduction of rosette-forming cells (RFC). Lymphocytotoxic antibodies were present in only 8 patients and correlated, with only one exception, with a reduced number of RFC. No significant deviation from normal ranges of the three major immunoglobulin classes in the patients' sera were found. C3 and C4 complement components were also, with one exception, within normal limits. In 18 of 19 patients no apparent association existed between the type or the amount of autoantibodies and/or complement components fixed on red cells and the levels of the respective immunoglobulins or complement in the sera. PMID:1084624

Krger, J; Rahman, A; Mogk, K U; Mueller-Eckhardt, C

1976-01-01

53

Erythrocytic Pyruvate Kinase Mutations Causing Hemolytic Anemia, Osteosclerosis, and Secondary Hemochromatosis in Dogs  

PubMed Central

Background Erythrocytic pyruvate kinase (PK) deficiency, first documented in Basenjis, is the most common inherited erythroenzymopathy in dogs. Objectives To report 3 new breed-specific PK-LR gene mutations and a retrospective survey of PK mutations in a small and selected group of Beagles and West Highland White Terriers (WHWT). Animals Labrador Retrievers (2 siblings, 5 unrelated), Pugs (2 siblings, 1 unrelated), Beagles (39 anemic, 29 other), WHWTs (22 anemic, 226 nonanemic), Cairn Terrier (n = 1). Methods Exons of the PK-LR gene were sequenced from genomic DNA of young dogs (<2 years) with persistent highly regenerative hemolytic anemia. Results A nonsense mutation (c.799C>T) resulting in a premature stop codon was identified in anemic Labrador Retriever siblings that had osteosclerosis, high serum ferritin concentrations, and severe hepatic secondary hemochromatosis. Anemic Pug and Beagle revealed 2 different missense mutations (c.848T>C, c.994G>A, respectively) resulting in intolerable amino acid changes to protein structure and enzyme function. Breed-specific mutation tests were developed. Among the biased group of 248 WHWTs, 9% and 35% were homozygous (affected) and heterozygous, respectively, for the previously described mutation (mutant allele frequency 0.26). A PK-deficient Cairn Terrier had the same insertion mutation as the affected WHWTs. Of the selected group of 68 Beagles, 35% were PK-deficient and 3% were carriers (0.37). Conclusions and Clinical Importance Erythrocytic PK deficiency is caused by different mutations in different dog breeds and causes chronic severe hemolytic anemia, hemosiderosis, and secondary hemochromatosis because of chronic hemolysis and, an as yet unexplained osteosclerosis. The newly developed breed-specific mutation assays simplify the diagnosis of PK deficiency. PMID:22805166

Gultekin, G. Inal; Raj, K.; Foureman, P.; Lehman, S.; Manhart, K.; Abdulmalik, O.; Giger, U.

2013-01-01

54

The simultaneous incidence of acute pancreatitis and autoimmune hemolytic anemia: a rare duo in a patient with SLE  

PubMed Central

A young female presented with acute abdominal pain of two days duration consistent with acute pancreatitis. During her stay in the hospital she had a sudden drop in hemoglobin to 6 g/dl without any overt blood loss. On evaluation, it was evident that she had acute pancreatitis, in addition to displaying features of autoimmune hemolytic anemia. She had been a known case of systemic lupus erythematosus (SLE) and had discontinued her treatment. She was managed with methylprednisolone pulse therapy. Her clinical condition improved, and she has been regularly attending our clinic for the last 2 years. According to a literature search in Medline, it would appear that this is the first report of a case in which SLE with autoimmune hemolytic anemia has been associated with acute pancreatitis in a single case. PMID:25276114

Masoodi, Ibrahim

2014-01-01

55

Hemolytic anemia as a result of piperacillin/tazobactam administration: a case report and discussion of pathophysiology.  

PubMed

We report a case of a 19-year-old woman with cystic fibrosis who presented with hemolytic anemia during a course of piperacillin/tazobactam. The patient was initially managed with the replacement of blood products; however, she continued to show signs of hemolysis. Laboratories were obtained confirming antibody formation to piperacillin/tazobactam, and she was given a single infusion of intravenous immunoglobulin. Following the infusion, the patient did not require administration of any further blood products and achieved stable red blood cell counts. Early recognition of hemolytic anemia secondary to piperacillin/tazobactam with the administration of intravenous immunoglobulin may shorten the duration of hospitalization and quantity of blood products required for the stabilization of red blood cell counts. PMID:24005557

Zanetti, Richard C; Biswas, Abhik K

2013-09-01

56

Coombs-positive hemolytic anemia secondary to brown recluse spider bite: a review of the literature and discussion of treatment.  

PubMed

The bite of the brown recluse spider (Loxosceles reclusa) typically results in local, dermonecrotic skin lesions. Rarely, these bites may precipitate systemic disturbances of varying severity collectively known as systemic loxoscelism. The more severe systemic alterations attributed to the venom of this arachnid include hemolytic anemia, multiorgan failure, disseminated intravascular coagulation, or even death. Coombs-positive hemolysis associated with brown recluse spider bites has rarely been documented in the literature. We report 2 cases of systemic loxoscelism in young women associated with severe Coombs-positive hemolytic anemia and systemic symptoms requiring hospitalization. Both patients were treated with aggressive wound care, hematologic monitoring with blood transfusion, and intravenous fluid replacement. Recovery was excellent in both cases. We review the literature and discuss the controversies surrounding the treatment of more severe brown recluse bite reactions. PMID:15663070

Lane, David R; Youse, Jeremy S

2004-12-01

57

Chapter 3 Hemolytic anemias due to erythrocyte enzyme deficiencies  

Microsoft Academic Search

Red blood cells can only fulfil their functions over the normal period of approximately 120 days with 1.7 105 circulatory cycles efficiently if they withstand external and internal loads. This requires ATP and redox equivalents, which have to be permanently regenerated by the energy and redox metabolism. These pathways are neccessary to maintain the biconcave shape of the cells,

Gisela Jacobasch; Samuel M. Rapoport

1996-01-01

58

Megadose Methylprednisolone (MDMP) Treatment in a Patient with Autoimmune Hemolytic Anemia (AIHA) Resistant to Conventional Corticosteroid Administration: A Case Report  

PubMed Central

A female in the Netherlands with severe autoimmune hemolytic anemia (AIHA) was treated with conventional corticosteroid (2 mg/kg/d in divided doses) and blood transfusions for 18 months without improvement. The presented patient responded to megadose methylprednisolone (MDMP) 30 mg/kg/d for 3 d, followed by 20 mg/kg for 4 d, and subsequently 10, 5, 2, and 1 mg/kg/d each for 1 week. Conflict of interest:None declared. PMID:24385786

Ozsoylu, Sinasi; Berenschot, Henriette WA

2013-01-01

59

Hemolytic uremic syndrome due to homozygous factorH deficiency  

Microsoft Academic Search

The majority of complement factorH mutations associated with atypical hemolytic uremic syndrome (HUS) are heterozygous. Homozygous\\u000a mutations causing atypical hemolytic uremic syndrome are rare. We report a 7-month-old boy with HUS, severe hypocomplementemia\\u000a (low C3 and normal C4 levels), and extremely low circulating levels of factorH. Genetic analysis showed homozygous 4bp deletion\\u000a in the gene encoding factorH in the patient,

Sidharth Kumar Sethi; Dragon-Durey Marie-Agnes; Neelam Thaker; Pankaj Hari; Arvind Bagga

2009-01-01

60

Establishment of permanent chimerism in a lactate dehydrogenase-deficient mouse mutant with hemolytic anemia  

SciTech Connect

Pluripotent hemopoietic stem cell function was investigated in the homozygous muscle type lactate dehydrogenase (LDH-A) mutant mouse using bone marrow transplantation experiments. Hemopoietic tissues of LDH-A mutants showed a marked decreased in enzyme activity that was associated with severe hemolytic anemia. This condition proved to be transplantable into wild type mice (+/+) through total body irradiation (TBI) at a lethal dose of 8.0 Gy followed by engraftment of mutant bone marrow cells. Since the mutants are extremely radiosensitive (lethal dose50/30 4.4 Gy vs 7.3 Gy in +/+ mice), 8.0-Gy TBI followed by injection of even high numbers of normal bone marrow cells did not prevent death within 5-6 days. After a nonlethal dose of 4.0 Gy and grafting of normal bone marrow cells, a transient chimerism showing peripheral blood characteristics of the wild type was produced that returned to the mutant condition within 12 weeks. The transfusion of wild type red blood cells prior to and following 8.0-Gy TBI and reconstitution with wild type bone marrow cells prevented the early death of the mutants and permanent chimerism was achieved. The chimeras showed all hematological parameters of wild type mice, and radiosensitivity returned to normal. It is concluded that the mutant pluripotent stem cells are functionally comparable to normal stem cells, emphasizing the significance of this mouse model for studies of stem cell regulation.

Datta, T.; Doermer, P.

1987-12-01

61

Alemtuzumab plus cyclosporine treatment of the autoimmune hemolytic anemia in an adult bowel transplant.  

PubMed

An adult male underwent a bowel transplant for tufting enteropathy, receiving alemtuzumab, tacrolimus, and steroids as immunosuppressants. Five years later, he developed an autoimmune hemolytic anemia (AIHA), anti-IgG positive, with reduced reticulocyte count, leukopenia, and thrombocytopenia with antiplatelet antibodies. After an unsuccessful initial treatment with high dose steroids, reduction in tacrolimus dose, and intravenous immunoglobulin (IVIG), a bone marrow biopsy revealed absence of erythroid maturation with precursor hyperplasia. The patient was switched to sirolimus and received four doses of rituximab plus two courses of plasmapheresis, which decreased his transfusion requirements. After a febrile episode one month later, the AIHA relapsed with corresponding decreases in platelet and leukocyte count: cyclosporine A (CsA) was started with a second course of rituximab and IVIG without response, even though repeat bone marrow biopsy did not reveal morphology correlated to an acquired pure red cell aplasia (APRCA). Considering the similarity in his clinical and laboratory findings to APRCA, alemtuzumab was added (three doses over a week) with CsA followed by steroids. The patient was eventually discharged transfusion-independent, with increasing hemoglobin (Hb) levels and normal platelet and leukocyte count. One year later he is still disease-free with functioning graft. PMID:25177510

Lauro, A; Stanzani, M; Finelli, C; Zanfi, C; Morelli, M C; Pasqualini, E; Dazzi, A; Ravaioli, M; Di Simone, M; Giudice, V; Pironi, L; Pinna, A D

2014-01-01

62

Acute generalized exanthematous pustulosis and Coombs-positive hemolytic anemia in a child following Loxosceles reclusa envenomation.  

PubMed

Previously reported cases of acute generalized exanthematous pustulosis secondary to brown recluse spider bite have been questioned due to lack of identification of the spider or because of the concomitant administration of antibiotics. We report a 9-year-old boy who arrived at the emergency department with a confirmed Loxosceles reclusa bite to the neck. On the third day of hospitalization, he developed hundreds of monomorphous, sterile pustules, initially in intertriginous areas. The eruption disseminated and was followed by pinpoint desquamation typical for acute generalized exanthematous pustulosis. During this he also developed late onset Coombs-positive hemolytic anemia and systemic loxoscelism. Sphingomyelinase in Loxosceles venom induces the production of interleukin-8 and granulocyte-macrophage colony-stimulating factor, cytokines involved in the pathogenesis of acute generalized exanthematous pustulosis, providing a mechanism by which Loxosceles reclusa bite may trigger acute generalized exanthematous pustulosis. We suggest that this case adds Loxosceles envenomation to the spectrum of agents that can trigger acute generalized exanthematous pustulosis. PMID:22082464

Lane, Leanna; McCoppin, Holly H; Dyer, Jonathan

2011-01-01

63

Use of human immunoglobulin in addition to glucocorticoids for the initial treatment of dogs with immune-mediated hemolytic anemia  

Microsoft Academic Search

OBJECTIVE: To determine the utility of human intravenous immunoglobulin (hIVIG) for the initial treatment of canine immune-mediated hemolytic anemia (IMHA).\\u000aDESIGN: Blinded, randomized, clinical trial.\\u000aSETTING: Veterinary teaching hospital.\\u000aANIMALS: Twenty-eight, client-owned dogs with primary IMHA.\\u000aINTERVENTIONS: At enrollment, after diagnosis of IMHA, dogs were randomly assigned to receive either hIVIG or placebo, in a blinded fashion. For the next

Megan F. Whelan; Therese E. OToole; Daniel L. Chan; Elizabeth A. Rozanski; Armelle M. deLaforcade; Sybil L. Crawford; Susan M. Cotter

2009-01-01

64

Alterations in Bone and Erythropoiesis in Hemolytic Anemia: Comparative Study in Bled, Phenylhydrazine-Treated and Plasmodium-Infected Mice  

PubMed Central

Sustained erythropoiesis and concurrent bone marrow hyperplasia are proposed to be responsible for low bone mass density (BMD) in chronic hemolytic pathologies. As impaired erythropoiesis is also frequent in these conditions, we hypothesized that free heme may alter marrow and bone physiology in these disorders. Bone status and bone marrow erythropoiesis were studied in mice with hemolytic anemia (HA) induced by phenylhydrazine (PHZ) or Plasmodium infection and in bled mice. All treatments resulted in lower hemoglobin concentrations, enhanced erythropoiesis in the spleen and reticulocytosis. The anemia was severe in mice with acute hemolysis, which also had elevated levels of free heme and ROS. No major changes in cellularity and erythroid cell numbers occurred in the bone marrow of bled mice, which generated higher numbers of erythroid blast forming units (BFU-E) in response to erythropoietin. In contrast, low numbers of bone marrow erythroid precursors and BFU-E and low concentrations of bone remodelling markers were measured in mice with HA, which also had blunted osteoclastogenesis, in opposition to its enhancement in bled mice. The alterations in bone metabolism were accompanied by reduced trabecular bone volume, enhanced trabecular spacing and lower trabecular numbers in mice with HA. Taken together our data suggests that hemolysis exerts distinct effects to bleeding in the marrow and bone and may contribute to osteoporosis through a mechanism independent of the erythropoietic stress. PMID:23029401

Moreau, Robert; Tshikudi Malu, Diane; Dumais, Mathieu; Dalko, Esther; Gaudreault, Veronique; Romero, Hugo; Martineau, Corine; Kevorkova, Olha; Dardon, Jaime Sanchez; Dodd, Erin Lynn; Bohle, David Scott; Scorza, Tatiana

2012-01-01

65

Hemolytic Disease of the Newborn Due to Anti-c Isoimmunization: A Case Report.  

PubMed

The Rhesus (Rh) blood group is one of the most complex blood groups known in humans. It has remained of primary importance in obstetrics, being the main cause of hemolytic disease of the newborn (HDN). Anti-D causes the most severe form of HDN. Other Rh allo antibodies that are capable of causing severe HDN include anti-c, which clinically is the most important Rh antigen after the D antigen. We report a case of hemolytic disease of the newborn due to Rh anti-c in an infant of an Rh positive mother. PMID:24426362

Sheeladevi, C S; Suchitha, S; Manjunath, G V; Murthy, Srinivas

2013-09-01

66

A Case of Hemolytic Disease of the Newborn Infant due to Anti-? (Cellano)  

Microsoft Academic Search

Hemolytic disease of the newborn infant (HDN) due to anti-? (Cellano) is very uncommon in Caucasians. We report here a case of anti-? HDN. The anti-? alloimmunization appeared in the mother during her fifth pregnancy. This HDN needed an exchange transfusion immediately after delivery. The clinical outcome of the newborn infant was good.Copyright 1991 S. Karger AG, Basel

P. Moncharmont; F. Juron-Dupraz; M. Doillon; M. Vignal; P. Debeaux

1991-01-01

67

Severe refractory autoimmune hemolytic anemia with five-year complete hematologic response to third course of treatment with rituximab: a case report  

PubMed Central

Introduction Rituximab is an emerging treatment for autoimmune hemolytic anemia. We report the case of a patient with a five-year complete hematologic response to a third course of treatment with rituximab. Cases of response to rituximab re-treatments have been reported, but none to our knowledge that failed multiple prior treatments and achieved as durable a response. Case presentation A 45-year-old Hispanic man presented at age 26 with darkening urine and cold intolerance. His blood tests revealed elevated lactic dehydrogenase and bilirubin, a hemoglobin level of 7.4g/dL, and a positive Coombs test for complement C3 and immunoglobulin G antibody. A diagnosis of autoimmune hemolytic anemia was made. After failing multiple therapies including prednisone, splenectomy, immunoglobulin, cyclosporine, danocrine and azathioprine, our patient was treated with a four-week course of rituximab at a dose of 375mg/m2 weekly, 10 years following initial presentation. He achieved a rapid and complete hematologic response that lasted 25 months. Re-treatment with the same course of rituximab prompted a second response that lasted 18 months. A third re-treatment has achieved an ongoing five-year complete hematologic response. Conclusions This is an unusual case of a durable five-year remission of autoimmune hemolytic anemia with rituximab re-treatment following relapse after two prior courses of rituximab and despite the persistence of immunoglobulin G and complement-coated red blood cells. No mechanistic explanations for improved response to rituximab re-treatment in autoimmune hemolytic anemia have been reported in the literature. Future studies of rituximab or other B cell-targeting antibodies in the treatment of autoimmune hemolytic anemia should explore autoantibody immunoglobulin G subclass switching and alterations in complement inhibitory proteins on red blood cell membranes as potential correlates of hematologic response. PMID:24889270

2014-01-01

68

Reappraisal of the Etiology of Extracorpuscular Non-Autoimmune Acquired Hemolytic Anemia in 2657 Hospitalized Patients with Non-Neoplastic Disease  

PubMed Central

INTRODUCTION Unlike autoimmune hemolytic anemia (AIHA), literature on the etiological study of non-autoimmune hemolytic anemia (non-AIHA) is scarce. The incidence and prevalence of non-AIHA in different geographic regions are largely unknown perhaps owing to the lack of perspective investigation and different profiles of etiologies from different geographic regions. We aimed to examine the real-world etiology or mechanisms of the non-hereditary non-AIHA from a nationwide population-based administrative claim database in Taiwan. PATIENTS AND METHODS The National Health Insurance Research Database of Taiwan was adopted for this research. The studied population was total inpatient claim records including both pediatric and adult patients, contributed by a population of 23 million insured individuals in Taiwan. From 2002 to 2008, we retrieved 3,903 patients having no pre-existing malignancy discharged after inpatient management for acquired hemolytic anemia, which was defined as coding in discharge diagnoses containing ICD-9-CM code 283. By contrast, ICD-9-CM code 282 and all of the sub-codes are for hereditary hemolytic anemias. RESULTS AIHA accounted for 32% of the total cases. Among 2,657 patients with non-AIHA, mechanical or microangiopathic mechanism accounted for 19% of cases; hemolytic-uremic syndrome (HUS) 4%, hemoglobinuria because of hemolysis from external causes such as paroxysmal nocturnal hemoglobinuria (PNH) and march hemoglobinuria 7%, and chronic idiopathic hemolytic anemia or other unspecified non-AIHA 69%. We looked further for specific etiology or mechanism for this group of patients with non-hereditary extrinsic non-AIHA (n = 2,657). The explanatory disease states or conditions were splenomegaly; alcohol use disorder (spur cell hemolysis); heart-valve prosthesis; malignant hypertension; disseminated intravascular coagulation; transfusion reaction; dengue fever-induced hemolytic anemia; direct parasitization; snake, lizard, or spider bite; and Wilsons disease with internal toxin mechanism. All these cases can explain up to 34.6% of all the non-hereditary extrinsic non-AIHA cases. Fragmentation hemolysis (HUS, heart-valve prosthesis, malignant hypertension, and disseminated intravascular coagulation) accounted for 7.4% of non-AIHA hospitalized patients with non-neoplastic disease. CONCLUSIONS This article is the first one to clearly demonstrate that the non-neoplastic-induced HUS requiring hospitalization cases in Taiwan, which has a population of over 23 million were 110 over a span of seven years, 16 cases per year. Although the etiologies of non-AIHA are well known and described in the literature, this work added the statistical percentages of the various etiologies of non-AIHA in Taiwan. PMID:24808725

Kok, Victor C; Lee, Chien-Kuan; Horng, Jorng-Tzong; Lin, Che-Chen; Sung, Fung-Chang

2014-01-01

69

Cocaine-induced microangiopathic hemolytic anemia mimicking idiopathic thrombotic thrombocytopenic purpura: A case report and review of the literature.  

PubMed

Our understanding of the pathogenesis of idiopathic thrombotic thrombocytopenic purpura (TTP) has increased, but remains incomplete, particularly with respect to cases of suspected TTP that are either unresponsive to therapeutic plasma exchange (TPE) or have normal ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type 1 motif 13) activity. A 53-year-old woman presented with severe anemia (hemoglobin 1.8 g/dL) and clinical and laboratory findings consistent with TTP in conjunction with acute cocaine use. The patient was treated with TPE until the pre-treatment ADAMTS13 activity was reported as normal without evidence of an inhibitor. TPE was stopped and the patient continued to improve without treatment. This patient's microangiopathic hemolytic anemia (MAHA) appeared to be secondary to cocaine use. The proposed pathogenesis is likely a combination of cocaine-induced vasoconstriction, vascular damage, platelet activation, and procoagulation. This is the fifth published report of cocaine-induced MAHA and to our knowledge the first with ADAMTS13 testing. J. Clin. Apheresis 29:284-289, 2014. 2014 Wiley Periodicals, Inc. PMID:24753113

Odronic, Shelley; Quraishy, NurJehan; Manroa, Pooja; Kier, Yelena; Koo, Anna; Figueroa, Priscilla; Hamilton, Aaron

2014-10-01

70

Clinical heterogeneity and predictors of outcome in primary autoimmune hemolytic anemia: a GIMEMA study of 308 patients.  

PubMed

The clinical outcome, response to treatment, and occurrence of acute complications were retrospectively investigated in 308 primary autoimmune hemolytic anemia (AIHA) cases and correlated with serological characteristics and severity of anemia at onset. Patients had been followed up for a median of 33 months (range 12-372); 60% were warm AIHA, 27% cold hemagglutinin disease, 8% mixed, and 5% atypical (mostly direct antiglobulin test negative). The latter 2 categories more frequently showed a severe onset (hemoglobin [Hb] levels ?6 g/dL) along with reticulocytopenia. The majority of warm AIHA patients received first-line steroid therapy only, whereas patients with mixed and atypical forms were more frequently treated with 2 or more therapy lines, including splenectomy, immunosuppressants, and rituximab. The cumulative incidence of relapse was increased in more severe cases (hazard ratio 3.08; 95% confidence interval, 1.44-6.57 for Hb ?6 g/dL; P < .001). Thrombotic events were associated with Hb levels ?6 g/dL at onset, intravascular hemolysis, and previous splenectomy. Predictors of a fatal outcome were severe infections, particularly in splenectomized cases, acute renal failure, Evans syndrome, and multitreatment (4 or more lines). The identification of severe and potentially fatal AIHA in a largely heterogeneous disease requires particular experienced attention by clinicians. PMID:25232059

Barcellini, Wilma; Fattizzo, Bruno; Zaninoni, Anna; Radice, Tommaso; Nichele, Ilaria; Di Bona, Eros; Lunghi, Monia; Tassinari, Cristina; Alfinito, Fiorella; Ferrari, Antonella; Leporace, Anna Paola; Niscola, Pasquale; Carpenedo, Monica; Boschetti, Carla; Revelli, Nicoletta; Villa, Maria Antonietta; Consonni, Dario; Scaramucci, Laura; De Fabritiis, Paolo; Tagariello, Giuseppe; Gaidano, Gianluca; Rodeghiero, Francesco; Cortelezzi, Agostino; Zanella, Alberto

2014-11-01

71

Evidence for a susceptibility gene (SLEH1) on chromosome 11q14 for systemic lupus erythematosus (SLE) families with hemolytic anemia  

PubMed Central

Hemolytic anemia is a forme fruste of systemic lupus erythematosus (SLE), being observed months or even years before the onset of other clinical manifestations in some patients. We hypothesized that hemolytic anemia in those SLE-affected patients would identify a group of SLE pedigrees that share a high degree of genetic homogeneity. From 160 multiplex SLE pedigrees, we sought evidence for linkage in 35 (16 African-American, 17 European-American, and 2 Hispanic) who had at least one SLE-affected patient with hemolytic anemia. Significant linkage was present at 11q14 in the 16 African-American pedigrees, yielding a maximum two-point logarithm of odds (LOD) score of 4.5 at D11S2002. The segregation pattern of SLE in these African-American pedigrees suggested a dominant mode of inheritance and, when maximized across penetrance and disease allele frequencies, produced a multipoint LOD of 4.7. Multipoint analysis yielded a multipoint heterogeneity LOD score of 3.6 (? = 0.63), again with maximum LOD at D11S2002. Finally, markers typed 7 centimorgans to either side of D11S2002 achieved LOD scores of 3 or better by using the maximized model, supporting linkage to 11q14. Clearly, pedigree ascertainment based on select clinical manifestations is an important tool, capable of revealing otherwise cryptic genetic linkages in complex genetic diseases. Thus, we show strong evidence for an SLE susceptibility gene, SLEH1, near D11S2002 in African-American pedigrees multiplex for SLE that have at least one SLE-affected patient with hemolytic anemia. PMID:12192084

Kelly, Jennifer A.; Thompson, Kevin; Kilpatrick, Jeff; Lam, Tom; Nath, Swapan K.; Gray-McGuire, Courtney; Reid, Jeff; Namjou, Bahram; Aston, Christopher E.; Bruner, Gail R.; Scofield, R. Hal; Harley, John B.

2002-01-01

72

Saudi Guidelines on the Diagnosis and Treatment of Pulmonary Hypertension: Pulmonary hypertension associated with hemolytic anemia  

PubMed Central

Hereditary hemoglobin disorders affecting the globin chain synthesis namely thalassemia syndromes and sickle cell disease (SCD) are the most common genetic disorders in human. Around 7% of the world population carries genes for these disorders, mainly the Mediterranean Basin, Middle and Far East, and Sub-Saharan Africa. An estimated 30 million people worldwide are living with sickle cell disease, while 60-80 million carry beta thalassemia trait. About 400,000 children are born with severe hemoglobinopathies each year. Cardiovascular complications of hemoglobinopathies include left and right ventricular (RV) dysfunction, arrhythmias, pericarditis, myocarditis, valvular heart disease, myocardial ischemia, and notably pulmonary hypertension (PH). Because of a unique pathophysiology, pulmonary hypertension associated with hemolytic disorders was moved from WHO group I to group V PH diseases. Treatment strategies are also unique and include blood transfusion, iron chelation, hydroxyurea, and oxygen therapy. The role of PH-specific agents has not been established. PMID:25077000

Saleemi, Sarfraz

2014-01-01

73

Saudi Guidelines on the Diagnosis and Treatment of Pulmonary Hypertension: Pulmonary hypertension associated with hemolytic anemia.  

PubMed

Hereditary hemoglobin disorders affecting the globin chain synthesis namely thalassemia syndromes and sickle cell disease (SCD) are the most common genetic disorders in human. Around 7% of the world population carries genes for these disorders, mainly the Mediterranean Basin, Middle and Far East, and Sub-Saharan Africa. An estimated 30 million people worldwide are living with sickle cell disease, while 60-80 million carry beta thalassemia trait. About 400,000 children are born with severe hemoglobinopathies each year. Cardiovascular complications of hemoglobinopathies include left and right ventricular (RV) dysfunction, arrhythmias, pericarditis, myocarditis, valvular heart disease, myocardial ischemia, and notably pulmonary hypertension (PH). Because of a unique pathophysiology, pulmonary hypertension associated with hemolytic disorders was moved from WHO group I to group V PH diseases. Treatment strategies are also unique and include blood transfusion, iron chelation, hydroxyurea, and oxygen therapy. The role of PH-specific agents has not been established. PMID:25077000

Saleemi, Sarfraz

2014-07-01

74

AMPD3-deficient mice exhibit increased erythrocyte ATP levels but anemia not improved due to PK deficiency.  

PubMed

AMP deaminase (AMPD) catalyzes AMP to IMP and plays an important role in energy charge and nucleotide metabolism. Human AMPD3 deficiency is a type of erythrocyte-specific enzyme deficiency found in individuals without clinical symptoms, although an increased level of ATP in erythrocytes has been reported. To better understand the physiological and pathological roles of AMPD3 deficiency, we established a line of AMPD3-deficient [A3(-/-)] mice. No AMPD activity and a high level of ATP were observed in erythrocytes of these mice, similar to human RBC-AMPD3 deficiency, while other characteristics were unremarkable. Next, we created AMPD3 and pyruvate kinase (PK) double-deficient [PKA(-/-,-/-)] mice by mating A3(-/-) mice with CBA-Pk-1slc/Pk-1slc mice [PK(-/-)], a spontaneous PK-deficient strain showing hemolytic anemia. In PKA(-/-,-/-) mice, the level of ATP in red blood cells was increased 1.5 times as compared to PK(-/-) mice, although hemolytic anemia in those animals was not improved. In addition, we observed osmotic fragility of erythrocytes in A3(-/-) mice under fasting conditions. In contrast, the ATP level in erythrocytes was elevated in A3(-/-) mice as compared to the control. In conclusion, AMPD3 deficiency increases the level of ATP in erythrocytes, but does not improve anemia due to PK deficiency and leads to erythrocyte dysfunction. PMID:23078545

Cheng, Jidong; Morisaki, Hiroko; Toyama, Keiko; Ikawa, Masahito; Okabe, Masaru; Morisaki, Takayuki

2012-11-01

75

Narrative Review: Paroxysmal Nocturnal Hemoglobinuria: The Physiology of Complement-Related Hemolytic Anemia  

NSDL National Science Digital Library

Physiology in Medicine review article. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare hematopoietic stem-cell disorder caused by a somatic mutation in a gene known as phosphatidylinositol glycan class A (PIGA). It may arise de novo or in the setting of acquired aplastic anemia.The absence of GPI-anchored proteins leads to complement-mediated intravascular hemolysis, because 2 important complement regulatory proteins (CD55 and CD59) are missing from PNH cells. Therapeutic options include supportive care, bone marrow transplantation, and monoclonal antibody therapy with the terminal complement inhibitor eculizumab.

Robert A. Brodsky (Johns Hopkins Medicine)

2008-04-15

76

High Pathogenic Potential of Low-Affinity Autoantibodies in Experimental Autoimmune Hemolytic Anemia  

Microsoft Academic Search

Summary To assess the potency of low-affinity anti-red blood cell (RBC) autoantibodies in the induc- tion of anemia, we generated an immunoglobulin (Ig)G2a class-switch variant of a 4C8 IgM anti-mouse RBC autoantibody, and compared its pathogenic potential with that of its IgM isotype and a high-affinity 34-3C IgG2a autoantibody. The RBC-binding activity of the 4C8 IgG2a variant was barely detectable,

Liliane Fossati-Jimack; Luc Reininger; Yves Chicheportiche; Raphael Clynes; Jeffrey V. Ravetch; Tasuku Honjo; Shozo Izui

2010-01-01

77

Rituximab is an effective and safe therapeutic alternative in adults with refractory and severe autoimmune hemolytic anemia.  

PubMed

Rituximab-induced B-cell depletion has been proven to be a useful therapy for autoimmune hemolytic anemia (AIHA). The aim of this retrospective study was to evaluate the effectiveness of rituximab in the treatment of 36 patients with AIHA refractory to several treatments. These patients had received a median of four (one to eight) previous treatments, and 13 patients had undergone splenectomy. Rituximab was administered by intravenous infusion at a dose of 375 mg/m(2) once weekly for four doses in 29 patients, and 7 patients received one to six doses. Overall, 28 (77%) of 36 patients achieved response. Twenty-two patients (61%) reached a complete response (CR), and 6 patients (16%) obtained a partial response. All patients that reached CR (61%) were able to maintain the response during more than 6 months, with a median follow-up of 14 months (1-86 months). Sixteen patients maintained response for more than 1 year. The predictors of maintained response were achievement of CR and negative Coombs test result. Splenectomized patients showed a better response rate than those nonsplenectomized. Rituximab was well tolerated, and only one patient presented a transitory rash during infusion. Rituximab induced clinical responses in multitreated severe refractory both warm and cold AIHA patients with little toxicity, and consequently, this therapy should be considered as an early therapeutic option in this setting. PMID:20526716

Pealver, Francisco Javier; Alvarez-Larrn, Alberto; Dez-Martin, Jose Luis; Gallur, Laura; Jarque, Isidro; Caballero, Dolores; Daz-Mediavilla, Joaqun; Bustelos, Rosala; Fernndez-Aceero, Mara Jess; Cabrera, Jos Rafael

2010-11-01

78

A Deep Intronic Mutation in the Ankyrin-1 Gene Causes Diminished Protein Expression Resulting in Hemolytic Anemia in Mice  

PubMed Central

Linkage between transmembrane proteins and the spectrin-based cytoskeleton is necessary for membrane elasticity of red blood cells. Mutations of the proteins that mediate this linkage result in various types of hemolytic anemia. Here we report a novel N-ethyl-N-nitrosourea?induced mutation of ankyrin-1, named hema6, which causes hereditary spherocytosis in mice through a mild reduction of protein expression. The causal mutation was traced to a single nucleotide transition located deep into intron 13 of gene Ank1. In vitro minigene splicing assay revealed two abnormally spliced transcripts containing cryptic exons from fragments of Ank1 intron 13. The inclusion of cryptic exons introduced a premature termination codon, which leads to nonsense-mediated decay of the mutant transcripts in vivo. Hence, in homozygous mice, only wild-type ankyrin-1 is expressed, albeit at 70% of the level in wild-type mice. Heterozygotes display a similar hereditary spherocytosis phenotype stemming from intermediate protein expression level, indicating the haploinsufficiency of the mutation. Weakened linkage between integral transmembrane protein, band 3, and underlying cytoskeleton was observed in mutant mice as the result of reduced high-affinity binding sites provided by ankyrin-1. Hema6 is the only known mouse mutant of Ank1 allelic series that expresses full-length canonical ankyrin-1 at a reduced level, a fact that makes it particularly useful to study the functional impact of ankyrin-1 quantitative deficiency. PMID:23934996

Huang, Hua; Zhao, PengXiang; Arimatsu, Kei; Tabeta, Koichi; Yamazaki, Kazuhisa; Krieg, Lara; Fu, Emily; Zhang, Tian; Du, Xin

2013-01-01

79

IgG red blood cell autoantibodies in autoimmune hemolytic anemia bind to epitopes on red blood cell membrane band 3 glycoprotein  

SciTech Connect

Red blood cell (RBC) autoantibodies from patients with IgG warm-type autoimmune hemolytic anemia were labeled with iodine 125 and their RBC binding behavior characterized. Epitope-bearing RBC membrane polypeptides were identified after autoantibody immunoprecipitation of labeled membranes and immunoblotting. Immunoaffinity isolation of labeled membrane proteins with 12 different IgG hemolytic autoantibodies with protein A-agarose revealed a major polypeptide at Mr 95 to 110 kd, which coelectrophoresed on sodium dodecylsulfate-polyacrylamide gel electrophoresis with a membrane component isolated with sheep IgG anti-band 3. Immunoprecipitation studies with chymotrypsinized RBCs resulted in the recovery of two labeled membrane polypeptides with molecular weights characteristically resulting from the chymotryptic fragmentation of band 3. Immunoblotting with sheep IgG anti-band 3 of the immunoprecipitated polypeptides confirmed that hemolytic autoantibody binding led to recovery of band 3 or its fragments. Two 125I-labeled IgG hemolytic autoantibodies showed binding behavior consistent with epitope localization on band 3. The labeled RBC autoantibodies bound immunospecifically to all types of human RBC tested, including those of rare Rh type (Rh-null, D--) at a site density of approximately 10(6) per RBC. The 125I-IgG in two labeled autoantibodies was 84% and 92% adsorbable by human and higher nonhuman primate RBCs. Antigen-negative animal RBC bound less than 10%, consistent with immunospecific RBC binding. IgG-1 was the major subclass in five autoantibodies tested; one of six fixed complement; and autoantibody IgG appeared polyclonal by isoelectric focusing. We conclude that IgG eluted from RBCs of patients with autoimmune hemolytic anemia consists predominantly of a single totally RBC-adsorbable antibody population that binds to antigenic determinants on band 3.

Victoria, E.J.; Pierce, S.W.; Branks, M.J.; Masouredis, S.P. (Univ. of California, San Diego (USA))

1990-01-01

80

Assessment of the Red Cell Proteome of Young Patients with Unexplained Hemolytic Anemia by Two-Dimensional Differential In-Gel Electrophoresis (DIGE)  

PubMed Central

Erythrocyte cytosolic protein expression profiles of children with unexplained hemolytic anemia were compared with profiles of close relatives and controls by two-dimensional differential in-gel electrophoresis (2D-DIGE). The severity of anemia in the patients varied from compensated (i.e., no medical intervention required) to chronic transfusion dependence. Common characteristics of all patients included chronic elevation of reticulocyte count and a negative workup for anemia focusing on hemoglobinopathies, morphologic abnormalities that would suggest a membrane defect, immune-mediated red cell destruction, and evaluation of the most common red cell enzyme defects, glucose-6-phosphate dehydrogenase and pyruvate kinase deficiency. Based upon this initial workup and presentation during infancy or early childhood, four patients classified as hereditary nonspherocytic hemolytic anemia (HNSHA) of unknown etiology were selected for proteomic analysis. DIGE analysis of red cell cytosolic proteins clearly discriminated each anemic patient from both familial and unrelated controls, revealing both patient-specific and shared patterns of differential protein expression. Changes in expression pattern shared among the four patients were identified in several protein classes including chaperons, cytoskeletal and proteasome proteins. Elevated expression in patient samples of some proteins correlated with high reticulocyte count, likely identifying a subset of proteins that are normally lost during erythroid maturation, including proteins involved in mitochondrial metabolism and protein synthesis. Proteins identified with patient-specific decreased expression included components of the glutathione synthetic pathway, antioxidant pathways, and proteins involved in signal transduction and nucleotide metabolism. Among the more than 200 proteins identified in this study are 21 proteins not previously described as part of the erythrocyte proteome. These results demonstrate the feasibility of applying a global proteomic approach to aid characterization of red cells from patients with hereditary anemia of unknown cause, including the identification of differentially expressed proteins as potential candidates with a role in disease pathogenesis. PMID:22509282

von Lohneysen, Katharina; Scott, Thomas M.; Soldau, Katrin; Xu, Xiuling; Friedman, Jeffrey S.

2012-01-01

81

[Anemia, this time without iron deficiency].  

PubMed

The approach to anemia by the primary care physician is to diagnose treatable causes like nutritional deficiencies, renal insufficiency, chronic inflammatory disease or hemolysis. Measurement of reticulocytes allows a distinction of hemolytic and non-hemolytic anemia. Among hemolytic anemias it is important to recognize rare but potentially severe diseases as autoimmune hemolytic anemia, microangiopathic anemia and certain hereditary anemias. Non-hemolytic anemias can be categorized in microcytic, normocytic and macrocytic subtypes. This allows a rational stepwise approach for each category. Most anemias can be correctly classified, evaluated for underlying disease and treated by the primary care physician. PMID:17405534

Gregor, M

2007-03-14

82

A case of successful management with splenectomy of intractable ascites due to congenital dyserythropoietic anemia type II-induced cirrhosis  

PubMed Central

The congenital dyserythropoietic anemias comprise a group of rare hereditary disorders of erythropoiesis, characterized by ineffective erythropoiesis as the predominant mechanism of anemia and by characteristic morphological aberrations of the majority of erythroblasts in the bone marrow. Congenital dyserythropoietic anemia type II is the most frequent type. All types of congenital dyserythropoietic anemias distinctly share a high incidence of iron loading. Iron accumulation occurs even in untransfused patients and can result in heart failure and liver cirrhosis. We have reported about a patient who presented with liver cirrhosis and intractable ascites caused by congenital dyserythropoietic anemia type II. Her clinical course was further complicated by the development of autoimmune hemolytic anemia. Splenectomy was eventually performed which achieved complete resolution of ascites, increase of hemoglobin concentration and abrogation of transfusion requirements. PMID:16521204

Vassiliadis, Themistoklis; Garipidou, Vassilia; Perifanis, Vassilios; Tziomalos, Konstantinos; Giouleme, Olga; Patsiaoura, Kalliopi; Avramidis, Michalis; Nikolaidis, Nikolaos; Vakalopoulou, Sofia; Tsitouridis, Ioannis; Antoniadis, Antonios; Semertzidis, Panagiotis; Kioumi, Anna; Premetis, Evangelos; Eugenidis, Nikolaos

2006-01-01

83

Anemia  

MedlinePLUS

... risk for developing anemia: Rheumatoid arthritis or other autoimmune disease Kidney disease Cancer Liver disease Thyroid disease Inflammatory ... viral infections, exposure to toxic chemicals, drugs, and autoimmune diseases. Idiopathic aplastic anemia is the term used when ...

84

Graves' Disease Causing Pancytopenia and Autoimmune Hemolytic Anemia at Different Time Intervals: A Case Report and a Review of the Literature  

PubMed Central

Graves' disease (GD) is associated with various hematologic abnormalities but pancytopenia and autoimmune hemolytic anemia (AIHA) are reported very rarely. Herein, we report a patient with GD who had both of these rare complications at different time intervals, along with a review of the related literature. The patient was a 70-year-old man who, during a hospitalization, was also noted to have pancytopenia and elevated thyroid hormone levels. Complete hematologic workup was unremarkable and his pancytopenia was attributed to hyperthyroidism. He was started on methimazole but unfortunately did not return for followup and stopped methimazole after a few weeks. A year later, he presented with fatigue and weight loss. Labs showed hyperthyroidism and isolated anemia (hemoglobin 7?g/dL). He had positive direct Coombs test and elevated reticulocyte index. He was diagnosed with AIHA and started on glucocorticoids. GD was confirmed with elevated levels of thyroid stimulating immunoglobulins and thyroid uptake and scan. He was treated with methimazole and radioactive iodine ablation. His hemoglobin improved to 10.7?g/dL at discharge without blood transfusion. Graves' disease should be considered in the differential diagnosis of hematologic abnormalities. These abnormalities in the setting of GD generally respond well to antithyroid treatment. PMID:24319463

Kumar, Geetika; Dewani, Shabana; Diedrich, William A.; Gupta, Ankur

2013-01-01

85

Anemia  

MedlinePLUS

If you have anemia, your blood does not carry enough oxygen to the rest of your body. The most common cause of anemia is not having enough ... rich protein that gives the red color to blood. It carries oxygen from the lungs to the ...

86

Hemolytic anemia in hereditary pyrimidine 5'-nucleotidase deficiency. II. Effect of pyrimidine nucleotides and their derivatives on glycolytic and pentose phosphate shunt enzyme activity.  

PubMed

We evaluated the glycolytic intermediate concentrations from the erythrocytes of a patient with hereditary pyrimidine 5'-nucleotidase (P5'N) deficiency. Conclusive evidence for a metabolic block was not found. We evaluated the effects of the pyrimidine (cytidine and uridine) tri- and diphosphate nucleotides (CTP, CDP, UTP, UDP) and the choline and ethanolamine derivatives of CDP (CDP-choline, CDP-ethanolamine) on the activities of key enzymes of the Embden-Meyerhof pathway. CTP and UTP inhibited fructose-6-phosphate competitively for phosphofructokinase and phosphoenolpyruvate competitively for pyruvate kinase. In both cases, the Ki of the pyrimidine nucleotide and Km of the glycolytic substrate were above their intraerythrocytic concentrations. CTP was a competitive inhibitor of ADP for pyruvate kinase with a Ki near its intraerythrocytic concentration. CDP-choline and CDP-ethanolamine had no effect on the activities of Embden-Meyerhof or pentose phosphate shunt enzymes. Thus, the nature of the hemolytic anemia in hereditary P5'N deficiency remains enigmatic. PMID:6091951

Oda, E; Oda, S; Tomoda, A; Lachant, N A; Tanaka, K R

1984-08-31

87

Refractory autoimmune hemolytic anemia in a patient with DiGeorge syndrome treated successfully with plasma exchange: a case report and review of the literature.  

PubMed

Warm antibody autoimmune hemolytic anemia (AIHA) results from targeted antibodies towards the red blood cells (RBCs) and can be either idiopathic or secondary to certain diseases, such as autoimmune disorders or malignancy, drugs, or infection. Patients with DiGeorge syndrome are particularly vulnerable to autoimmune conditions secondary to thymic hypoplasia and dysfunction of the immune system. First-line therapy for AIHA consists of corticosteroids, with most patients showing signs of response. Relapses are not uncommon and are treated with splenectomy or rituximab. There is a paucity of reports in the literature regarding treatment options beyond this stage. Herein, we describe an unusual case of a 20-year-old female affected by DiGeorge syndrome with a history of immune thrombocytopenia (ITP), who presented with life-threatening AIHA. Standard first- and second-line therapeutic modalities were ineffective in controlling her disease and she ultimately underwent plasma exchange therapy with successful resolution of hemolysis. At her last follow-up, one year after her initial presentation, she remains clinically well without signs of hemolysis. We conclude that in refractory cases of warm AIHA, plasma exchange therapy can be a valuable tool in the therapeutic armamentarium. PMID:25079091

Damlaj, Moussab; Sguin, Chantal

2014-11-01

88

Molecular basis of inherited microcytic anemia due to defects in iron acquisition or heme synthesis  

PubMed Central

Microcytic anemia is the most commonly encountered anemia in general medical practice. Nutritional iron deficiency and ? thalassemia trait are the primary causes in pediatrics, whereas bleeding disorders and anemia of chronic disease are common in adulthood. Microcytic hypochromic anemia can result from a defect in globin genes, in heme synthesis, in iron availability or in iron acquisition by the erythroid precursors. These microcytic anemia can be sideroblastic or not, a trait which reflects the implications of different gene abnormalities. Iron is a trace element that may act as a redox component and therefore is integral to vital biological processes that require the transfer of electrons as in oxygen transport, oxidative phosphorylation, DNA biosynthesis and xenobiotic metabolism. However, it can also be pro-oxidant and to avoid its toxicity, iron metabolism is strictly controlled and failure of these control systems could induce iron overload or iron deficient anemia. During the past few years, several new discoveries mostly arising from human patients or mouse models have highlighted the implication of iron metabolism components in hereditary microcytic anemia, from intestinal absorption to its final inclusion into heme. In this paper we will review the new information available on the iron acquisition pathway by developing erythrocytes and its regulation, and we will consider only inherited microcytosis due to heme synthesis or to iron metabolism defects. This information could be useful in the diagnosis and classification of these microcytic anemias. PMID:19181781

Iolascon, Achille; De Falco, Luigia; Beaumont, Carole

2009-01-01

89

Anemia  

MedlinePLUS

... the first step toward anemia. If the body's iron stores aren't replenished at this point, continuing iron ... for several months to build back your body's iron stores. Back Continue Getting Enough Iron Some people feel ...

90

Anemia  

MedlinePLUS

... type of anemia happens when your red blood cells are destroyed by disease. Updated: March 2012 Posted: March 2012 2014 Health in Aging. All rights reserved. Feedback Site Map Privacy Policy ...

91

Iron-Deficiency Anemia Leading to Transient Ischemic Attacks due to Intraluminal Carotid Artery Thrombus  

PubMed Central

Reactive thrombocytosis secondary to iron-deficiency anemia (IDA) is a rare but recognized cause of stroke. We report the case of a patient with iron-deficiency anemia presenting with multiple transient ischemic attacks (TIA) due to intraluminal thrombus of an internal carotid artery. The putative mechanisms underlying anemia and stroke syndromes are not completely understood, and it is believed that iron deficiency may cause ischemic stroke by several potential mechanisms. Thrombocytosis is often associated with iron deficiency, and microcytosis produces a reduction in the red cell deformability and could produce a hypercoagulable state. The platelet count and function observed in iron-deficiency anemia could act synergistically to promote thrombus formation, especially in the setting of an underlying atherosclerotic disease. The presence of floating thrombus in a patient with clinical and MRI evidence of stroke represents a significant therapeutic dilemma and requires immediate decision about treatment. PMID:24109530

Batur Caglayan, H. Z.; Nazliel, B.; Irkec, C.; Dumlu, A.; Filiz, A.; Panpalli Ates, M.

2013-01-01

92

Hemolytic disease of the newborn due to anti-jkb: case report and review of the literature.  

PubMed

Although anti-Jkb is a well-defined cause of severe acute or delayed hemolytic transfusion reactions, it is rarely associated with severe Hemolytic Disease of the Newborn (HDN), even with high antibody titer. To date, only 13 cases have been reported, so the possible reasons for that still remain unclear. Most of HDN due to anti-Jkb are mild-to-moderate, and usually have a good prognosis. A 41-years-old woman, who had a positive antibody screening test in her 13th week of pregnancy, was sent to the blood bank for study before an amniocentesis. Antibody identification and red blood cell (RBC) phenotyping of the patient and his husband were performed, plus arrays study in the amniotic fluid. An anti-Jkb was identified in the patient's serum with a titer of 1:1, and her RBC phenotype was O Rh(D) positive, C(+), c(+), E(-), e(+), K(-), Jka(+), Jkb(-). The RBC genotype of the fetus was B Rh(D) positive, Jka(+), Jkb(+). Antibody titer remained stable and the pregnancy was uneventful. At birth, there was no need of phototherapy or exchange transfusion for the newborn and her Jk(b+) typing result was confirmed in a cord blood sample. Although most of HDN cases due to anti-Jkb have a good outcome, monitoring antibody titer should be done to prevent fatal complications. Furthermore, antenatal antibody screening should be performed in every pregnant woman irrespective of her Rh(D) antigen status in order to detect red cell alloimmunization to other clinically significant blood group antigens. PMID:24839369

Velasco Rodrguez, Diego; Prez-Segura, G; Jimnez-Ubieto, A; Rodrguez, M A; Montejano, L

2014-06-01

93

Hemolytic uremic syndrome associated with Clostridium difficile infection.  

PubMed

We report 3 cases of Clostridium difficile-associated hemolytic uremic syndrome (HUS) with biopsy proven renal thrombotic microangiopathy. Two patients with acute renal failure were kidney transplants recipients whereas the third patient developed renal failure in the native kidneys. The presentation was preceded by acute diarrhea and stool. Clostridium difficile toxin was detected in all the 3 patients. Stool studies were negative for Escherichia coli, Shigella dysenteriae and other enteric pathogens. The diagnosis of Clostridium difficile-associated hemolytic uremic syndrome was suspected due to presence of thrombocytopenia, microangiopathic hemolytic anemia and biopsy proven renal thrombotic microangiopathy without another clinically apparent cause. This case series suggest that Clostridium difficile infection may cause renal failure due to thrombotic microangiopathy (TMA) and should be considered in the differential diagnosis of diarrhea-associated HUS. PMID:23320969

Alvarado, Anthony S; Brodsky, Sergey V; Nadasdy, Tibor; Singh, Neeraj

2014-04-01

94

Lenoir et al., 1 Iron deficiency anemia due to matriptase-2 inactivation is dependent upon  

E-print Network

the reticuloendothelial system and dietary iron absorption by duodenal enterocytes1 . The liver-iron regulatory hormone expression is tightly regulated by body iron status and is dependent upon bone morphogenetic protein 6 (Bmp6Lenoir et al., 1 1 Iron deficiency anemia due to matriptase-2 inactivation is dependent upon

Paris-Sud XI, Université de

95

Acute hemolytic transfusion reactions due to multiple alloantibodies including anti-E, anti-c and anti-Jkb.  

PubMed Central

We report a case of two consecutive episodes of acute hemolytic transfusion reactions (HTRs) due to multiple alloantibodies in a 34-yr-old man who suffered from avascular necrosis of left femoral head. He received five units of packed red blood cells (RBCs) during surgery. Then the transfusion of packed RBCs was required nine days after the surgery because of the unexplained drop in hemoglobin level. The transfusion of the first two units resulted in fever and brown-colored urine, but he received the transfusion of another packed RBCs the next day. He experienced even more severe symptoms during the transfusion of the first unit. We performed antibody screening test, and it showed positive results. Multiple alloantibodies including anti-E, anti-c and anti-Jkb were detected by antibody identification study. Acute HTRs due to multiple alloantibodies were diagnosed, and the supportive cares were done for 6 days. We suggest the antibody screening test should be included in the panel of pretransfusion tests for safer transfusion, and it is particularly mandatory for the patients with multiple transfusions, pregnant women, and preoperative patients. PMID:14676451

Park, Tae Sung; Kim, Ki Uk; Jeong, Woo Jin; Kim, Hyung Hoi; Chang, Chulhun L.; Chung, Joo Seop; Cho, Goon Jae; Lee, Eun Yup; Son, Han Chul

2003-01-01

96

Atypical hemolytic uremic syndrome  

PubMed Central

Hemolytic uremic syndrome (HUS) is defined by the triad of mechanical hemolytic anemia, thrombocytopenia and renal impairment. Atypical HUS (aHUS) defines non Shiga-toxin-HUS and even if some authors include secondary aHUS due to Streptococcus pneumoniae or other causes, aHUS designates a primary disease due to a disorder in complement alternative pathway regulation. Atypical HUS represents 5 -10% of HUS in children, but the majority of HUS in adults. The incidence of complement-aHUS is not known precisely. However, more than 1000 aHUS patients investigated for complement abnormalities have been reported. Onset is from the neonatal period to the adult age. Most patients present with hemolytic anemia, thrombocytopenia and renal failure and 20% have extra renal manifestations. Two to 10% die and one third progress to end-stage renal failure at first episode. Half of patients have relapses. Mutations in the genes encoding complement regulatory proteins factor H, membrane cofactor protein (MCP), factor I or thrombomodulin have been demonstrated in 20-30%, 5-15%, 4-10% and 3-5% of patients respectively, and mutations in the genes of C3 convertase proteins, C3 and factor B, in 2-10% and 1-4%. In addition, 6-10% of patients have anti-factor H antibodies. Diagnosis of aHUS relies on 1) No associated disease 2) No criteria for Shigatoxin-HUS (stool culture and PCR for Shiga-toxins; serology for anti-lipopolysaccharides antibodies) 3) No criteria for thrombotic thrombocytopenic purpura (serum ADAMTS 13 activity > 10%). Investigation of the complement system is required (C3, C4, factor H and factor I plasma concentration, MCP expression on leukocytes and anti-factor H antibodies; genetic screening to identify risk factors). The disease is familial in approximately 20% of pedigrees, with an autosomal recessive or dominant mode of transmission. As penetrance of the disease is 50%, genetic counseling is difficult. Plasmatherapy has been first line treatment until presently, without unquestionable demonstration of efficiency. There is a high risk of post-transplant recurrence, except in MCP-HUS. Case reports and two phase II trials show an impressive efficacy of the complement C5 blocker eculizumab, suggesting it will be the next standard of care. Except for patients treated by intensive plasmatherapy or eculizumab, the worst prognosis is in factor H-HUS, as mortality can reach 20% and 50% of survivors do not recover renal function. Half of factor I-HUS progress to end-stage renal failure. Conversely, most patients with MCP-HUS have preserved renal function. Anti-factor H antibodies-HUS has favourable outcome if treated early. PMID:21902819

2011-01-01

97

How Is Hemolytic Anemia Treated?  

MedlinePLUS

... Search Form Advanced Search Search the NHLBI, use radio buttons below to select whole site or Disease and Conditions Index ... Research Research Resources Scientific Reports Technology Transfer ...

98

Hemolytic disease of newborn due to anti-Jk b in a woman with high risk pregnancy  

Microsoft Academic Search

This case illustrates the importance of blood group antibodies in antenatal serology other than Rh system as a cause of hemolytic disease of newborn (HDN). In India, antenatal antibody screening is done at majority of transfusion centers in only Rh (D) negative mothers. In this multigravida woman with high risk obstetrical history, an antenatal antibody screening by indirect antiglobulin test

Beenu Thakral; Sheetal Malhotra; Karan Saluja; Praveen Kumar; Neelam Marwaha

2010-01-01

99

Case Report: Severe Hemolytic Disease of the Newborn Due to anti-Dib Treated with Phototherapy and Intravenous Immunoglobulin  

Microsoft Academic Search

The Di b antigen usually occurs with high incidence, except in certain Asian and South American Indian populations. In general, hemolysis caused by anti-Dib is not severe and its clinical course is benign. We report a Korean neonate with severe hemolytic disease of the newborn caused by anti-Dib. The phenotype and genotype of the Diego blood group system of the

Eun-Jee Oh; Dong Wook Jekarl; Hyun-Sik Jang; Hae-Il Park; Yeon-Joon Park; Hyun Ah Choi; Chung-Sik Chun; Yonggoo Kim; Hyung Hoi Kim

100

Fanconi's anemia  

MedlinePLUS

... of blood cells. Fanconi's anemia is different from Fanconi syndrome , a rare kidney disorder. ... Fanconi's anemia is due to an abnormal gene that damages cells, which keeps them from repairing damaged DNA. ...

101

Anti-erythropoietin receptor antibody-associated pure red cell aplasia accompanied by Coombs-negative autoimmune hemolytic anemia in a patient with T cell/histiocyte-rich large B cell lymphoma.  

PubMed

A 79-year-old female diagnosed with T cell/histiocyte-rich large B cell lymphoma in complete remission after six cycles of rituximab-combined chemotherapy developed severe anemia, reticulocytopenia, and bone marrow erythroid hypoplasia. She was diagnosed with pure red cell aplasia (PRCA) accompanied by Coombs-negative autoimmune hemolytic anemia evidenced by a lack of glycophorin-A-positive cells in the bone marrow, haptoglobin under the detection level, and a high titer of RBC-bound IgG. Anti-erythropoietin receptor (EPOR) antibody was detected in the serum, and oligoclonal ?/? and ?/? T cells were also detected in her peripheral blood by Southern blotting analysis. Parvovirus B19 DNA was not detected by PCR. Although the treatment with rituximab had limited efficacy (specifically, only for hemolysis), subsequent cyclosporine therapy led to prompt recovery of erythropoiesis with the disappearance of anti-EPOR antibody and oligoclonal T cells. This is the first case report of anti-EPOR antibody-associated PRCA in a patient with malignant lymphoma treated successfully with cyclosporine. PMID:25096221

Fujimi, Akihito; Kamihara, Yusuke; Kanisawa, Yuji; Hashimoto, Akari; Nakajima, Chisa; Hayasaka, Naotaka; Uemura, Naoki; Okuda, Toshinori; Minami, Shinya; Iyama, Satoshi; Takada, Koichi; Sato, Tsutomu; Hara, Akinori; Iwata, Yasunori; Furuichi, Kengo; Wada, Takashi; Kato, Junji

2014-11-01

102

Iron deficiency anemia among Alaska Natives may be due to fecal loss rather than inadequate intake.  

PubMed

To define more fully the nature of a persistently high prevalence of iron deficiency anemia observed among Alaska Native children, we examined dietary iron intake, hemoglobin concentrations, and storage iron (serum ferritin) based on multiple cross-sectional surveys of Alaska Natives between 1983 and 1989. Approximately 30 to 50% of the children studied < 12 y of age had depleted iron stores. Anemia and depleted iron stores also were prevalent among adult men and women, about twice as prevalent as in the U.S. population based on the Second National Health and Nutrition Examination Survey (NHANES II). The higher rate of iron deficiency, occurring even when the dietary assessment found Alaska Native iron intake to be higher than the U.S. average with an ample intake of food high in bioavailable iron, suggests blood loss as a possible cause of the unusual pattern of iron deficiency observed. In a pilot study of stool blood loss in two villages, 65% of the samples had a significantly elevated stool heme concentration. Further investigation of iron deficiency due to gastrointestinal blood loss for the Alaska Native is warranted. PMID:8914948

Petersen, K M; Parkinson, A J; Nobmann, E D; Bulkow, L; Yip, R; Mokdad, A

1996-11-01

103

Prevalence of Anemia in Children with Congestive Heart Failure due to Dilated Cardiomyopathy  

PubMed Central

Introduction. Anemia is prevalent in adult heart failure patients and appears to be an independent risk factor for morbidity and mortality. The purpose of this work is to determine the prevalence of anemia in children with heart failure from dilated cardiomyopathy (DCM) and to evaluate its influence on morbidity and mortality. Methods. A homogenous group of 58 children with congestive heart failure from DCM was evaluated for heart failure symptoms, appearance of anemia, hospitalization, age of first clinical appearance, necessity of transfusion, and death during medical attendance. Anemic and nonanemic patients were analyzed for differences in age distribution, morbidity, and mortality. Results. Anemia was present in 64% of DCM patients. Hospitalization secondary to heart failure was significantly elevated in heart failure patients with anemia (mean 35.1 40.5 versus 9.97 9.65 days per year, P < 0.05). However, mortality was not elevated. Significant relations of age and prevalence of anemia or age and severity of anemia did not appear. Conclusion. Anemia is prevalent in pediatric patients with congestive heart failure from DCM and appears in all age classes. Hospitalization as a surrogate of morbidity is elevated in heart failure patients developing anemia, but mortality risk did not increase. PMID:23213342

Mueller, Goetz Christoph; Schlueter, Emmy Lou; Arndt, Florian; Dodge-Khatami, Ali; Weil, Jochen; Mir, Thomas S.

2012-01-01

104

Laboratory Evaluation of Anemia  

PubMed Central

The laboratory evaluation of anemia begins with a complete blood count and reticulocyte count. The anemia is then categorized as microcytic, macrocytic or normocytic, with or without reticulocytosis. Examination of the peripheral smear and a small number of specific tests confirm the diagnosis. The serum iron level, total iron-binding capacity, serum ferritin level and hemoglobin electrophoresis generally separate the microcytic anemias. The erythrocyte size-distribution width may be particularly helpful in distinguishing iron deficiency from thalassemia minor. Significant changes have occurred in the laboratory evaluation of macrocytic anemia, and a new syndrome of nitrous oxide-induced megaloblastosis and neurologic dysfunction has been recognized. A suggested approach to the hemolytic anemias includes using the micro-Coombs' test and ektacytometry. Finally, a number of causes have been identified for normocytic anemia without reticulocytosis, including normocytic megaloblastic anemia and the acquired immunodeficiency syndrome. PMID:3577135

Wallerstein, Ralph O.

1987-01-01

105

Anemia in older persons.  

PubMed

Anemia in older persons is commonly overlooked despite mounting evidence that low hemoglobin levels are a significant marker of physiologic decline. Using the World Health Organization definition of anemia (hemoglobin level less than 13 g per dL [130 g per L] in men and less than 12 g per dL [120 g per L] in women), more than 10 percent of persons older than 65 years are anemic. The prevalence increases with age, approaching 50 percent in chronically ill patients living in nursing homes. There is increasing evidence that even mild anemia is associated with increased morbidity and mortality. Anemia warrants evaluation in all older persons, except those at the end of life or who decline interventions. About one third of persons have anemia secondary to a nutritional deficiency, one third have anemia caused by chronic inflammation or chronic kidney disease, and one third have unexplained anemia. Nutritional anemia is effectively treated with vitamin or iron replacement. Iron deficiency anemia often is caused by gastrointestinal bleeding and requires further investigation in most patients. Anemia of chronic inflammation or chronic kidney disease may respond to treatment of the underlying disease and selective use of erythropoiesis-stimulating agents. The treatment of unexplained anemia is difficult, and there is little evidence that treatment decreases morbidity and mortality, or improves quality of life. Occasionally, anemia may be caused by less common but potentially treatable conditions, such as autoimmune hemolytic anemia, malignancy, or myelodysplastic syndrome. PMID:20822082

Bross, Michael H; Soch, Kathleen; Smith-Knuppel, Teresa

2010-09-01

106

Folate-deficiency anemia  

MedlinePLUS

Folate-deficiency anemia is a decrease in red blood cells ( anemia ) due to a lack of folate. Folate is a type ... B vitamin. It is also called folic acid. Anemia is a condition in which the body does ...

107

Blueberry muffin rash, hyperbilirubinemia, and hypoglycemia: A case of hemolytic disease of the fetus and newborn due to anti-Kpa  

Microsoft Academic Search

Hemolytic disease of the fetus and newborn occurs when maternal IgG antibodies cross the placenta and cause hemolysis of fetal red blood cells. Kpa is a low frequency red blood cell antigen that has rarely been implicated in hemolytic disease of the fetus and newborn. The few reported cases attributed to anti-Kpa have typically had minimal clinical consequences. We report

J E Brumbaugh; S Morgan; J C Beck; N Zantek; S Kearney; C M Bendel; K D Roberts

2011-01-01

108

A case of atypical hemolytic uremic syndrome.  

PubMed

A 9-year-old boy presented with fever not responding to antibiotic therapy and elevated blood urea and serum creatinine levels. The patient developed microangiopathic hemolytic anemia and thrombocytopenia during the hospital stay. Kidney biopsy confirmed the diagnosis of atypical hemolytic uremic syndrome (HUS). The patient had sufficient urine output, normal blood pressure, and no evidence of peripheral edema during the whole course of his disease. Serum levels of anti-Epstein-Barr virus immunoglobulin M was elevated, indicating the possible role of Epstein-Barr virus infection in inducing atypical HUS in this patient. The patient underwent hemodialysis with dramatic response. He was discharged with normal kidney function after a few days. Kidney function and platelet count were normal 12 months after the initial presentation. This case report shows that atypical hemolytic uremic syndrome could have unusual presentations such as the absence of oliguria, hypertension, and edema, with rapid recovery and good prognosis. PMID:25001143

Fallahzadeh, Mohammad Amin; Fallahzadeh, Mohammad Kazem; Derakhshan, Ali; Shorafa, Eslam; Mojtahedi, Yusof; Geramizadeh, Bita; Fallahzadeh, Mohammad Hossein

2014-07-01

109

Iron deficiency anemia due to lymphocytic gastritis with Helicobacter pylori infection in childhood: case report.  

PubMed

Lymphocytic gastritis (LG) is a chronic inflammatory process of poorly understood pathogenesis. We report the case of a 12-year-old premenstrual girl with refractory iron deficiency anemia in which the oral iron absorption challenge suggested iron malabsorption. Laboratory studies ruled out celiac disease and autoimmune gastritis, and carbon-13 urea breath test for Helicobacter pylori was also negative. Upper endoscopy with gastric body and antral mucosa biopsies revealed a LG with focal intestinal metaplasia and H. pylori infection. H. pylori eradication was undertaken with success and 3 months later her hematologic parameters normalized. Histologic reevaluation showed disappearance of LG. This case shows that investigation of malabsorption disease in the presence of refractory iron deficiency anemia can lead to the diagnosis of important gastric diseases, even in the absence of gastrointestinal symptoms. This nonceliac child was diagnosed with a severe histopathologic pattern of LG, with potential risk of malignant transformation, which was completely reverted with adequate H. pylori eradication treatment. PMID:23528908

Santalha, Marta F F; Costa, Emlia; Miguel, Natalina; Vizcano, Ramn; Barbot, Jos; Pereira, Fernando

2013-05-01

110

How atypical can Atypical Hemolytic Uremic Syndrome be?  

PubMed Central

Key Clinical Message A 24-year-old man with diarrhea found to have acute renal failure with microangiopathic hemolytic anemia (MAHA). A diagnosis of hemolytic uraemic syndrome (HUS) was made. He was initiated on plasma exchange and hemodialysis. On day 6, he was started on eculizumab. His renal functions progressively improved. His main complication during eculizumab therapy was hypertension-related posterior reversible encephalopathy syndrome.

Sajan, Thomas; Vinay, Srinivasa; Sonu, Nigam; Alan, Parnham

2014-01-01

111

Two novel ADAMTS13 gene mutations in thrombotic thrombocytopenic purpura\\/hemolytic-uremic syndrome (TTP\\/HUS)  

Microsoft Academic Search

Two novel ADAMTS13 gene mutations in thrombotic thrombocytopenic purpura\\/hemolytic-uremic syndrome (TTP\\/HUS).BackgroundThrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS) are now considered to be variants of one single syndrome called thrombotic thrombocytopenic purpura\\/hemolytic-uremic syndrome (TTP\\/HUS). Key features are thrombocytopenia, hemolytic anemia, and subsequently impaired function of different organs, especially the kidneys and the central nervous system (CNS). One possible reason is

CHRISTOPH LICHT; LUDWIG STAPENHORST; THORSTEN SIMON; ULRICH BUDDE; REINHARD SCHNEPPENHEIM; BERND HOPPE

2004-01-01

112

Erythropoiesis during recovery from macrocytic anemia: macrocytes, normocytes, and microcytes.  

PubMed

In seven patients with marked megaloblastic anemia (MCV greater than 110 fl), red cell size distribution curves (erythrograms) demonstrated the size of red cells produced after therapy. In six, the new red cells were normocytic throughout recovery. In the seventh patient, folate repletion along produced a new population of microcytes, due to unsuspected iron deficiency; after iron repletion normocytes were produced. Three patients with autoimmune hemolytic anemia had macrocytosis (MCV greater than 110 fl) without folate or vitamin B12 deficiency. During recovery with predisone therapy, instead of a discrete new normocytic population appearing, the entire population progressively returned to normal size. Normal rather than "stress" reticulocytes, and remodeled stress reticulocytes remaining, may explain this different pattern of recovery. Two patients initially had minor subpopulations of smaller red cells that disappeared soon after therapy. These probably reflected the dyserythropoiesis of severe megaloblastic anemia. PMID:922166

Bessman, D

1977-12-01

113

Hemolytic Disease of the Newborn Due to Anti-S A Case Report with a Review of 12 Anti-S Sera Cited in the Literature  

Microsoft Academic Search

his co-workers3 described the Guth factor, s, as the genetic allele of 5, with the aid of an antibody associated with hemolytic disease. In terms of the Ss system, there are three genotypes, the incidence of which in the white populations are as follows: 6545 12.28, ?Ss 46.4 and ss 41.4 per cent. In the Negro group, the value of

PHILIP LEVINE; LouiS R. FERRARO; ELIZABETH KOCH

1952-01-01

114

Pernicious anemia  

MedlinePLUS

Macrocytic achylic anemia; Congenital pernicious anemia; Juvenile pernicious anemia; Vitamin B12 deficiency (malabsorption) ... Pernicious anemia is a type of vitamin B12 anemia. The body needs vitamin B12 to make red blood cells. ...

115

Practice guidelines for the diagnosis and management of microcytic anemias due to genetic disorders of iron metabolism or heme synthesis.  

PubMed

During recent years, our understanding of the pathogenesis of inherited microcytic anemias has gained from the identification of several genes and proteins involved in systemic and cellular iron metabolism and heme syntheses. Numerous case reports illustrate that the implementation of these novel molecular discoveries in clinical practice has increased our understanding of the presentation, diagnosis, and management of these diseases. Integration of these insights into daily clinical practice will reduce delays in establishing a proper diagnosis, invasive and/or costly diagnostic tests, and unnecessary or even detrimental treatments. To assist the clinician, we developed evidence-based multidisciplinary guidelines on the management of rare microcytic anemias due to genetic disorders of iron metabolism and heme synthesis. These genetic disorders may present at all ages, and therefore these guidelines are relevant for pediatricians as well as clinicians who treat adults. This article summarizes these clinical practice guidelines and includes background on pathogenesis, conclusions, and recommendations and a diagnostic flowchart to facilitate using these guidelines in the clinical setting. PMID:24665134

Donker, Albertine E; Raymakers, Reinier A P; Vlasveld, L Thom; van Barneveld, Teus; Terink, Rieneke; Dors, Natasja; Brons, Paul P T; Knoers, Nine V A M; Swinkels, Dorine W

2014-06-19

116

[Treating severe acute anemia due to vaginal bleeding in the Jehovah's Witness: a report of 2 cases].  

PubMed

For reasons of religious belief, Jehova's Witnesses do not accept blood transfusions or the infusion of blood products. In situations in which severe, life-threatening anemia develops, patient refusal to receive a transfusion can create serious ethical and legal problems. The principle of patient autonomy, which implies the freedom to accept or reject treatment, comes into conflict with the physician's obligation to safeguard the patient's life using all means possible. We report 2 cases of severe anemia in Jehova's Witnesses. One was due to menorrhagia and the other to postpartum bleeding. The physician should be aware of alternatives to infusion of blood products and know how to cope with an unexpected critical event in these patients. The measures we took were effective in our patients. In the case of menorrhagia, hormone treatment is effective when the woman wishes to preserve the ability to conceive and avoid surgery (endometrial ablation and hysterectomy). In postpartum bleeding refractory to conservative treatment, selective embolization of bleeding vessels may make it unnecessary to resort to more aggressive treatment, such as obstetric hysterectomy. PMID:20151526

Gredilla, E; Prez-Ferrer, A; Canser, E; Alonso, E; Martnez Serrano, B; Gilsanz, F

2009-12-01

117

Shared Copy Number Variation in Simultaneous Nephroblastoma and Neuroblastoma due to Fanconi Anemia  

PubMed Central

Concurrent emergence of nephroblastoma (Wilms Tumor; WT) and neuroblastoma (NB) is rare and mostly observed in patients with severe subtypes of Fanconi anemia (FA) with or without VACTER-L association (VL). We investigated the hypothesis that early consequences of genomic instability result in shared regions with copy number variation in different precursor cells that originate distinct embryonal tumors. We observed a newborn girl with FA and VL (aplasia of the thumbs, cloacal atresia (urogenital sinus), tethered cord at L3/L4, muscular ventricular septum defect, and horseshoe-kidney with a single ureter) who simultaneously acquired an epithelial-type WT in the left portion of the kidney and a poorly differentiated adrenal NB in infancy. A novel homozygous germline frameshift mutation in PALB2 (c.1676_c1677delAAinsG) leading to protein truncation (pGln526ArgfsX1) inherited from consanguineous parents formed the genetic basis of FA-N. Spontaneous and induced chromosomal instability was detected in the majority of cells analyzed from peripheral lymphocytes, bone marrow, and cultured fibroblasts. Bone marrow cells also showed complex chromosome rearrangements consistent with the myelodysplastic syndrome at 11 months of age. Array-comparative genomic hybridization analyses of both WT and NB showed shared gains or amplifications within the chromosomal regions 11p15.5 and 17q21.31-q25.3, including genes that are reportedly implicated in tumor development such as IGF2, H19, WT2, BIRC5, and HRAS. PMID:23112754

Serra, A.; Eirich, K.; Winkler, A.K.; Mrasek, K.; Gohring, G.; Barbi, G.; Cario, H.; Schlegelberger, B.; Pokora, B.; Liehr, T.; Leriche, C.; Henne-Bruns, D.; Barth, T.F.; Schindler, D.

2012-01-01

118

Severe hemolytic disease of the newborn from anti-e  

Microsoft Academic Search

Maternal antibody-mediated fetal red blood cell destruction secondary to non-D Rhesus (Rh) antibodies is a significant cause of hemolytic disease of the newborn (HDN). Here, we report a rare case of severe HDN associated with maternal antibody to Rh e. In addition to severe anemia, the infant developed thrombocytopenia, conjugated hyperbilirubinemia and cholelithiasis. Resolution of the infant's cholelithiasis occurred following

R M McAdams; S A Dotzler; L W Winter; J D Kerecman

2008-01-01

119

[Diagnosis and clinical features of hemolytic uremic syndrome].  

PubMed

The hemolytic-uremic syndrome (HUS) is an acute disorder, characterized by the triad of microangiopathic hemolytic anemia, nephropathy and thrombocytopenia. The great majority of patients are children, usually under 4 years of age, although adults can be affected. The onset is abrupt and usually follows gastroenteritis or upper respiratory infection. Later, clinical manifestations based on the triad, such as pallor, jaundice, edema, hypertension and purpura soon develop. The urinary output is reduced and the urine may appear dark yellow or tea-colored. Laboratory tests of peripheral blood show severe hemolytic anemia associated with fragmented red blood cells and thrombocytopenia, usually below 50,000/microliters. The blood urea nitrogen, serum creatinine and lactate dehydrogenase concentrations are elevated. Proteinuria and microscopic hematuria, which are indicative of active glomerular damage are also seen. Profound understanding of these manifestations is sufficient to permit an early diagnosis of HUS. PMID:8433521

Nakajima, M; Yoshioka, A

1993-01-01

120

Megaloblastic anemia.  

PubMed

Most, but not all, megaloblastic anemia is produced by "ineffective erythropoiesis" in the bone marrow due to either folic acid or vitamin B12 deficiency. In folic acid deficiency the cause frequently is inadequate dietary intake, whereas vitamin B12 deficiency is almost always conditioned by some specific type of malabsorption. Anemia with oval macrocytes, few reticulocytes, moderate leukopenia, and thrombocytopenia is typical of both. Aplastic anemia, refractory anemias with cellular marrow, preleukemia, aleukemia, and erythroleukemia may have somewhat similar blood findings but are usually recognizable from bone marrow biopsy. Decreased levels of folate or vitamin B12 are the most reliable criteria of megaloblastic anemia. With these available in advance, therapy with the appropriate vitamin can be begun at once. If serum levels are unavailable or available only in retrospect, initial treatment, especially of severe anemia, should be with both vitamins. Differentiation between folate and vitamin B12 deficiency is important but impossible by blood and bone marrow morphology alone. Thus, if serum levels are unavailable, the distinction must be made, sometimes retrospectively, on the basis of other laboratory examinations, such as gastric analysis, small-bowel x-ray films, and the Schilling test. PMID:704501

Castle, W B

1978-10-01

121

Anemia in inflammatory bowel disease.  

PubMed

Anemia is a frequent extraenteric complication of inflammatory bowel disease (IBD, Crohn's disease and ulcerative colitis). A systematic review of the literature shows that the overall prevalence of anemia ranges from 8.8% to 73.7% but differs whether in a setting of Crohn's disease or ulcerative colitis. A disabling complication of IBD, anemia worsens the patient's general condition and quality of life, and increases hospitalization rates. Different factors, including vitamin B12 and folic acid deficiency, bone marrow suppression secondary to drug therapy, autoimmune hemolytic anemia and the coexistence of myelodysplastic syndromes are involved in the pathogenesis of anemia in IBD. The main types of anemia in IBD are iron deficiency anemia and anemia accompanying chronic diseases. Correct diagnostic definition of anemia is a fundamental step in guiding the choice of therapeutic options, since the co-presence of different pathogenetic factors may sometimes require a more complex treatment plan. A review of anemia in IBD, its pathogenetic features, epidemiology, diagnosis and therapy based on evidence from recent studies is the focus of this article. PMID:16971872

Giannini, S; Martes, C

2006-09-01

122

Aplastic Anemia  

MedlinePLUS

... from the NHLBI on Twitter. What Is Aplastic Anemia? Aplastic anemia (a-PLAS-tik uh-NEE-me-uh) is ... heart, heart failure , infections, and bleeding. Severe aplastic anemia can even cause death. Overview Aplastic anemia is ...

123

A case of atypical hemolytic uremic syndrome successfully treated with eculizumab.  

PubMed

Atypical hemolytic uremic syndrome (aHUS) is a rare thrombotic microangiopathy (TMA) characterized by the triad of hemolytic anemia, thrombocytopenia, and acute renal failure. Eculizumab, a monoclonal complement C5 antibody which prevents the induction of the terminal complement cascade, has recently emerged as a therapeutic option for aHUS. We report a case of aHUS successfully treated with eculizumab. A 51-year-old male was admitted to the hospital following a mechanical fall. His past medical history was significant for rheumatic valve disease and mitral valve replacement; he was on warfarin for anticoagulation. A computed tomography scan of the head revealed a right-sided subdural hematoma due to coagulopathy resulting from a supratherapeutic international normalized ratio (INR). Following treatment with prothrombin complex concentrate to reverse the INR, urine output dropped and his serum creatinine subsequently increased to 247.52 ?mol/l from the admission value of 70.72 ?mol/l. Laboratory evaluation was remarkable for hemolytic anemia, thrombocytopenia, elevated lactate dehydrogenase (LDH), low haptoglobin, and low complement C3. A renal biopsy was consistent with TMA, favoring a diagnosis of aHUS. Treatment with eculizumab was initiated which resulted in the stabilization of his hemoglobin, platelets, and LDH. Hemodialysis was terminated after 2.5 months due to improvement in urine output and solute clearance. The interaction between thrombin and complement pathway might be responsible for the pathogenesis of aHUS in this case. Eculizumab is an effective therapeutic agent in the treatment of aHUS. Early targeting of the complement system may modify disease progression and thus treat aHUS more effectively. PMID:24570684

Thajudeen, B; Sussman, A; Bracamonte, E

2013-07-01

124

The Hypochromic Anemias  

PubMed Central

Hypochromic anemia is the commonest type of anemia encountered in family practice. Although iron deficiency is by far the most common cause, it cannot be readily distinguished from hypochromic anemia due to other causes (thalassemia, secondary anemia and sideroblastic anemia) without knowing the state of the tissue iron stores. Treatment with iron should not be commenced until this is known. To establish the reason for the hypochromic state, the following tests are suggested: serum ferritin, bone marrow assessment of iron stores, plus serum iron and iron binding capacity. PMID:20469272

Ali, M. A. M.

1976-01-01

125

Hemolytic activity of Serratia marcescens  

Microsoft Academic Search

A cell-bound hemolytic activity was found in several strains of Serratia marcescens. One Serratia cell per ten erythrocytes was sufficient to cause complete lysis of human erythrocytes within 2 h in the liquid assay. The hemolytic activity resided in the membrane fraction and could be inactivated by incubating cells with proteases. The hemolytic activity was greatly enhanced in actively metabolizing

Volkmar Braun; Hannelore Gnther; Burkard Neu; Christiane Tautz

1985-01-01

126

X-linked sideroblastic anemia due to ALAS2 intron 1 enhancer element GATA-binding site mutations.  

PubMed

X-linked sideroblastic anemia (XLSA) is the most common form of congenital sideroblastic anemia. In affected males, it is uniformly associated with partial loss-of-function missense mutations in the erythroid-specific heme biosynthesis protein 5-aminolevulinate synthase 2 (ALAS2). Here, we report five families with XLSA owing to mutations in a GATA transcription factor binding site located in a transcriptional enhancer element in intron 1 of the ALAS2 gene. As such, this study defines a new class of mutations that should be evaluated in patients undergoing genetic testing for a suspected diagnosis of XLSA. PMID:24166784

Campagna, Dean R; de Bie, Charlotte I; Schmitz-Abe, Klaus; Sweeney, Marion; Sendamarai, Anoop K; Schmidt, Paul J; Heeney, Matthew M; Yntema, Helger G; Kannengiesser, Caroline; Grandchamp, Bernard; Niemeyer, Charlotte M; Knoers, Nine V A M; Swart, Sonia; Marron, Gordon; van Wijk, Richard; Raymakers, Reinier A; May, Alison; Markianos, Kyriacos; Bottomley, Sylvia S; Swinkels, Dorine W; Fleming, Mark D

2014-03-01

127

Pernicious Anemia  

MedlinePLUS

... from the NHLBI on Twitter. What Is Pernicious Anemia? Pernicious anemia (per-NISH-us uh-NEE-me-uh) is ... nervous system working properly. People who have pernicious anemia can't absorb enough vitamin B12 from food. ...

128

Eculizumab Therapy Leads to Rapid Resolution of Thrombocytopenia in Atypical Hemolytic Uremic Syndrome  

PubMed Central

Eculizumab is highly effective in controlling complement activation in patients with the atypical hemolytic uremic syndrome (aHUS). However, the course of responses to the treatment is not well understood. We reviewed the responses to eculizumab therapy for aHUS. The results show that, in patients with aHUS, eculizumab therapy, when not accompanied with concurrent plasma exchange therapy, led to steady increase in the platelet count and improvement in extra-renal complications within 3 days. By day 7, the platelet count was normal in 15 of 17 cases. The resolution of hemolytic anemia and improvement in renal function were less predictable and were not apparent for weeks to months in two patients. The swift response in the platelet counts was only observed in one of five cases who received concurrent plasma exchange therapy and was not observed in a case of TMA due to gemcitabine/carboplatin. In summary, eculizumab leads to rapid increase in the platelet counts and resolution of extrarenal symptoms in patients with aHUS. Concurrent plasma exchange greatly impedes the response of aHUS to eculizumab therapy. Eculizumab is ineffective for gemcitabine/carboplatin associated TMA.

Kuo, Elizabeth

2014-01-01

129

Aplastic anemia  

MedlinePLUS

Aplastic anemia is a condition in which the bone marrow does not make enough new blood cells. Bone marrow ... Aplastic anemia results from injury to the blood stem cells. These are immature cells in the bone marrow that ...

130

Aplastic Anemia  

MedlinePLUS

Aplastic anemia is a rare but serious blood disorder. If you have it, your bone marrow doesn't make ... cause is unknown. Your doctor will diagnose aplastic anemia based on your medical and family histories, a ...

131

Anemia due to coadministration of renin-angiotensin-system inhibitors and PPAR? agonists in uncomplicated diabetic patients.  

PubMed

Therapy with either angiotensin converting enzyme inhibitors and angiotensin receptor blockers (ACEI/ARB) or thiazolidinediones (TZD) is associated with dose-dependent decrements in hematocrit and hemoglobin levels. We aimed to investigate the impact of the coadministration of TZD and ACEI/ARB on hematocrit and hemoglobin values in uncomplicated patients with type 2 diabetes mellitus and normal serum creatinine.Data from patients with type 2 diabetes currently followed, were reviewed and patients treated with ACEI/ARB and/or TZD were identified. For the purpose of this study the following 4 groups of 30 stable non-anemic diabetic patients each matched for age, gender, and BMI were formed. Group ACEI/ARB included patients on ACEI/ARB without TZD, group TZD included patients on TZD and antihypertensive agents other than ACEI/ARB, group ACEI/ARB/TZD consisted of patients on combined therapy with ACEI/ARB and TZD and the control group C included patients never exposed to ACEI/ARB or TZD. Clinical and laboratory data were collected prior to initiation of treatment and after 6 months.Neither hematocrit nor hemoglobin showed any significant change from baseline at the end of the study in group C. In both group ACEI/ARB and group TZD a small, but statistically significant reduction in hematocrit (~ 1% point) and hemoglobin levels (~ 0.3 g/dl) was seen. A greater statistically and clinically important reduction in hematocrit (~ 3% points) and hemoglobin (~ 1 g/dl) levels was observed in group ACEI/ARB/TZD. Furthermore, incident anemia at the end reached 7% in group TZD and 23% in group ACEI/ARB/TZD.Coadministration of RAS inhibitors and PPAR-? agonists should be considered in the differential diagnosis of hematocrit lowering and anemia in uncomplicated type 2 diabetic patients with normal serum creatinine. Further studies are required to clarify the mechanism(s), the cardiovascular consequences and the cost utility of anemia workup in such patients. PMID:22441720

Raptis, A E; Bacharaki, D; Mazioti, M; Marathias, K P; Markakis, K P; Raptis, S A; Dimitriadis, G D; Vlahakos, D V

2012-07-01

132

Hemolytic uremic syndrome caused by Bordetella pertussis infection.  

PubMed

We report the case of a 4-week-old infant with severe Bordetella pertussis infection resulting in hemolytic anemia, thrombocytopenia, and acute renal failure leading to a diagnosis of hemolytic uremic syndrome (HUS) associated with pertussis. In addition to antibiotic and supportive therapy, he was treated with plasma transfusions based on the possibility of underlying complement defect, and he improved. The association of B. pertussis infection and HUS has previously been described in a patient with a mutation in the gene encoding complement factor H (CFH). However, whereas a genetic workup for complement regulator mutations was performed, no mutation was found in our patient. This case demonstrates the possible association between pertussis infection and HUS and highlights the need for increased vigilance for renal complications in this diagnosis. Despite negative results in this case, in-depth workup of the complement system may be important to guide treatment efforts and strategies. PMID:20145955

Chaturvedi, Swasti; Licht, Christoph; Langlois, Valerie

2010-07-01

133

A case of hemolytic uremic syndrome preceded by intussusception  

PubMed Central

Hemolytic-uremic syndrome (HUS) is the most common cause of acute renal failure in young children. It is classically characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and uremia. Further, not only is intussusception one of the differential diagnoses of HUS but it may also become a complication during disease progression. We report a case of HUS preceded by intussusception in a previously healthy 17-month-old boy. The patient presented at the emergency department with bloody stools that developed the day after reduction of intussusception. HUS was diagnosed 4 days after the reduction of intussusception. The patient was provided only supportive care and his laboratory test findings were normal at discharge. PMID:21738552

Ko, Eun Young; Kim, Joo Young; Lee, Hye Jin; Lee, Hyun Seung; Han, Ji Whan; Kim, Young Hoon; Kim, Jin Tack; Cheong, Hae Il

2011-01-01

134

How to approach chronic anemia.  

PubMed

We present herein an approach to diagnosing the cause of chronic anemia based on a patient's history and complete blood cell count (CBC). Four patterns that are encountered frequently in CBCs associated with chronic anemias are considered: (1) anemia with abnormal platelet and/or leukocyte counts, (2) anemia with increased reticulocyte counts, (3) life-long history of chronic anemia, and (4) anemia with inappropriately low reticulocytes. The pathophysiologic bases for some chronic anemias with low reticulocyte production are reviewed in terms of the bone marrow (BM) events that reduce normal rates of erythropoiesis. These events include: apoptosis of erythroid progenitor and precursor cells by intrinsic and extrinsic factors, development of macrocytosis when erythroblast DNA replication is impaired, and development of microcytosis due to heme-regulated eIF2? kinase inhibition of protein synthesis in iron-deficient or thalassemic erythroblasts. PMID:23233579

Koury, Mark J; Rhodes, Melissa

2012-01-01

135

Glucose-6-phosphate dehydrogenase deficiency  

MedlinePLUS

G-6-PD deficiency; Hemolytic anemia due to G6PD deficiency; Anemia - hemolytic due to G6PD deficiency ... Churchill Livingston; 2008:chap 45. Golan DER. Hemolytic anemias: red cell membrane and metabolic defects. In: Goldman ...

136

[A case presenting with ataxic gait and dementia due to vitamin B?? deficiency without megaloblastic anemia or subacute combined degeneration of the spinal cord].  

PubMed

A 36-year-old man was admitted to our hospital because of subacute progressive ataxic gait and dementia. His blood test results vitamin B?? deficiency due to presence of anti-intrinsic factor antibody and his endoscopic examination findings showed chronic gastritis. Treatment was administered on the bass of on a diagnosis of vitamin B?? deficiency. Consequently, ataxic gait improved and dementia regressed. I-IMP cerebral blood flow scintigraphy conducted at 8 months after treatment initiation showed increased blood flow the area around the parietal lobe to the corpus callosum, and flow both temporal lobes to the hippocampus compared. The diagnosis was difficult in this case because the patient did not show the typical symptoms and complications associated with vitamin B?? deficiency, such as megaloblastic anemia, or subacute combined degeneration of the spinal cord. However, the disturbance in cerebral blood flow may be related to the dysfunction of higher brain function caused by vitamin B?? deficiency. PMID:21386128

Iwanami, Hisatake; Tanaka, Michito; Iwakawa, Hideki; Takiguti, Yoshimitu; Inukai, Toshihiko

2011-03-01

137

A neonate with Coombs-negative hemolytic jaundice with spherocytes but normal erythrocyte indices: a rare case of autosomal-recessive hereditary spherocytosis due to alpha-spectrin deficiency.  

PubMed

The diagnosis of hereditary spherocytosis (HS) in a newborn infant is generally made on the basis of a positive family history, spherocytes on blood film and Coombs-negative hemolytic jaundice of variable severity with an elevated mean corpuscular hemoglobin concentration (MCHC) and a low mean corpuscular volume (MCV). In general, sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) quantification of erythrocyte membrane proteins is not needed to make the clinical diagnosis of HS. However, we observed that a neonate with no family history of HS, but with abundant spherocytosis on repeated blood films, Coombs-negative hemolytic jaundice and normal MCHC and MCV measurements, where SDS-PAGE revealed alpha-spectrin deficiency, a rare autosomal-recessive variety of HS that generally has a severe clinical phenotype. PMID:23624969

Yaish, H M; Christensen, R D; Agarwal, A

2013-05-01

138

About Anemia  

MedlinePLUS

... vessels in the skin. A fast heartbeat can be another sign of anemia, because when you don't have as many RBCs, the heart has to work harder to get the same amount of blood and oxygen to the body. If anemia worsens, a kid who was once very active may become worn out quickly. He or she ...

139

Management of renal anemia.  

PubMed

Normochromic normocytic anemia is common in children with chronic renal failure (CRF) when their glomerular filtration rate is below 35 ml/min/1.73 m2 BSA, but it may develop earlier in some forms of renal disease. An inadequate erythropoiesis due to insufficient erythropoietin synthesis in the kidneys is the main cause of renal anemia. Other reasons include reduced red blood cell lifespan, chronic blood loss, iron deficiency, inhibitors of erythropoiesis, and malnutrition. The presence of anemia contributes to many of the symptoms of uremia, including decreased appetite, decreased energy, poor cardiac function, and poor school performance. Therefore, correction of anemia dramatically improves the life of the child with CRF. Presently, the goal of anemia management is to maintain hematocrit concentrations at 33% to 36% and a hemoglobin concentration of at least 11 g/L. This can be accomplished by intravenous or subcutaneous administration of recombinant erythropoietin (rHuEPO, 100-300 U/kg/week) and iron preparations. If adequate iron stores cannot be maintained with oral therapy (2-3, max 6 mg/kg/day), intravenous iron should be administered. In order to optimize anemia management in children with CRF, future research should be concentrated on the normalization of hemoglobin early in the course of CRF, and the long-term effects on the child's development. PMID:15884663

Peco-Antic, Amira

2005-01-01

140

[Severe hemolytic disease of the newborn as a result of late and undiagnosed alloimmunization--case report].  

PubMed

We report a case of a hemolytic disease in a newborn from the first pregnancy due to anti-D antibodies. The maternal blood group was A Rhesus negative. She had an antibody screening test twice during the pregnancy (in the second trimester) and it was negative. The pregnancy was uneventful, without any invasive procedures and bleeding. The infant was born at 39 weeks of gestation in good overall condition. After the delivery the blood group of the neonate was indicated - A Rhesus positive, BOC positive. Anti-D antibodies were detected in maternal blood. Neonatal blood tests revealed severe anemia (hemoglobin level: 6.0g/dl, hematocrit: 22.2%, erythrocytes: 2.01T/L). During the first day of neonatal life, the newborn received two transfusions of red blood cells. Bilirubin level and rate of rise were not recommendation enough for exchange transfusion. The newborn was treated with continuous phototherapy since the delivery The perinatal period was complicated with intrauterine infection and respiratory failure. Hematopoietic vitamins and iron supplementation was initiated in the second week of neonatal life due to persistent anemia. The child remained under medical care of a hematologic clinic and received human recombinant erythropoietin treatment. PMID:24783436

Drozdowska-Szymczak, Agnieszka; Czapli?ska, Natalia; Borek-Dziecio?, Beata; Kociszewska-Najman, Bozena; Bartkowiak, Robert; Wielgo?, Miros?aw

2014-03-01

141

Diamond-Blackfan anemia and nutritional deficiency-induced anemia in children.  

PubMed

Diamond-Blackfan anemia is a rare, inherited disease that characteristically presents as a chronic, normochromic macrocytosis due to red cell lineage bone marrow failure. Although studies are elaborating on the genetic basis for its associated comorbidities, little has been published comparing this anemia to other chronic anemias that have similar laboratory results in children. This article offers a global perspective of the disease and compares it with anemia due to vitamin B12 and folate deficiency in children. PMID:24662257

Gelbart, David

2014-04-01

142

Genetics Home Reference: Anemia  

MedlinePLUS

... Home Conditions Genes Chromosomes Handbook Glossary Resources Conditions > Anemia Related topics on Genetics Home Reference: acute promyelocytic ... syndrome beta thalassemia Coats plus syndrome congenital dyserythropoietic anemia Diamond-Blackfan anemia Fanconi anemia Ghosal hematodiaphyseal dysplasia ...

143

Anemia and Pregnancy  

MedlinePLUS

... For Patients / Blood Disorders / Anemia / Anemia and Pregnancy Anemia & Pregnancy Your body goes through significant changes when ... becoming anemic. back to top Is Pregnancy-Related Anemia Preventable? Good nutrition is the best way to ...

144

What Causes Anemia?  

MedlinePLUS

... page from the NHLBI on Twitter. What Causes Anemia? The three main causes of anemia are: Blood ... the blood and can lead to anemia. Aplastic Anemia Some infants are born without the ability to ...

145

Anemia and Fatigue  

MedlinePLUS

Anemia And Fatigue Anemia And Fatigue htmAnemiaAndFatigue Left untreated, anemia can lead to a lack of energy and, more seriously, strokes, heart attacks ... InteliHealth Medical Content 2014-12-08 What Is Anemia? Anemia means that your hemoglobin level is below ...

146

Hemolytic Disease of the Newborn Anti c Antibody Induced Hemolysis  

Microsoft Academic Search

Hemolytic disease in the newborn, as a cause of early jaundice, is not uncommon. This is mostly due to Rh (D), ABO incompatibility\\u000a and rarely due to other minor blood group incompatibility. The authors report two cases of Rh anti c isoimmunization presenting\\u000a as significant early neonatal jaundice within the 20h of life. Both the babies were treated with intensive

Srinivas Murki; Hemasree Kandraju; Surekha A. Devi

147

Recessive mutations in DGKE cause atypical hemolytic-uremic syndrome  

PubMed Central

Pathologic thrombosis is a major cause of mortality. Hemolytic-uremic syndrome (HUS) features episodes of small vessel thrombosis resulting in microangiopathic hemolytic anemia, thrombocytopenia and renal failure1. Atypical HUS (aHUS) can result from genetic or autoimmune factors2 that lead to pathologic complement cascade activation3. By exome sequencing we identify recessive mutations in DGKE (diacylglycerol kinase epsilon) that co-segregate with aHUS in 9 unrelated kindreds, defining a distinctive Mendelian disease. Affected patients present with aHUS before age 1, have persistent hypertension, hematuria and proteinuria (sometimes nephrotic range), and develop chronic kidney disease with age. DGKE is found in endothelium, platelets, and podocytes. Arachidonic acid-containing diacylglycerols (DAG) activate protein kinase C, which promotes thrombosis. DGKE normally inactivates DAG signaling. We infer that loss of DGKE function results in a pro-thrombotic state. These findings identify a new mechanism of pathologic thrombosis and kidney failure and have immediate implications for treatment of aHUS patients. PMID:23542698

Lemaire, Mathieu; Fremeaux-Bacchi, Veronique; Schaefer, Franz; Choi, Murim; Tang, Wai Ho; Le Quintrec, Moglie; Fakhouri, Fadi; Taque, Sophie; Nobili, Francois; Martinez, Frank; Ji, Weizhen; Overton, John D.; Mane, Shrikant M.; Nurnberg, Gudrun; Altmuller, Janine; Thiele, Holger; Morin, Denis; Deschenes, Georges; Baudouin, Veronique; Llanas, Brigitte; Collard, Laure; Majid, Mohammed A.; Simkova, Eva; Nurnberg, Peter; Rioux-Leclerc, Nathalie; Moeckel, Gilbert W.; Gubler, Marie Claire; Hwa, John; Loirat, Chantal; Lifton, Richard P.

2013-01-01

148

Shiga toxin-associated hemolytic uremic syndrome complicated by intestinal perforation in a child with typical hemolytic uremic syndrome  

PubMed Central

Hemolytic uremic syndrome (HUS) is one of the most common causes of acute renal failure in childhood and is primarily diagnosed in up to 4.5% of children who undergo chronic renal replacement therapy. Escherichia coli serotype O157:H7 is the predominant bacterial strain identified in patients with HUS; more than 100 types of Shiga toxin-producing enterohemorrhagic E. coli (EHEC) subtypes have also been isolated. The typical HUS manifestations are microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency. In typical HUS cases, more serious EHEC manifestations include severe hemorrhagic colitis, bowel necrosis and perforation, rectal prolapse, peritonitis, and intussusceptions. Colonic perforation, which has an incidence of 1%-2%, can be a fatal complication. In this study, we report a typical Shiga toxin-associated HUS case complicated by small intestinal perforation with refractory peritonitis that was possibly because of ischemic enteritis. Although the degree of renal damage is the main concern in HUS, extrarenal complications should also be considered in severe cases, as presented in our case. PMID:24678335

Chang, Hye Jin; Kim, Hwa Young; Choi, Jae Hong; Choi, Hyun Jin; Ko, Jae Sung; Ha, Il Soo; Cheong, Hae Il; Choi, Yong

2014-01-01

149

Shiga toxin-associated hemolytic uremic syndrome complicated by intestinal perforation in a child with typical hemolytic uremic syndrome.  

PubMed

Hemolytic uremic syndrome (HUS) is one of the most common causes of acute renal failure in childhood and is primarily diagnosed in up to 4.5% of children who undergo chronic renal replacement therapy. Escherichia coli serotype O157:H7 is the predominant bacterial strain identified in patients with HUS; more than 100 types of Shiga toxin-producing enterohemorrhagic E. coli (EHEC) subtypes have also been isolated. The typical HUS manifestations are microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency. In typical HUS cases, more serious EHEC manifestations include severe hemorrhagic colitis, bowel necrosis and perforation, rectal prolapse, peritonitis, and intussusceptions. Colonic perforation, which has an incidence of 1%-2%, can be a fatal complication. In this study, we report a typical Shiga toxin-associated HUS case complicated by small intestinal perforation with refractory peritonitis that was possibly because of ischemic enteritis. Although the degree of renal damage is the main concern in HUS, extrarenal complications should also be considered in severe cases, as presented in our case. PMID:24678335

Chang, Hye Jin; Kim, Hwa Young; Choi, Jae Hong; Choi, Hyun Jin; Ko, Jae Sung; Ha, Il Soo; Cheong, Hae Il; Choi, Yong; Kang, Hee Gyung

2014-02-01

150

Chickens treated with a nitric oxide inhibitor became more resistant to Plasmodium gallinaceum infection due to reduced anemia, thrombocytopenia and inflammation  

PubMed Central

Malaria is a serious infectious disease caused by parasites of the Plasmodium genus that affect different vertebrate hosts. Severe malaria leads to host death and involves different pathophysiological phenomena such as anemia, thrombocytopenia and inflammation. Nitric oxide (NO) is an important effector molecule in this disease, but little is known about its role in avian malaria models. Plasmodium gallinaceum- infected chickens were treated with aminoguanidine (AG), an inhibitor of inducible nitric oxide synthase, to observe the role of NO in the pathogenesis of this avian model. AG increased the survival of chickens, but also induced higher parasitemia. Treated chickens demonstrated reduced anemia and thrombocytopenia. Moreover, erythrocytes at different stages of maturation, heterophils, monocytes and thrombocytes were infected by Plasmodium gallinaceum and animals presented a generalized leucopenia. Activated leukocytes and thrombocytes with elongated double nuclei were observed in chickens with higher parasitemia; however, eosinophils were not involved in the infection. AG reduced levels of hemozoin in the spleen and liver, indicating lower inflammation. Taken together, the results suggest that AG reduced anemia, thrombocytopenia and inflammation, explaining the greater survival rate of the treated chickens. PMID:23398940

2013-01-01

151

Case Report: Severe Hemolytic Disease of the Newborn in a Group B African-American Infant Delivered by a Group O Mother  

Microsoft Academic Search

Maternal-fetal ABO incompatibility is a common hematological problem affecting the newborn. In general, hemolysis is minimal and the clinical course is relatively benign, rarely causing the escalating levels of hyperbilirubinemia and significant anemia commonly associated with Rh hemolytic disease of the newborn (HDN). The incidence of HDN ranges from one in 150 births to 1:3000 births, depending on the degree

Kathryn Drabik-Clary; Vishnu V. B. Reddy; William H. Benjamin; Fouad N. Boctor

152

Anemia in the Newborn  

MedlinePLUS

... Caregivers > Children's Health Issues > Problems in Newborns 4 Anemia in the Newborn Anemia is a disorder in which there are too few red blood cells in the blood. Anemia can occur when red blood cells are broken ...

153

Anemia of chronic disease  

MedlinePLUS

Anemia of inflammation; AOCD; ACD ... Anemia is a lower-than-normal number of red blood cells in the blood. Some conditions can lead to anemia of chronic disease include: Autoimmune disorders , such as ...

154

Living with Anemia  

MedlinePLUS

... page from the NHLBI on Twitter. Living With Anemia Often, you can treat and control anemia. If ... by an inherited or chronic disease or trauma. Anemia and Children/Teens Infants and young children have ...

155

Sickle Cell Anemia  

MedlinePLUS

... not have the disease itself. What Is Sickle Cell Anemia? Sickle cell anemia is a blood disorder ... blood vessels. Continue What Happens With Sickle-Shaped Cells Sickle cell anemia occurs because an abnormal form ...

156

Sequences responsible for the distinctive hemolytic potentials of Friend and Moloney murine leukemia viruses are dispersed but confined to the psi-gag-PR region.  

PubMed Central

Friend and Moloney murine leukemia viruses (F- and M-MuLV) induce distinct diseases in hematopoietic tissues following inoculation of newborn mice of susceptible strains. F-MuLV induces erythroleukemia preceded by severe early hemolytic anemia; M-MuLV induces thymomas and only very mild hemolysis. The major viral determinant of severe early hemolytic anemia residues in the env gene, but sequences located outside this gene can modulate this effect. By means of genetic chimeras of F- and M-MuLV, we have found that although they are confined to the 5' portion of the env gene intron, sequences that determine the distinctive hemolytic potentials of F- and M-MuLV are widely distributed over a region spanning the RNA encapsidation domain, the gag gene, and the portion of the pol gene encoding the viral protease. Within this large region, two fragments of M-MuLV, a 1.3-kb region encoding the matrix, pp12, and capsid proteins and a 0.8-kb region encoding the nucleocapsid and the viral protease, were capable, individually, of partially attenuating the capacity of F-MuLV for induction of severe early hemolytic anemia. In association, these two fragments conferred complete attenuation. Moreover, a second pair of adjacent fragments within this large region appeared to behave cooperatively to confer complete attenuation; a 0.36-kb region roughly corresponding to the encapsidation domain, although not detectably altering hemolytic potential on its own, deepened the attenuation conferred by the adjacent 1.3-kb region. Whether capable of inducing severe early hemolytic anemia or not and despite different efficiencies of induction of recombinant polytropic viruses, all chimeric viruses retained the erythroleukemogenicity of the F-MuLV parent. PMID:8350407

Richardson, J; Corbin, A; Pozo, F; Orsoni, S; Sitbon, M

1993-01-01

157

Humanized mouse model of glucose 6-phosphate dehydrogenase deficiency for in vivo assessment of hemolytic toxicity  

PubMed Central

Individuals with glucose 6-phosphate dehydrogenase (G6PD) deficiency are at risk for the development of hemolytic anemia when given 8-aminoquinolines (8-AQs), an important class of antimalarial/antiinfective therapeutics. However, there is no suitable animal model that can predict the clinical hemolytic potential of drugs. We developed and validated a human (hu)RBC-SCID mouse model by giving nonobese diabetic/SCID mice daily transfusions of huRBCs from G6PD-deficient donors. Treatment of SCID mice engrafted with G6PD-deficient huRBCs with primaquine, an 8-AQ, resulted in a dose-dependent selective loss of huRBCs. To validate the specificity of this model, we tested known nonhemolytic antimalarial drugs: mefloquine, chloroquine, doxycycline, and pyrimethamine. No significant loss of G6PD-deficient huRBCs was observed. Treatment with drugs known to cause hemolytic toxicity (pamaquine, sitamaquine, tafenoquine, and dapsone) resulted in loss of G6PD-deficient huRBCs comparable to primaquine. This mouse model provides an important tool to test drugs for their potential to cause hemolytic toxicity in G6PD-deficient populations. PMID:24101478

Rochford, Rosemary; Ohrt, Colin; Baresel, Paul C.; Campo, Brice; Sampath, Aruna; Magill, Alan J.; Tekwani, Babu L.; Walker, Larry A.

2013-01-01

158

Comparison of methods for extraction of nucleic acid from hemolytic serum for PCR amplification of hepatitis B virus DNA sequences.  

PubMed Central

The sensitivity of PCR for the amplification of target nucleic acid sequences in clinical diagnostics may often be reduced due to the presence of inhibitory factors. Hemolytic serum contains a number of PCR inhibitors, one of which is hemin. In this study we have found that conventional methods of DNA extraction were not sufficient for the removal of PCR-inhibitory compounds in hemolytic serum. We have therefore compared the efficiency of several commercial and noncommercial methods of nucleic acid purification from hemolytic serum samples prior to PCR amplification. Separation with the QIAamp HCV kit, dialysis with Millipore filters, and bovine serum albumin absorption were all found to be suitable extraction methods for eliminating inhibitors from hemolytic serum for PCR amplification. Using these methods we were able to detect very low levels of hepatitis B virus DNA in hemolytic serum. PMID:9196220

Klein, A; Barsuk, R; Dagan, S; Nusbaum, O; Shouval, D; Galun, E

1997-01-01

159

Sexuality and sickle cell anemia  

PubMed Central

Background Sickle cell disease, the most common hereditary blood disease in the world, is the result of an atypical hemoglobin called S (Hb S) which, when homozygous (Hb SS) is the cause of sickle cell anemia. Changes of puberty, correlated with a delayed growth spurt, begin late in both male and female sickle cell anemia individuals with repercussions on sexuality and reproduction. The objectives of this exploratory and descriptive study were to characterize the development of sexuality in adults with sickle cell anemia by investigating the patient's perception of their sex life, as well as the information they had and needed on this subject. Methods Twenty male and female sickle cell anemia patients treated at the Hemocentro Regional de Uberaba (UFTM) with ages between 19 and 47 years old were enrolled. A socioeconomic questionnaire and a semi-structured interview on sexuality, reproduction and genetic counseling were applied. Results This study shows that the sickle cell anemia patients lacked information on sexuality especially about the risks of pregnancy and the possible inheritance of the disease by their children. Moreover, the sexual life of the patients was impaired due to pain as well as discrimination and negative feelings experienced in close relationships. Conclusion The health care of sickle cell anemia patients should take into account not only the clinical aspects of the disease, but also psychosocial aspects by providing counseling on sexuality, reproduction and genetics, in order to give this population the possibility of a better quality of life. PMID:23741184

Cobo, Viviane de Almeida; Chapadeiro, Cibele Alves; Ribeiro, Joao Batista; Moraes-Souza, Helio; Martins, Paulo Roberto Juliano

2013-01-01

160

Iron refractory iron deficiency anemia  

PubMed Central

Iron refractory iron deficiency anemia is a hereditary recessive anemia due to a defect in the TMPRSS6 gene encoding Matriptase-2. This protein is a transmembrane serine protease that plays an essential role in down-regulating hepcidin, the key regulator of iron homeostasis. Hallmarks of this disease are microcytic hypochromic anemia, low transferrin saturation and normal/high serum hepcidin values. The anemia appears in the post-natal period, although in some cases it is only diagnosed in adulthood. The disease is refractory to oral iron treatment but shows a slow response to intravenous iron injections and partial correction of the anemia. To date, 40 different Matriptase-2 mutations have been reported, affecting all the functional domains of the large ectodomain of the protein. In vitro experiments on transfected cells suggest that Matriptase-2 cleaves Hemojuvelin, a major regulator of hepcidin expression and that this function is altered in this genetic form of anemia. In contrast to the low/undetectable hepcidin levels observed in acquired iron deficiency, in patients with Matriptase-2 deficiency, serum hepcidin is inappropriately high for the low iron status and accounts for the absent/delayed response to oral iron treatment. A challenge for the clinicians and pediatricians is the recognition of the disorder among iron deficiency and other microcytic anemias commonly found in pediatric patients. The current treatment of iron refractory iron deficiency anemia is based on parenteral iron administration; in the future, manipulation of the hepcidin pathway with the aim of suppressing it might become an alternative therapeutic approach. PMID:23729726

De Falco, Luigia; Sanchez, Mayka; Silvestri, Laura; Kannengiesser, Caroline; Muckenthaler, Martina U.; Iolascon, Achille; Gouya, Laurent; Camaschella, Clara; Beaumont, Carole

2013-01-01

161

Clostridium septicum infection and hemolytic uremic syndrome.  

PubMed Central

Five cases of Clostridium septicum infection secondary to Escherichia coli O157-induced hemolytic uremic syndrome have been reported. We report on three cases (one of which is included in the above five) of dual Cl. septicum and E. coil infection; all three patients were exposed to farm animals. A common zoonotic source for Cl. septicum and E. coli O157 infections should be considered. Patients with hemolytic uremic syndrome should be treated aggressively and monitored closely for Cl. septicum superinfection. PMID:9621207

Barnham, M.; Weightman, N.

1998-01-01

162

Imaging diagnosis of neonatal anemia: report of two unusual etiologies.  

PubMed

Anemia in neonatal period is rare, with the common causes being Rh and ABO blood group incompatibility, hemorrhagic disease of newborn, congenital hemolytic anemia, hemoglobinopathies, and TORCH (toxoplasmosis, rubella, cytomegalovirus, herpes virus) infections. Congenital leukemia and infantile osteopetrosis (OP) are among the rare causes of neonatal anemia. A review of the literature shows approximately 200 reported cases of congenital leukemia. Articles describing the imaging features of congenital leukemia are still rarer. Infantile OP, another rare disorder with a reported incidence of 1 in 250,000 has characteristic imaging features, which are diagnostic of the disease. We report a case each, of two rare diseases: Congenital leukemia and infantile osteopetrosis. Additionally, our report highlights the radiological and imaging features of congenital leukemia and infantile OP and their crucial role in arriving at an early diagnosis. PMID:24605254

Grover, Shabnam Bhandari; Preethi, G Rajalakshmi; Saluja, Sumita; Bhargava, Ankit

2013-01-01

163

Nitrite-induced anemia in channel catfish, Ictalurus punctatus Rafinesque  

SciTech Connect

Since 1983 numerous cases of anemia have been reported in populations of channel catfish Ictalurus punctatus Rafinesque cultured in the southeastern United States. Environmental nitrite-nitrogen concentrations of 4 mg/L or more occur sporadically in channel catfish culture ponds, and the frequency of occurrence is greatest in the fall and spring. The authors have observed that some cases of anemia in populations of pond-raised channel catfish follow prolonged exposure to high concentrations of environmental nitrite. However, there was no evidence that exposure of channel catfish to environmental nitrite was the cause of the observed anemia. Hemolytic anemia following nitrite exposure has been described for sea bass Dicentrarchus labrax (L.) and rainbow trout Salmo gairdneri, but not for channel catfish. In the present study the authors show that a variable, but generally mild, anemia develops in channel catfish exposed to nitrite. They also offer a management procedure for preventing the development of anemia during periods of elevated environmental nitrite concentrations.

Tucker, C.S. (Mississippi Agricultural and Forestry Experiment Station, Stoneville (USA)); Francis-Floyd, R.; Beleau, M.H. (College of Veterinary Medicine, Stoneville, MS (USA))

1989-08-01

164

Recognition of sickle cell anemia in skeletal remains of children.  

PubMed

The present study discusses in detail the osteological changes associated with sickle cell anemia in children and their importance in differential diagnosis. Posterior calcaneal and specific articular surface disruptive metacarpal lesions are diagnostic for sickle cell anemia. Calvarial thickening, tibial and femoral cortical bone thickening, and bowing are of more limited utility in differential diagnosis. Granular osteoporosis, pelvic demineralization and rib broadening are nonspecific. Localized calvarial "ballooning," previously not described, may have diagnostic significance. Bone marrow hyperplastic response (porotic hyperostosis) in sickle cell anemia produces minimal radiologic changes contrasted with that observed in thalassemia and blood loss/hemolytic phenomenon. Two other issues, the osteological criteria for discriminating among the anemias and the purported relationship between porotic hyperostosis and iron deficiency anemia, are also discussed. There is sufficient information to properly diagnose the four major groups of anemias, and further, to establish that iron deficiency is only indirectly associated with porotic hyperostosis. The hyperproliferative bone marrow response (manifest as porotic hyperostosis) to blood loss or hemolysis exhausts iron stores, resulting in secondary iron deficiency. PMID:9386828

Hershkovitz, I; Rothschild, B M; Latimer, B; Dutour, O; Lonetti, G; Greenwald, C M; Rothschild, C; Jellema, L M

1997-10-01

165

Assessment of hematopoietic failure due to Rpl11 deficiency in a zebrafish model of Diamond-Blackfan anemia by deep sequencing  

PubMed Central

Background DiamondBlackfan anemia is a rare congenital red blood cell dysplasia that develops soon after birth. RPL11 mutations account for approximately 4.8% of human DBA cases with defective hematopoietic phenotypes. However, the mechanisms by which RPL11 regulates hematopoiesis in DBA remain elusive. In this study, we analyzed the transcriptome using deep sequencing data from an Rpl11-deficient zebrafish model to identify Rpl11-mediated hematopoietic failure and investigate the underlying mechanisms. Results We characterized hematological defects in Rpl11-deficient zebrafish embryos by identifying affected hematological genes, hematopoiesis-associated pathways, and regulatory networks. We found that hemoglobin biosynthetic and hematological defects in Rpl11-deficient zebrafish were related to dysregulation of iron metabolism-related genes, including tfa, tfr1b, alas2 and slc25a37, which are involved in heme and hemoglobin biosynthesis. In addition, we found reduced expression of the hematopoietic stem cells (HSC) marker cmyb and HSC transcription factors tal1 and hoxb4a in Rpl11-deficient zebrafish embryos, indicating that the hematopoietic defects may be related to impaired HSC formation, differentiation, and proliferation. However, Rpl11 deficiency did not affect the development of other blood cell lineages such as granulocytes and myelocytes. Conclusion We identified hematopoietic failure of Rpl11-deficient zebrafish embryos using transcriptome deep sequencing and elucidated potential underlying mechanisms. The present analyses demonstrate that Rpl11-deficient zebrafish may serve as a model of DBA and may provide insights into the pathogenesis of mutant RPL11-mediated human DBA disease. PMID:24341334

2013-01-01

166

Sickle cell anemia  

MedlinePLUS

Anemia - sickle cell; Hemoglobin SS disease (Hb SS); Sickle cell disease ... Sickle cell anemia is caused by an abnormal type of hemoglobin called hemoglobin S. Hemoglobin is a protein inside red blood cells ...

167

Living with Fanconi Anemia  

MedlinePLUS

... from the NHLBI on Twitter. Living With Fanconi Anemia Improvements in blood and marrow stem cell transplants ... FA can be costly). Rate This Content: Fanconi Anemia Clinical Trials Clinical trials are research studies that ...

168

The Anemias of Athletes.  

ERIC Educational Resources Information Center

Diagnosing anemia in athletes is complicated because athletes normally have a pseudoanemia that needs no treatment. Athletes, however, can develop anemia from iron deficiency or footstrike hemolysis, which require diagnosis and treatment. (Author/MT)

Eichner, Edward R.

1986-01-01

169

Group A ?-hemolytic streptococcal pharyngotonsillitis outbreak.  

PubMed

The aim was to describe an outbreak of group A ?-hemolytic streptococcal pharyngotonsillitis in health care professionals. This is a cross-sectional descriptive study of 17 clients who dined at the same table in a restaurant in Barcelona in July 2012. The frequency, timing and severity of symptoms were analyzed, as were demographic variables and others concerning the food ingested. The attack rate was 58.8%. Six of the 10 clients were positive for group A ?-hemolytic streptococcal. Six of the 13 individuals who handled the food involved in the dinner had symptoms. No association was identified with the food consumed. There is epidemiological evidence of foodborne group A ?-hemolytic streptococcal transmission, but respiratory transmission could not be ruled out. PMID:24897054

Culqui, Dante R; Manzanares-Laya, Sandra; Van Der Sluis, Sarah Lafuente; Fanlo, Albert Anton; Comas, Rosa Bartolom; Rossi, Marcello; Cayl, Jon A

2014-04-01

170

Myeloma and pernicious anemia.  

PubMed

Four cases of pernicious anemia developing in association with multiple myeloma are described. The description now of 14 cases demonstrating the association of these two disorders suggest a causative relationship. These observations, in addition to the previously well-documented increased coincidence of pernicious anemia and benign monoclonal gammopathy and pernicious anemia and hypoglobulinemia, suggest that screening for vitamine B12 deficiency in patients with gammopathies and for protein abnormalities in patients with pernicious anemia is indicated. PMID:665715

Perillie, P E

1978-01-01

171

Effects of immunosuppressive therapy in a patient with aplastic anemia-paroxysmal nocturnal hemoglobinuria (AA-PNH) syndrome during ongoing eculizumab treatment.  

PubMed

A 65-year-old woman experienced a hemolytic attack triggered by sepsis. She presented with markedly increased CD55(-) CD59(-) erythrocytes and the signs of bone marrow failure, which led to a diagnosis of aplastic anemia-paroxysmal nocturnal hemoglobinuria (AA-PNH) syndrome. There was a possibility of increasing hemolysis, as large PNH clones remained after immunosuppressive therapy (IST). Accordingly, eculizumab was first used to control the hemolytic attack followed by IST with antithymocyte globulin and cyclosporine A. The patient was successfully weaned from blood transfusions and has been followed up without any recurrence of hemolytic attacks. PMID:24429452

Asano, Jin; Ueda, Ryosuke; Tanaka, Yasuhiro; Shinzato, Isaku; Takafuta, Toshiro

2014-01-01

172

Post-liver-transplant anemia: etiology and management.  

PubMed

Anemia is common after liver transplantation, with the incidence ranging from 4.3% to 28.2% depending on the criteria used to define anemia. The cause of anemia is unidentified in the majority of patients, and it is likely to be multifactorial. Immunosuppressive-medication-induced bone marrow suppression is perhaps the most common cause of unexplained anemia. Chronic blood loss, iron deficiency, hemolysis, and renal insufficiency are other potential causes of chronic anemia. Rare causes, somewhat unique to transplantation, include aplastic anemia, graft-versus-host disease (GVHD), and lymphoproliferative disease. Anemia due to immunosuppressive medication is challenging, since almost all drugs currently used for this purpose cause anemia, but the renal-sparing property of sirolimus may benefit the subgroup in which renal insufficiency is contributing to anemia. Aplastic anemia is seen in young patients transplanted for non-A, non-B, non-C, fulminant hepatic failure. It is thought to be immunologically mediated, secondary to an unknown viral infection, and is associated with a grave prognosis. GVHD is another infrequent (approximately 1% of transplant recipients) but serious cause of severe anemia that carries a dismal prognosis. Lymphoproliferative disorder, too may rarely rare cause anemia and it may respond to reduction of immunosuppression. Recipients of solid-organ transplants do not mount a significant increase in erythropoietin in response to anemia. In conclusion, though there are no data on the response of anemia to erythropoietin in liver transplant recipients, it appears to benefit other solid-organ-transplant recipients with anemia. PMID:14762852

Maheshwari, Anurag; Mishra, Rajnish; Thuluvath, Paul J

2004-02-01

173

Hemolytic disease of the newborn due to rare alloantibodies  

Microsoft Academic Search

SummaryIn the period January 1975 to December 1981, serum sampies from 9,525 pregnant women were examined for irregular red cell\\u000a antibodies. Red cell, antibodies were found in 719 cases (7.5%); anti D antibodies were present in 532 cases (5.5% of the\\u000a whole series), rare antibodies (other than anti-D) in 187 cases (2%). Seven pregnant women with rare red cell antibodies

Guglielmo Zuliani; Gian Alessandro Moroni; Mauro Buscaglia; Raffaella Morotti; Giorgio Pardi

1983-01-01

174

Haptoglobin blood test  

MedlinePLUS

... normal levels may be due to: Chronic liver disease Collection of blood (hematoma) Drug-induced immune hemolytic anemia Blood disorder in a fetus or newborn called erythroblastosis fetalis Hemolytic anemia due to G6PD ...

175

Cyclosporine therapy during pregnancy in a patient with ?-thalassemia major and autoimmune haemolytic anemia: a case report and review of the literature  

PubMed Central

Recent advances in the management of hemoglobinopathies offer an improved potential for safe pregnancy with favourable outcome in patients with ?-thalassemia major. Autoimmune diseases that are common in women at reproductive age might be fulminant and hardly manageable in pregnant women with thalassemia. Thus immunosuppressant drugs like cyclosporine A could be necessary in order to maintain good maternal and foetal health. We present a case report of a 35-year-old woman with ?-thalassemia major, splenectomy, autoimmune hemolytic anemia and insulin treated diabetes mellitus who was treated with cyclosporine A during her pregnancy, and delivered a healthy male infant. First line therapy with steroids was ineffective, due to deregulation of diabetes mellitus. PMID:23935353

Agapidou, A; Vlachaki, E; Theodoridis, T; Economou, M; Perifanis, V

2013-01-01

176

Isolated microcytic anemia disclosing a unicentric Castleman disease: The interleukin-6/hepcidin pathway?  

PubMed

Castleman disease (CD) is a rare lymphoproliferative disorder of uncertain origin. Anemia is commonly reported and is related to an inflammatory mechanism. Occasionally an autoimmune hemolytic anemia appears as the leading clinical feature. Three histological types have been differentiated, a hyaline-vascular type (HV), a plasma cell type (PC), and a mixed type. Clinically CD is separated into unicentric (localized) or multicentric (generalized) forms. The former is most frequently of HV type (80-90%), affecting a single lymph node. The PC type is encountered in 10-20% of the unicentric CD and in almost all of the multicentric cases. Numerous systemic manifestations have been described usually associated with PC type. An isolated and markedly microcytic anemia revealing a unicentric CD has never been reported in English literature. Recent data concerning iron metabolism, interleukin-6 and hepcidin provide interesting clues to understand the particular microcytic anemia of CD. PMID:18549942

Vinzio, Stphane; Ciarloni, Laetitia; Schlienger, Jean-Louis; Rohr, Serge; Mchine, Agns; Goichot, Bernard

2008-07-01

177

Anemia of inflammation.  

PubMed

Anemia of inflammation (AI, also called anemia of chronic disease) is a common, typically normocytic, normochromic anemia that is caused by an underlying inflammatory disease. It is diagnosed when serum iron concentrations are low despite adequate iron stores, as evidenced by serum ferritin that is not low. In the setting of inflammation, it may be difficult to differentiate AI from iron deficiency anemia, and the 2 conditions may coexist. Treatment should focus on the underlying disease. Recent advances in molecular understanding of AI are stimulating the development of new pathophysiologically targeted experimental therapies. PMID:25064707

Nemeth, Elizabeta; Ganz, Tomas

2014-08-01

178

Iron deficiency anemia  

PubMed Central

Iron is essential to virtually all living organisms and is integral to multiple metabolic functions. The most important function is oxygen transport in hemoglobin. Iron deficiency anemia in dogs and cats is usually caused by chronic blood loss and can be discovered incidentally as animals may have adapted to the anemia. Severe iron deficiency is characterized by a microcytic, hypochromic, potentially severe anemia with a variable regenerative response. Iron metabolism and homeostasis will be reviewed, followed by a discussion of diagnostic testing and therapeutic recommendations for dogs and cats with iron deficiency anemia. PMID:22942439

Naigamwalla, Dinaz Z.; Webb, Jinelle A.; Giger, Urs

2012-01-01

179

How Is Pernicious Anemia Treated?  

MedlinePLUS

... from the NHLBI on Twitter. How Is Pernicious Anemia Treated? Doctors treat pernicious anemia by replacing the missing vitamin B12 in the body. People who have pernicious anemia may need lifelong treatment. The goals of treating ...

180

Genetics Home Reference: Fanconi anemia  

MedlinePLUS

... Recent literature OMIM Genetic disorder catalog Conditions > Fanconi anemia On this page: Description Genetic changes Inheritance Diagnosis ... Glossary definitions Reviewed January 2012 What is Fanconi anemia? Fanconi anemia is a condition that affects many ...

181

How Is Aplastic Anemia Treated?  

MedlinePLUS

... from the NHLBI on Twitter. How Is Aplastic Anemia Treated? Treatments for aplastic anemia include blood transfusions , blood and marrow stem cell ... a transplant. Removing a known cause of aplastic anemia, such as exposure to a toxin, also may ...

182

Managing Chemotherapy Side Effects: Anemia  

MedlinePLUS

... National Institutes of Health Managing Chemotherapy Side Effects Anemia Call your doctor or nurse if you feel: ? ... tired ? Your heart beating very fast What is anemia? Anemia is when your body doesnt have ...

183

Fatal hemolysis induced by ceftriaxone in a child with sickle cell anemia  

Microsoft Academic Search

A 2-year-old boy with sickle cell anemia had a massive, fatal hemolytic reaction after administration of an intravenous dose of ceftriaxone. Laboratory studies demonstrated the presence of an IgM antibody against ceftriaxone, binding to and destroying the patient's erythrocytes by an immune complex mechanism. This rare complication should be considered in the differential diagnosis when hemoglobinuria develops in a child

Juan C. Bernini; Mahmoud M. Mustafa; Laurie J. Sutor; George R. Buchanan

1995-01-01

184

Distribution of hemolytic complement in the normal cornea.  

PubMed

Hemolytic activities in the central cornea were compared with hemolytic activities in the peripheral cornea for each of the following complement components: C1, C4, C2, C3, C5, C6, and C7. For all seven complement components studied, hemolytic activities in the peripheral cornea were higher than hemolytic activities in the central cornea, and the differences were statistically significant. The most striking difference was for C1, which had a ratio of mean hemolytic activity in the peripheral cornea to that in the central cornea of almost 5:1. For the other six complement components, the ratio of the mean hemolytic activity in the peripheral cornea to that in the central cornea was approximately 1.2:1. This distribution of complement activity in the cornea suggests that the major source of complement components is the limbal vessels and that complement components diffuse from the limbus to the central cornea. PMID:7020664

Mondino, B J; Brady, K J

1981-08-01

185

Sickle Cell Anemia  

MedlinePLUS

Sickle cell anemia is a disease in which your body produces abnormally shaped red blood cells. The cells are shaped like a crescent or sickle. They ... last as long as normal, round red blood cells. This leads to anemia. The sickle cells also ...

186

Fifth Cooley's anemia symposium  

SciTech Connect

This book discusses the topics presented at the symposium on the subject of 'Thalassemia'. Sickle cell anemia is also briefly discussed. The aspects discussed are chromosomal defects of anemias particularly globin synthesis, and the role of messenger RNA and other chromosomes.

Bank, A.; Anderson, W.F.; Zaino, E.C.

1985-01-01

187

Initiation and Regulation of Complement during Hemolytic Transfusion Reactions  

PubMed Central

Hemolytic transfusion reactions represent one of the most common causes of transfusion-related mortality. Although many factors influence hemolytic transfusion reactions, complement activation represents one of the most common features associated with fatality. In this paper we will focus on the role of complement in initiating and regulating hemolytic transfusion reactions and will discuss potential strategies aimed at mitigating or favorably modulating complement during incompatible red blood cell transfusions. PMID:23118779

Stowell, Sean R.; Winkler, Anne M.; Maier, Cheryl L.; Arthur, C. Maridith; Smith, Nicole H.; Girard-Pierce, Kathryn R.; Cummings, Richard D.; Zimring, James C.; Hendrickson, Jeanne E.

2012-01-01

188

Clomiphene-responsive hypogonadism in sickle cell anemia.  

PubMed

Two 19-year-old men with sickle cell anemia and hypogonadism had hypothalamic dysfunction that responded to oral clomiphene therapy. The patients had no nutritional deficiencies or anatomic lesions known to result in the hypogonadism associated with sickle cell anemia. Their sickle cell disease was characterized by infrequent crises, severe hemolytic anemia, urinary iron loss, and iron deficiency. Partial hypothalamic hypogonadism was shown by low levels of testosterone, low to low-normal levels of luteinizing hormone and follicle-stimulating hormone, and a nearly normal rise in gonadotropin levels in response to exogenous gonadotropin releasing hormone. Treatment with oral clomiphene raised luteinizing hormone, follicle-stimulating hormone, and testosterone levels to normal, and induced puberty in both patients. Treatment was discontinued in one patient because of the onset of priapism, but was continued for 10 months without side effects in the other. Severe hypogonadism in patients with sickle cell anemia should be thoroughly evaluated and clomiphene therapy considered in patients with hypothalamic dysfunction. PMID:6414355

Landefeld, C S; Schambelan, M; Kaplan, S L; Embury, S H

1983-10-01

189

Response of Paroxysmal Nocturnal Hemoglobinuria Clone with Aplastic Anemia to Rituximab  

PubMed Central

Paroxysmal nocturnal hemoglobinuria is caused by expansion of a hematopoietic stem cell clone with an acquired somatic mutation in the PIG-A gene. This mutation aborts the synthesis and expression of the glycosylphosphatidylinositol anchor proteins CD55 and CD59 on the surface of blood cells, thereby making them more susceptible to complement-mediated damage. A spectrum of disorders occurs in PNH ranging from hemolytic anemia and thrombosis to myelodysplasia, aplastic anemia and, myeloid leukemias. Aplastic anemia is one of the most serious and life-threatening complications of PNH, and a PNH clone is found in almost a third of the cases of aplastic anemia. While allogeneic bone marrow transplantation and T cell immune suppression are effective treatments for aplastic anemia in PNH, these therapies have significant limitations. We report here the first case, to our knowledge, of PNH associated with aplastic anemia treated with the anti-CD20 monoclonal antibody rituximab, which was associated with a significant reduction in the size of the PNH clone and recovery of hematopoiesis. We suggest that this less toxic therapy may have a significant role to play in treatment of PNH associated with aplastic anemia. PMID:22937317

Raghupathy, Radha; Derman, Olga

2012-01-01

190

Anemia in the Elderly  

PubMed Central

As the population ages, increasing attention has become focused on the prevalence of anemia in elderly individuals. Anemia occurs in more than 10% of individuals who are older than the age of 65 years, and it increases to more than 50% in individuals who are older than the age of 80 years. Although the anemia is typically mild and unlikely to result in symptoms, it is uniformly associated with increased morbidity and mortality as assessed in large cohort studies. Anemia is an independent predictor of these adverse outcomes both in healthy community-dwelling subjects and in patients with significant co-morbidities. Efforts to understand the pathophysiology of anemia in this population, especially the one third of patients with unexplained anemia, have focused on the potential contributions of inflammatory pathways, erythropoietin resistance, and changes in hematopoietic stem cells to the age-dependent decrease in red cell mass. We would argue that these pathways are closely interrelated and combine to lead to anemia in aging individuals. This brief review summarizes the current understanding of this entity and our studies aimed at further delineating its pathophysiology. PMID:23874029

Berliner, Nancy

2013-01-01

191

Renal recovery with eculizumab in atypical hemolytic uremic syndrome following prolonged dialysis.  

PubMed

Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy (TMA) which encompasses hemolytic anemia, thrombocytopenia, and organ impairment. Around 10% of cases are atypical HUS (aHUS), a rare disease with poor outcomes caused by uncontrolled activation of the alternative complement pathway. This case describes a young woman with clinical manifestations compatible with TMA during childhood and adolescence who was formally diagnosed with aHUS at the age of 21. She was managed with intensive plasma exchange and hemodialysis, which failed to improve her severe acute kidney injury and other hematological manifestations of aHUS. This was further compounded by several episodes of flash pulmonary edema and the posterior reversible encephalopathy syndrome (PRES). Treatment with the monoclonal anti-C5 inhibitor, eculizumab, improved all hematological parameters with almost full renal recovery following 3.5 months of dialysis. So far, long-term use of eculizumab (> 11 months) continues to be effective and without complication. Our case illustrates the difficulty but importance of early consideration of aHUS in patients presenting with TMA. More importantly, we highlight that near-normal renal recovery may be attained with eculizumab in adults even after a long dependence on dialysis - an observation that has not been reported in the literature so far. PMID:23557793

Povey, Hannah; Vundru, Rahul; Junglee, Naushad; Jibani, Mahdi

2014-11-01

192

Familial Atypical Hemolytic Uremic Syndrome: A Review of Its Genetic and Clinical Aspects  

PubMed Central

Atypical hemolytic uremic syndrome (aHUS) is a rare renal disease (two per one million in the USA) characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. Both sporadic (80% of cases) and familial (20% of cases) forms are recognized. The study of familial aHUS has implicated genetic variation in multiple genes in the complement system in disease pathogenesis, helping to define the mechanism whereby complement dysregulation at the cell surface level leads to both sporadic and familial disease. This understanding has culminated in the use of Eculizumab as first-line therapy in disease treatment, significantly changing the care and prognosis of affected patients. However, even with this bright outlook, major challenges remain to understand the complexity of aHUS at the genetic level. It is possible that a more detailed picture of aHUS can be translated to an improved understanding of disease penetrance, which is highly variable, and response to therapy, both in the short and long terms. PMID:23251215

Bu, Fengxiao; Borsa, Nicolo; Gianluigi, Ardissino; Smith, Richard J. H.

2012-01-01

193

Postoperative Atypical Hemolytic Uremic Syndrome Associated with Complement C3 Mutation  

PubMed Central

Atypical hemolytic uremic syndrome (aHUS) can be distinguished from typical or Shiga-like toxin-induced HUS. The clinical outcome is unfavorable; up to 50% of affected patients progress to end-stage renal failure and 25% die during the acute phase. Multiple conditions have been associated with aHUS, including infections, drugs, autoimmune conditions, transplantation, pregnancy, and metabolic conditions. aHUS in the nontransplant postsurgical period, however, is rare. An 8-month-old boy underwent surgical repair of tetralogy of Fallot. Neurological disturbances, acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia developed 25 days later, and aHUS was diagnosed. Further evaluation revealed that his complement factor H (CFH) level was normal and that anti-FH antibodies were not detected in his plasma. Sequencing of his CFH, complement factor I, membrane cofactor protein, complement factor B, and thrombomodulin genes was normal. His ADAMTS-13 (a disintegrin-like and metalloprotease with thrombospondin-1 repeats 13) activity was also normal. However, he had a potentially causative mutation (R425C) in complement component C3. Restriction fragment length polymorphism analysis revealed that his father and aunt also had this mutation; however, they had no symptoms of aHUS. We herein report a case of aHUS that developed after cardiovascular surgery and was caused by a complement C3 mutation.

Matsukuma, Eiji; Imamura, Atsushi; Iwata, Yusuke; Takeuchi, Takamasa; Yoshida, Yoko; Fujimura, Yoshihiro; Fan, Xinping; Miyata, Toshiyuki; Kuwahara, Takashi

2014-01-01

194

Refractory anemia with ring sideroblasts.  

PubMed

Refractory anemia with ring sideroblasts (RARS) is a subtype of myelodysplastic syndrome (MDS) characterized by 15% or more ring sideroblasts in the bone marrow according to the WHO classification. After Perls staining, ring sideroblasts are defined as erythroblasts in which there are 5 or more siderotic granules covering at least a third of the nuclear circumference. The iron deposited in perinuclear mitochondria of ring sideroblasts is present in the form of mitochondrial ferritin. The molecular basis of MDS with ring sideroblasts has remained unknown until recently. In 2011, whole exome sequencing studies revealed somatic mutations of SF3B1, a gene encoding a core component of RNA splicing machinery, in myelodysplasia with ring sideroblasts. The close relationship between SF3B1 mutation and ring sideroblasts is consistent with a causal relationship, and makes SF3B1 the first gene to be associated with a specific morphological feature in MDS. RARS is mainly characterized by isolated anemia due to ineffective erythropoiesis, and its clinical course is generally benign, although there is a tendency to worsening of anemia in most patients over time. By contrast, refractory cytopenia with multilineage dysplasia and ring sideroblasts (RCMD-RS) is characterized by pancytopenia and dysplasia in two or more myeloid cell lineages. More importantly, patients with RCMD-RS have a higher risk of developing bone marrow failure or progressing to acute myeloid leukemia (AML). Refractory anemia with ring sideroblasts (RARS-T) associated with marked thrombocytosis is a myelodysplastic/myeloproliferative neoplasm associated with both SF3B1 and JAK2 or MPL mutations. RARS-T may develop from an SF3B1 mutated RARS through the acquisition of a JAK2 or MPL mutations in a subclone of hematopoietic cells. PMID:24507814

Malcovati, Luca; Cazzola, Mario

2013-12-01

195

Iron deficiency anemia  

MedlinePLUS

... You get iron deficiency anemia when your body's iron stores run low. This can occur because: You lose ... ferrous sulfate) are needed to build up the iron stores in your body. Most of the time, your ...

196

Sickle Cell Anemia.  

National Technical Information Service (NTIS)

The bibliography is composed of 9 annotated, unclassified references to reports on sickle cell anemia. The entries were selected from references processed into the AD data bank from January 1953 trough February 1971. Corporate author-monitoring agency, su...

1971-01-01

197

Hemolytic activity of five different calcium silicates.  

PubMed Central

Mineral characteristics and the in vitro hemolytic activity of three synthetic and two natural calcium silicates (CaSi) are compared. Hemolysis is higher for the synthetic compounds than for the natural ones. The difference is accentuated by weak ultrasonication of the minerals. No variation was observed within the two groups, including both acicular and fibrous forms. Calcium was released from the minerals during storage in Tris-buffered saline. At the same time, hemolysis decreased, and crystallographic alterations occurred in the leached minerals. Treatment of the CaSi with calcium chelators (EGTA and EDTA) did not change hemolytic activity. An increase was observed when 30 mM calcium was added. Hemolysis is related to specific surface areas and the crystalline structure of the minerals. Calcium may also be a contributing factor. Images FIGURE 1. a FIGURE 1. b FIGURE 1. c FIGURE 1. d FIGURE 1. e FIGURE 1. f FIGURE 7. a FIGURE 7. b FIGURE 7. c FIGURE 7. d FIGURE 7. e FIGURE 7. f PMID:6315361

Skaug, V; Gylseth, B

1983-01-01

198

Generation of hemolytic activity in ozone-treated phosphatidylcholine  

SciTech Connect

When liposomes prepared from purified soybean phosphatidylcholine were treated with ozone, at least two types of hemolytic agents were formed. One type was stable at 0 degree C but was destroyed rapidly at 37 degrees C. A second type was evolved during storage of ozone-treated phosphatidylcholine at 37 degrees C in the absence of EDTA. This study is concerned mainly with the heat-labile type. The hemolytic activity was not associated with lipid hydroperoxides. A number of substances were shown to inhibit the hemolytic activity and these may be divided into two classes. The first included cysteine, polyamines, n-heptylamine, semicarbazide, and tryptophan. Preincubation of the ozone-treated phosphatidylcholine was necessary with a Class 1 inhibitor, presumably for the interaction of the inhibitor with a functional group of the hemolytic agents. The Class II inhibitors, including BHT and vitamin C, required no preincubation. These possibly abolished the hemolytic activity by scavenging free radicals in the process.

Butterman, J.; Chan, P.C.; Kesner, L.

1987-04-01

199

Mouse models of Fanconi anemia  

PubMed Central

Fanconi anemia is a rare inherited disease characterized by congenital anomalies, growth retardation, aplastic anemia and an increased risk of acute myeloid leukemia and squamous cell carcinomas. The disease is caused by mutation in genes encoding proteins required for the Fanconi anemia pathway, a response mechanism to replicative stress, including that caused by genotoxins that cause DNA interstrand crosslinks. Defects in the Fanconi anemia pathway lead to genomic instability and apoptosis of proliferating cells. To date, thirteen complementation groups of Fanconi anemia were identified. Five of these genes have been deleted or mutated in the mouse, as well as a sixth key regulatory gene, to create mouse models of Fanconi anemia. This review summarizes the phenotype of each of the Fanconi anemia mouse models and highlights how genetic and interventional studies using the strains have yielded novel insight into therapeutic strategies for Fanconi anemia and into how the Fanconi anemia pathway protects against genomic instability. PMID:19427003

Parmar, Kalindi; D'Andrea, Alan; Niedernhofer, Laura J.

2009-01-01

200

Hemolytic-uremic syndrome in Switzerland: a nationwide surveillance 19972003  

Microsoft Academic Search

Hemolytic-uremic syndrome (HUS) is a leading cause of acute renal failure in childhood. In its typical presentation, it is\\u000a preceded by an episode of diarrhea mostly due to Shiga-toxin-producing Escherichia coli. There is important geographical variation of many aspects of this syndrome. Nationwide data on childhood HUS in Switzerland\\u000a have not been available so far. In a prospective national study

Alexandra Schifferli; Rodo O. von Vigier; Matteo Fontana; Giuseppina Spart; Hans Schmid; Mario G. Bianchetti; Christoph Rudin

2010-01-01

201

Physicochemical properties and inhibition effect on iron deficiency anemia of a novel polysaccharide-iron complex (LPPC).  

PubMed

Porphyran (P) was extracted from red algae Porphyra by boiling water. A novel polysaccharide-iron complex (LPPC) was prepared under the alkaline condition by adding a ferric chloride solution to the low molecular weight porphyran (LP) solution. Physicochemical properties and inhibition effect on iron deficiency anemia of this complex were studied. The content of iron(III) in the complex is 21.57% determined with iodometry. The results indicate that LPPC was product required. The complex can increase red blood cell count (RBC), hemoglobin (Hb), Serum iron (SI), spleen index, spleen mass and mass of mice with iron deficiency anemia (IDA). Although the structure and deeper mechanisms on hemolytic anemia of LPPC should be further studied, LPPC is hoped to be developed as a late-model iron supplement which has a synergism on anemia. PMID:22153938

Zhang, Zhong-Shan; Wang, Xiao-Mei; Han, Zhi-Ping; Yin, Li; Zhao, Ming-Xing; Yu, Shu-Chi

2012-01-01

202

How Is Iron-Deficiency Anemia Treated?  

MedlinePLUS

... the NHLBI on Twitter. How Is Iron-Deficiency Anemia Treated? Treatment for iron-deficiency anemia will depend ... may be advised. Treatments for Severe Iron-Deficiency Anemia Blood Transfusion If your iron-deficiency anemia is ...

203

Special Issues for People with Aplastic Anemia  

MedlinePLUS

... Aplastic Anemia Special Issues for People with Aplastic Anemia Because you have aplastic anemia , everyday events can ... doctor if it is safe Pregnancy and Aplastic Anemia Pregnancy is possible for women who have been ...

204

Iron deficiency anemia.  

PubMed

The prevalence of iron deficiency anemia is 2 percent in adult men, 9 to 12 percent in non-Hispanic white women, and nearly 20 percent in black and Mexican-American women. Nine percent of patients older than 65 years with iron deficiency anemia have a gastrointestinal cancer when evaluated. The U.S. Preventive Services Task Force currently recommends screening for iron deficiency anemia in pregnant women but not in other groups. Routine iron supplementation is recommended for high-risk infants six to 12 months of age. Iron deficiency anemia is classically described as a microcytic anemia. The differential diagnosis includes thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning. Serum ferritin is the preferred initial diagnostic test. Total iron-binding capacity, transferrin saturation, serum iron, and serum transferrin receptor levels may be helpful if the ferritin level is between 46 and 99 ng per mL (46 and 99 mcg per L); bone marrow biopsy may be necessary in these patients for a definitive diagnosis. In children, adolescents, and women of reproductive age, a trial of iron is a reasonable approach if the review of symptoms, history, and physical examination are negative; however, the hemoglobin should be checked at one month. If there is not a 1 to 2 g per dL (10 to 20 g per L) increase in the hemoglobin level in that time, possibilities include malabsorption of oral iron, continued bleeding, or unknown lesion. For other patients, an endoscopic evaluation is recommended beginning with colonoscopy if the patient is older than 50. PMID:17375513

Killip, Shersten; Bennett, John M; Chambers, Mara D

2007-03-01

205

[An uncommon etiology of anemia: copper deficiency].  

PubMed

A 58-year-old patient, without any notable medical history, except for alcoholism and treated hypertension, developed anemia and leukopenia with macrocytosis. Folate deficiency was diagnosed and subsequently treated. Despite folate supplementation, the hematological parameters did not normalize. Further diagnosis investigations were led to search for uncommon etiologies of anemia and leukoneutropenia. We diagnosed severe copper deficiency on the basis of decreased plasma levels of copper and ceruloplasmin. Copper supplementation improved blood counts within three months. This case illustrates hematological disorders due to copper deficiency, initially masked by an associated folate deficiency. The copper deficiency etiology was not identified in this case. PMID:23906580

Kouamou, Edwige; Stpanian, Alain; Khadra, Fadi; de Prost, Dominique; Teillet, France

2013-01-01

206

Screening for Hemolytic Disease of the Newborn by Cord Blood Coombs TestingAnalysis of a Five-Year xperience  

Microsoft Academic Search

An accepted diagnostic feature of hemo lytic disease of the newborn due to isoimmu nization by any of the Rh factors is a posi tive direct antiglobulin reaction (Coombs test) with umbilical cord blood.Not so well documented is the usefulness of the direct antiglobulin test for the recog nition of hemolytic disease associated with ABO grouping differences. Some believe the

John H. Clifford; Pat Mathews; C. W. Reiquam; H. D. Palmer

1968-01-01

207

Hemolytic Uremic Syndrome following Infection with O111 Shiga Toxin-Producing Escherichia coli Revealed through Molecular Diagnostics  

PubMed Central

We report a case of hemolytic uremic syndrome in a 69-year-old woman due to Shiga toxin-producing Escherichia coli, possibly serotype O111, to illustrate the potentially deleterious implications of a Campylobacter enzyme immunoassay (EIA) result and the increasing importance of molecular testing when conventional methods are limited. PMID:24371241

Operario, Darwin J.; Moonah, Shannon

2014-01-01

208

What Causes Sickle Cell Anemia?  

MedlinePLUS

... from the NHLBI on Twitter. What Causes Sickle Cell Anemia? Sickle cell anemia is an inherited disease. ... can also raise the risk for infection. Sickle Cell Trait People who inherit a sickle hemoglobin gene ...

209

Selection of peptides for serological detection of equine infectious anemia.  

PubMed

Equine infectious anemia caused by equine infectious anemia virus is an important disease due to its high severity and incidence in animals. We used a phage display library to isolate peptides that can be considered potential markers for equine infectious anemia diagnosis. We selected peptides using IgG purified from a pool comprised of 20 sera from animals naturally infected with equine infectious anemia virus. The diagnostic potential of these peptides was investigated by ELISA, Western blot and dot blot with purified IgG and serum samples. Based on the results, we chose a peptide mimetic for glycoprotein gp45 epitopes of equine infectious anemia virus, with potential for use as an antigen in indirect diagnostic assays. Synthesis of this peptide has possible applications for the development of new diagnostic tools for this disease. PMID:22653674

Santos, E M; Cardoso, R; Souza, G R L; Goulart, L R; Heinemann, M B; Leite, R C; Reis, J K P

2012-01-01

210

Acute methemoglobinemia with hemolytic anemia following bio-organic plant nutrient compound exposure: Two case reports.  

PubMed

Two young women, were reffered to our hospital on two different occasions with history of breathlessness and mental confusion, following consumption of two different bio-organic plant nutrient compounds with a suicidal intent. On examination, they had cyanotic mucous membranes, and their blood samples showed the classic 'dark chocolate brown' appearance. Work up revealed cyanosis unresponsive to oxygen supplementation and absence of cardiopulmonary abnormality. Pulse oximetry revealed saturation of 75% in case 1 and 80% in case 2, on 8 liters oxygen supplementation via face masks, although their arterial blood gas analysis was normal, suggestive of "saturation gap". Methemoglobinemia was suspected based on these findings and was confirmed by Carbon monoxide-oximetry (CO-oximetry). Methylene blue was administered and the patients showed dramatic improvement. Both the patients developed evidence of hemolysis approximately 72 hours following admission which improved with blood transfusion and supportive treatment. The patients were eventually discharged without any neurological sequalae. PMID:24678158

Malkarnekar, Santoshi Balkrishna; Anjanappa, Raveesha; Naveen, L; Kiran, B G

2014-02-01

211

Reticulocytopenia in severe autoimmune hemolytic anemia (AIHA) of the warm antibody type.  

PubMed

A patient with severe AIHA of the warm antibody type, absence of reticulocytes and red cell hyperplasia of the bone marrow is described. In order to maintain a reasonable hemoglobin level 38 units of washed packed red cells were required within 24 days. The treatment with high doses of steroids showed no permanent beneficial effect. After splenectomy the red cell destruction was immediately reduced and the patient went into a remission. Bone marrow culture studies during the acute phase of the disease and at the time of complete hemato- and immunological remission, i.e. 4 months after splenectomy suggested a circulating autoantibody directed to early erythroid progenitors (BFU-E). The inhibitory activity in the patient's plasma did not influence granulocytic or mixed colony formation (CFU-GEMM). In addition to autoantibodies directed to erythroblasts and erythropoietin involved in the pathogenic mechanisms leading to red cell aplasia type I and II the culture studies suggest an unusual autoantibody that might cause the observed reticulocytopenia and erythropoietic hyperplasia of the bone marrow in AIHA. After the splenectomy the patient recovered, he required no further blood transfusions and his disease has not recurred. PMID:6850101

Hauke, G; Fauser, A A; Weber, S; Maas, D

1983-06-01

212

Acute methemoglobinemia with hemolytic anemia following bio-organic plant nutrient compound exposure: Two case reports  

PubMed Central

Two young women, were reffered to our hospital on two different occasions with history of breathlessness and mental confusion, following consumption of two different bio-organic plant nutrient compounds with a suicidal intent. On examination, they had cyanotic mucous membranes, and their blood samples showed the classic dark chocolate brown appearance. Work up revealed cyanosis unresponsive to oxygen supplementation and absence of cardiopulmonary abnormality. Pulse oximetry revealed saturation of 75% in case 1 and 80% in case 2, on 8 liters oxygen supplementation via face masks, although their arterial blood gas analysis was normal, suggestive of saturation gap. Methemoglobinemia was suspected based on these findings and was confirmed by Carbon monoxide-oximetry (CO-oximetry). Methylene blue was administered and the patients showed dramatic improvement. Both the patients developed evidence of hemolysis approximately 72 hours following admission which improved with blood transfusion and supportive treatment. The patients were eventually discharged without any neurological sequalae. PMID:24678158

Malkarnekar, Santoshi Balkrishna; Anjanappa, Raveesha; Naveen, L.; Kiran, B. G.

2014-01-01

213

The characterization of gene mutations for human glucose phosphate isomerase deficiency associated with chronic hemolytic anemia.  

PubMed Central

DNA was isolated from four unrelated glucose phosphate isomerase-deficient patients. Seven new mutations in the coding region were found: 247 C-->T, 671 C-->T, 818 G-->A, 833 C-->T, 1039 C-->T, 1459 C-->T, and 1483 G-->A. Three patients were compound heterozygotes, and one patient was a homozygote of 247 C-->T/247 C-->T. Six mutations were found to involve highly conserved amino acids of glucose phosphate isomerase, suggesting that these residues are crucial for the maintenance of biological activity. Two polymorphic sites were also identified, 489 A-->G and 1356 G-->C, which do not produce a change in the amino acid sequence. PMID:7989588

Xu, W; Beutler, E

1994-01-01

214

How Is Aplastic Anemia Diagnosed?  

MedlinePLUS

... from the NHLBI on Twitter. How Is Aplastic Anemia Diagnosed? Your doctor will diagnose aplastic anemia based on your medical and family histories, a ... your primary care doctor thinks you have aplastic anemia, he or she may refer you to a ...

215

How Is Fanconi Anemia Treated?  

MedlinePLUS

... from the NHLBI on Twitter. How Is Fanconi Anemia Treated? Doctors decide how to treat Fanconi anemia (FA) based on a person's age and how ... Long-term treatments for FA can: Cure the anemia. Damaged bone marrow cells are replaced with healthy ...

216

Anemia and School Participation  

ERIC Educational Resources Information Center

Anemia is among the most widespread health problems for children in developing countries. This paper evaluates the impact of a randomized health intervention delivering iron supplementation and deworming drugs to Indian preschool children. At baseline, 69 percent were anemic and 30 percent had intestinal worm infections. Weight increased among

Bobonis, Gustavo J.; Miguel, Edward; Puri-Sharma, Charu

2006-01-01

217

Sickle Cell Anemia Bibliography.  

ERIC Educational Resources Information Center

Presents sources for the acquisition of medical, social, psychological, educational, and practical knowledge of sickle cell anemia. The materials listed are designed to help parents, educators, and public service workers. Materials include journal articles, films, brochures, slides, and fact sheets. The usual bibliographic information is given.

Christy, Steven C.

218

Anemia of inflammation.  

PubMed

Inflammation arising from various etiologies, including infection, autoimmune disorders, chronic diseases, and aging, can promote anemia. The anemia of inflammation (AI) is most often normocytic and normochromic and is usually mild. Characteristic changes in systemic iron handling, erythrocyte production, and erythrocyte life span all contribute to AI. The preferred treatment is directed at the underlying disease. However, when the inflammatory insult is intractable, or the cause has not been diagnosed, there are limited options for treatment of AI. Because anemia is a comorbid condition that is associated with poor outcomes in various chronic disease states, understanding its pathogenesis and developing new tools for its treatment should remain a priority. Hepcidin antimicrobial peptide has taken center stage in recent years as a potent modulator of iron availability. As the technology for quantitative hepcidin analysis improves, hepcidin's role in various disease states is also being revealed. Recent insights concerning the regulatory pathways that modify hepcidin expression have identified novel targets for drug development. As the field advances with such therapeutics, the analysis of the impact of normalized hemoglobin on disease outcomes will confirm whether anemia is a reversible independent contributor to the morbidity and mortality associated with inflammatory diseases. PMID:21239806

Roy, Cindy N

2010-01-01

219

Treatment of iron deficiency anemia in pediatric inflammatory bowel disease.  

PubMed

Anemia is a frequent extraintestinal manifestation of inflammatory bowel disease (IBD) that is commonly overlooked, despite its significant impact on quality of life. Characteristic symptoms include chronic fatigue, headache, and subtle impairment of cognitive function, although some less common symptoms include dyspnea, dizziness, pica, angular stomatitis, shortened attention span, and esophageal webs. Several types of anemia are associated with IBD, but iron deficiency anemia (IDA) accounts for the majority of cases and others include anemia of chronic disease, anemia associated with vitamin deficiency (vitamin B12 and folate), autoimmune anemia, and anemia caused by medication used to treat IBD. The diagnosis of IDA relies on laboratory blood tests. Therefore, these tests should be obtained on a regular basis because characteristic symptoms may be absent or not readily recognized by patients and their clinicians. Complete blood count may suffice; however, iron studies and serum vitamin levels may be necessary to differentiate between specific types of anemia. During the diagnostic process, it is important to consider coexistence of different types of anemia, especially if no response to therapy is noted. The therapy for anemia is directed towards treatment of the underlying inflammatory process and supplemental therapy, depending on the type of deficiency. Iron deficiency anemia is treated with iron preparations, first orally, and if unresponsive or if associated with untoward adverse events leading to decrease in adherence with the therapeutic regimen, with intravenous preparations. Intramuscular therapy has been abandoned due to high rate of complications. Intravenous therapy may be administered as a multiple-dose regimen (intravenous iron sucrose and gluconate) or as a single intravenous dose (iron dextran), which is associated with a higher risk of allergic infusion reactions and requires obligatory test dose administration. Treatment with erythropoietin is reserved for a select subgroup of patients with anemia of chronic disease. With appropriate treatment, the majority of patients with IBD will have significant improvement or resolution of anemia, which can lead to a better quality of life. However, a high index of suspicion should be maintained in order to identify the precise cause of anemia and to prescribe the appropriate therapy. PMID:16162307

Thayu, Meena; Mamula, Petar

2005-10-01

220

Change in Serum Ferritin Concentration in Experimentally Induced Anemia of Chronic Inflammation in Dogs  

PubMed Central

ABSTRACT In veterinary medicine, hyperferritinemia is often observed in dogs with various diseases (e.g., histiocytic sarcoma and immune-mediated hemolytic anemia) without evidence of iron overload. The mechanism underlying hyperferritinemia development is not well understood. Anemia caused by inflammation is termed as anemia of chronic disease (ACD), and experimentally induced ACD is known to cause slight hyperferritinemia. However, almost all these studies were based on short-term acute inflammation. Hepcidin, a protein mainly produced by hepatocytes, is thought to be a key regulator in iron release from reticuloendothelial cells (RECs), and its expression is related to ACD. We hypothesized that in the case of long-term ACD, iron deposition in RECs increases through hepcidin, causing a diachronic increase in serum ferritin levels. In the present study, we used a canine model with repeated subcutaneous administration of turpentine oil every 3 days over a period of 42 days (15 injections) and induced long-term inflammatory conditions; furthermore, we evaluated the change in serum ferritin concentration. Hypoproliferative anemia, bone marrow iron deposition and hypoferremia, which are characteristic of ACD, were observed on administering the turpentine injections. Hepatic iron content, hepatic hepcidin mRNA expression and serum ferritin concentration increased during the early period after turpentine injection, but returned to normal levels later. These results show that experimentally induced long-term ACD caused hypoproliferative anemia without sustained increase in hepcidin expression and did not cause systemic iron overload. Thus, chronic inflammation may not contribute greatly to increase in hyperferritinemia. PMID:23803460

CHIKAZAWA, Seishiro; NAKAZAWA, Takafumi; HORI, Yasutomo; HOSHI, Fumio; KANAI, Kazutaka; ITO, Naoyuki; ORINO, Koichi; WATANABE, Kiyotaka; HIGUCHI, Seiichi

2013-01-01

221

21 CFR 866.5490 - Hemopexin immunological test system.  

Code of Federal Regulations, 2010 CFR

...of various hematologic disorders, such as hemolytic anemia (anemia due to shortened in vivo survival of mature red blood...compensate for their decreased life span) and sickle cell anemia. (b) Classification. Class II (special...

2010-04-01

222

Investigation of macrocytic anemia.  

PubMed

The three most common causes of macrocytosis--vitamin B12 or folate deficiency, liver disease, and reticulocytosis--usually can be differentiated on the basis of red cell indexes and morphologic findings. Bone marrow studies are not indicated. In reticulocytosis, the mean corpuscular volume (MCV) rarely exceeds ll0 cu mu and a reticulocyte count quickly establishes the diagnosis. In liver disease, macrocytosis is also mild and uniform. The RBCs are round. In megaloblastic anemia, the MCV may exceed 150 cu mu. The RBCs vary considerably in size and shape. The macrocytes tend to be oval. Serum vitamin B12 determination remains the best test for unmasking vitamin B12 deficiency. It should be ordered in conjunction with serum and red cell folate determinations in the course of investigating a macrocytic anemia. When vitamin B12 deficiency has been established, a Schilling test or plasma uptake test is indicated to pinpoint the cause. PMID:368738

Ward, P C

1979-02-01

223

Current treatment of atypical hemolytic uremic syndrome  

PubMed Central

Summary Tremendous advances have been made in understanding the pathogenesis of atypical Hemolytic Uremic Syndrome (aHUS), an extremely rare disease. Insights into the molecular biology of aHUS resulted in rapid advances in treatment with eculizumab (Soliris, Alexion Pharmaceuticals Inc.). Historically, aHUS was associated with very high rates of mortality and morbidity. Prior therapies included plasma therapy and/or liver transplantation. Although often life saving, these were imperfect and had many complications. We review the conditions included under the rubric of aHUS: S. pneumoniae HUS (SpHUS), inborn errors of metabolism, and disorders of complement regulation, emphasizing their differences and similarities. We focus on the clinical features, diagnosis, and pathogenesis, and treatment of aHUS that results from mutations in genes encoding alternative complement regulators, SpHUS and HUS associated with inborn errors of metabolism. Mutations in complement genes, or antibodies to their protein products, result in unregulated activity of the alternate complement pathway, endothelial injury, and thrombotic microangiopathy (TMA). Eculizumab is a humanized monoclonal antibody that inhibits the production of the terminal complement components C5a and the membrane attack complex (C5b-9) by binding to complement protein C5a. This blocks the proinflammatory and cytolytic effects of terminal complement activation. Eculizumab use has been reported in many case reports, and retrospective and prospective clinical trials in aHUS. There have been few serious side effects and no reports of tachphylaxis or drug resistance. The results are very encouraging and eculizumab is now recognized as the treatment of choice for aHUS. PMID:25343125

Kaplan, Bernard S.; Ruebner, Rebecca L.; Spinale, Joann M.; Copelovitch, Lawrence

2014-01-01

224

Anemia of chronic disease.  

PubMed

Anemia of chronic disease (ACD) or inflammation may be secondary to infections, autoimmune disorders, chronic renal failure, or malignancies. It is characterized by an immune activation with an increase in inflammatory cytokines and resultant increase in hepcidin levels. In addition, inappropriate erythropoietin levels or hyporesponsiveness to erythropoietin and reduced red blood cell survival contribute to the anemia. Hepcidin being the central regulator of iron metabolism plays a key role in the pathophysiology of ACD. Hepcidin binds to the iron export protein, ferroportin, present on macrophages, hepatocytes, and enterocytes, causing degradation of the latter. This leads to iron trapping within the macrophages and hepatocytes, resulting in functional iron deficiency. Production of hepcidin is in turn regulated by iron stores, inflammation, and erythropoiesis via the BMP-SMAD and JAK-STAT signaling pathways. Treatment of anemia should primarily be directed at the underlying disease, and conventional therapy such as red blood cell transfusions, iron, erythropoietin, and novel agents targeting the hepcidin-ferroportin axis and signaling pathways (BMP-SMAD, JAK-STAT) involved in hepcidin production also may be considered. PMID:23953340

Gangat, Naseema; Wolanskyj, Alexandra P

2013-07-01

225

Anemia in Heart Failure Patients  

PubMed Central

Heart failure is a very common disease, with severe morbidity and mortality, and a frequent reason of hospitalization. Anemia and a concurrent renal impairment are two major risk factors contributing to the severity of the outcome and consist of the cardio renal anemia syndrome. Anemia in heart failure is complex and multifactorial. Hemodilution, absolute or functional iron deficiency, activation of the inflammatory cascade, and impaired erythropoietin production and activity are some pathophysiological mechanisms involved in anemia of the heart failure. Furthermore other concomitant causes of anemia, such as myelodysplastic syndrome and chemotherapy, may worsen the outcome. Based on the pathophysiology of cardiac anemia, there are several therapeutic options that may improve hemoglobin levels, tissues' oxygenation, and probably the outcome. These include administration of iron, erythropoiesis-stimulating agents, and blood transfusions but still the evidence provided for their use remains limited. PMID:22536520

Alexandrakis, Michael G.; Tsirakis, George

2012-01-01

226

Hemolytic disease of the fetus and newborn owing to anti-U, successfully treated with repeated intrauterine transfusions.  

PubMed

Hemolytic disease of the fetus and newborn (HDFN) owing to anti-U has rarely been reported. U is part of the MNS system.M and N glycoproteins are located on glycophorin A (GPA); Sand s antigens are on glycophorin B (GPB). Individuals who lack GPB are S- and s- and also lack U. The U- phenotype occurs almost exclusively in the African population and has a very low frequency (0.25%). Anti-U is of immunoglobulin G class and can cause hemolytic transfusion reaction and HDFN. In this report we present the use of a noninvasive method to detect anemia in the fetus and the subsequent use of intrauterine transfusion(IUT) with blood of a very rare phenotype. For the first time, we used deglycerolized and 3-week-old red blood cell units for IUT without signs of adverse reactions and with the expected effect on the hemoglobin value. We conclude that this transfusion strategy could be applied safely. PMID:24094236

Strindberg, Johanna; Lundahl, Joachim; Ajne, Gunilla

2013-01-01

227

Genetics Home Reference: Dyserythropoietic anemia and thrombocytopenia  

MedlinePLUS

... Recent literature OMIM Genetic disorder catalog Conditions > Dyserythropoietic anemia and thrombocytopenia On this page: Description Genetic changes ... Glossary definitions Reviewed October 2014 What is dyserythropoietic anemia and thrombocytopenia? Dyserythropoietic anemia and thrombocytopenia is a ...

228

Genetics Home Reference: Diamond-Blackfan anemia  

MedlinePLUS

... literature OMIM Genetic disorder catalog Conditions > Diamond-Blackfan anemia On this page: Description Genetic changes Inheritance Diagnosis ... definitions Reviewed February 2012 What is Diamond-Blackfan anemia? Diamond-Blackfan anemia is a disorder of the ...

229

Avoiding Anemia: Boost Your Red Blood Cells  

MedlinePLUS

... link, please review our exit disclaimer . Subscribe Avoiding Anemia Boost Your Red Blood Cells If youre ... and sluggish, you might have a condition called anemia. Anemia is a common blood disorder that many ...

230

Failure of Clindamycin To Eradicate Infection with Beta-Hemolytic Streptococci Inducibly Resistant to Clindamycin in an Animal Model and in Human Infections  

PubMed Central

Inducible clindamycin resistance in beta-hemolytic streptococci remains an underrecognized phenomenon of unknown clinical significance. We performed an evaluation of inducible clindamycin resistance using an animal model as well as retrospectively reviewing the charts of patients treated with clindamycin monotherapy who were infected with beta-hemolytic streptococci inducibly resistant to clindamycin. The neutropenic mouse thigh model of infection was used to evaluate the in vivo activity of clindamycin against beta-hemolytic streptococci, including isolates susceptible, inducibly resistant, or constitutively resistant to clindamycin. The clinical microbiology laboratory information system and pharmacy databases were cross-referenced to identify patients with infections due to inducibly clindamycin-resistant beta-hemolytic streptococci who were treated with clindamycin monotherapy. Medical records of these patients were reviewed to evaluate microbiologic and clinical outcomes. Inducible clindamycin resistance resulted in impaired killing of beta-hemolytic streptococci in the animal model. Though suppressed initially, compared to those with constitutive resistance (P = 0.0429), by 48 h, colony counts of inducibly clindamycin-resistant organisms were similar to those of constitutively resistant isolates (P = 0.1142). In addition, we identified 8 patients infected with inducibly clindamycin-resistant beta-hemolytic streptococci who experienced clinical and microbiologic failure when treated with clindamycin monotherapy. These patients either improved initially and subsequently failed or never responded to clindamycin therapy. We have demonstrated in a murine model of infection and from human cases that inducible clindamycin resistance in beta-hemolytic streptococci is clinically significant. Routine testing and reporting by clinical laboratories should be encouraged and alternative antimicrobial agents considered when these organisms are encountered in clinical care. PMID:24323478

Lewis, James S.; Lepak, Alex J.; Thompson, George R.; Craig, William A.; Andes, David R.; Sabol-Dzintars, Kathryn E.

2014-01-01

231

A mouse model of hemolytic disease of the newborn.  

PubMed

In this issue of Blood, Stowell et al describe a novel mouse model of hemolytic disease of the fetus and newborn (HDFN) that recapitulates many of the key features of human disease.1 Recently, this same group of researchers described a transgenic mouse that expresses the human KEL2 (Chellano) red cell surface protein from the Kell system on red cells, and subsequently demonstrated that Kell differences on transfused blood induce antibody responses and hemolytic transfusion reactions similar to those seen in patients. In this latest report, Stowell et al demonstrate that similar to some patients, Kell differences between mother and father can lead to maternal antibody generation and hemolytic disease in utero. In so doing, they provide experimental confirmation of a long sought after animal model of HDFN. PMID:23970354

Luckey, Chance John; Silberstein, Leslie E

2013-08-22

232

Racial difference in incidence of ABO hemolytic disease.  

PubMed Central

In this review of 7,464 consecutive infants born at North Carolina Memorial Hospital, hemolytic disease from ABO incompatibility was found to be two to three times as common in black infants as in white infants. The statistical significance of the difference remained high as more restrictive criteria for ABO hemolytic disease were applied. ABO disease, serious enough to cause an indirect serum bilirubin of 15 mg/100ml or higher, had an incidence in black newborns as great as the incidence of Rh hemolytic disease in whites. In contrast, the general prevalence and severity of hyperbilirubinemia was not found to be higher in black newborns than in white infants. The difference cannot be attributed to differences in the prevalence of ABO blood groups between the two races. Policies of early discharge of newborns could be affected by the finding that ABO erythroblastosis is two to three times as common in black infants as in white infants. PMID:961953

Bucher, K A; Patterson, A M; Elston, R C; Jones, C A; Kirkman, H N

1976-01-01

233

Hyperemic peripheral red marrow in a patient with sickle cell anemia demonstrated on Tc-99m labeled red blood cell venography  

SciTech Connect

A 25-year-old gravid woman, homozygous for sickle cell anemia, with a history of recent deep venous thrombosis, was examined using Tc-99m labeled red blood cell venography for recurrent thrombosis. Although negative for thrombus, the study presented an unusual incidental finding: the patient's peripheral bone marrow was hyperemic in a distribution consistent with peripheral red bone marrow expansion. Such a pattern has not been documented before using this technique. This report supports other literature that has demonstrated hyperemia of peripheral red bone marrow in other hemolytic anemias. This finding may ultimately define an additional role of scintigraphy in assessing the pathophysiologic status of the sickle cell patient.

Heiden, R.A.; Locko, R.C.; Stent, T.R. (Columbia Univ. College of Physicians and Surgeons, New York, NY (USA))

1991-03-01

234

78 FR 79469 - Strategies To Address Hemolytic Complications of Immune Globulin Infusions; Public Workshop  

Federal Register 2010, 2011, 2012, 2013

...Hemolytic Complications of Immune Globulin Infusions; Public Workshop AGENCY: Food and Drug...Hemolytic Complications of Immune Globulin Infusions.'' The purpose of the public workshop...Globulin Intravenous (IGIV) (Human) infusion. Complications of hemolysis...

2013-12-30

235

Anemia associated with chronic heart failure: current concepts  

PubMed Central

Anemia is a frequent comorbidity of heart failure and is associated with poor outcomes. Anemia in heart failure is considered to develop due to a complex interaction of iron deficiency, kidney disease, and cytokine production, although micronutrient insufficiency and blood loss may contribute. Currently, treatment of anemia of heart failure lacks clear targets and specific therapy is not defined. Intravenous iron use has been shown to benefit anemic as well as nonanemic patients with heart failure. Treatment with erythropoietin-stimulating agents has been considered alone or in combination with iron, but robust evidence to dictate clear guidelines is not currently available. Available and emerging new agents in the treatment of anemia of heart failure will need to be tested in randomized, controlled studies. PMID:23403618

Shah, Ravish; Agarwal, Anil K

2013-01-01

236

Hematopoietic stem cell transplantation for aplastic anemia and paroxysmal nocturnal hemoglobinuria: current evidence and recommendations.  

PubMed

Aplastic anemia (AA) is a bone marrow failure syndrome characterized by pancytopenia and an empty bone marrow. Standard treatments for AA include immunosuppressive therapy and bone marrow transplantation (BMT). BMT is the preferred option for young AA patients with a sibling donor, whereas in older patients or in those to be grafted from an unrelated donor BMT is exploited as second-line treatment. Current results of BMT for AA demonstrate cure rates up to 80 and 70% in BMT from HLA-matched siblings and unrelated donor, respectively, with age and stem cell source largely affecting the outcome. BMT is also a potential treatment option for paroxysmal nocturnal hemoglobinuria, a rare hematological disorder characterized by complement-mediated intravascular hemolytic anemia, thrombophilia and bone marrow failure. PMID:25331515

Marotta, Serena; Pagliuca, Simona; Risitano, Antonio M

2014-12-01

237

Studies on the factors affecting the growth and hemolytic activity of Anabaena variabilis  

Microsoft Academic Search

The hemolytic activity of the cell-free culture supernatant of Anabaena variabilis OL S1 was investigated using the hemolysis of rabbit erythrocytes as an assay. The culture medium of A. variabilis started to exhibit hemolytic activity at the late exponential growth phase, and maximized at the stationary phase. The hemolytic\\u000a toxin is heat-stable and can be extracted in dichloromethane. The hemolytic

Wei Wang; Xiu-Kai Song; Shao-Guo Ru

2007-01-01

238

Sickle Cell Anemia  

NSDL National Science Digital Library

In this case study on sickle cell anemia, students are introduced to some of the key researchers responsible for determining the molecular basis of the disease and learn about the functioning of erythrocytes as well as the notion that changes in the environment can influence the functioning of cells.  Students also become familiar with the process of osmosis and how it can influence the sickling of the erythrocytes.  Throughout the case, students must address experimental design questions. The case was designed for use in the first semester of an introductory majors biology course.

Stamper, Debra L.

2000-01-01

239

FA (Fanconi Anemia) Family Newsletter  

MedlinePLUS

Family Newsletter The Fanconi Anemia Research Fund publishes the FA Family Newsletter twice a year and mails it to all FA patients and their ... 888-326-2664 | 541-687-4658 Copyright 2014 Fanconi Anemia Research Fund, Inc. | Privacy Policy | Translate: Google Translate ...

240

Isolated abducens nerve palsy in hemolytic uremic syndrome.  

PubMed

Isolated abducens nerve (VI cranial nerve) palsies are reported in a dialyzed child with Escherichia coli 0157:H7-associated hemolytic uremic syndrome (HUS). There were no other neurological manifestations and he made a complete recovery, suggesting that isolated abducens nerve palsy in HUS may represent a minor neurological complication. PMID:15185136

Durkan, Anne; Menascu, Shay; Langlois, Valerie

2004-08-01

241

Hemolytic reactions mechanically induced by kinked hemodialysis lines.  

PubMed

Ten hemolytic reactions occurred in our outpatient hemodialysis unit over a 12-month period (December 1989 to December 1990). Eight patients were hospitalized and one died. All patients developed severe abdominal or back pain an average of 2.5 hours into a 4-hour hemodialysis session using a bleach/formaldehyde reprocessed hollow-fiber cupraphan dialyzer (average reuse, three times) with blood flow rates of 375 mL/min. All had visible hemolysis in a spun hematocrit, seven had a significant decrease in hematocrit, and six developed pancreatitis. Hemolysis was further confirmed by a decrease in haptoglobin in all patients and an increase in lactic dehydrogenase in all but the last case. Investigation of each episode failed to find an abnormality in dialysate temperature or tonicity; dialysate or water levels of copper, zinc, nitrates, chloramine, or formaldehyde; or blood pump or venous alarm. Hemolytic reactions continued despite changing to 15-gauge needles, removing bleach from the reuse procedure, or stopping reuse. During the eighth episode, a kink was noted in the arterial blood line. Two subsequent hemolytic reactions occurred, and in each kinks were found in the arterial blood line, either in the excess tubing between the blood pump and drip chamber or in the predialyzer. No further hemolytic reactions occurred after changing to a new arterial blood line without redundant tubing and securing all lines. Hemolytic reactions occurring during hemodialysis have many etiologies, including mechanical trauma, which we report may result from kinking of dialyzer lines. With new blood lines on the market, attention to this aspect of dialysis is mandatory. PMID:8659503

Sweet, S J; McCarthy, S; Steingart, R; Callahan, T

1996-02-01

242

Do You Know about Sickle Cell Anemia?  

MedlinePLUS

Do You Know About Sickle Cell Anemia? KidsHealth > Kids > Health Problems > Blood > Do You Know About Sickle Cell Anemia? Print A A A Text Size What's in ... to stay in the hospital. What Causes Sickle Cell Anemia? Sickle cell anemia is an inherited (say: ...

243

Hemolytic-uremic syndrome in Switzerland: a nationwide surveillance 1997-2003.  

PubMed

Hemolytic-uremic syndrome (HUS) is a leading cause of acute renal failure in childhood. In its typical presentation, it is preceded by an episode of diarrhea mostly due to Shiga-toxin-producing Escherichia coli. There is important geographical variation of many aspects of this syndrome. Nationwide data on childhood HUS in Switzerland have not been available so far. In a prospective national study through the Swiss Pediatric Surveillance Unit 114 cases (median age 21 months, 50% boys) were reported between April 1997 and March 2003 by 38 pediatric units (annual incidence 1.42 per 10(5) children < or =16 years). Shiga-toxin-producing E. coli were isolated in 32 (60%) of tested stool samples, serotype O157:H7 in eight. Sixteen children presented with only minimal renal involvement, including three with underlying urinary tract infection. Six patients presented with atypical hemolytic-uremic syndrome, and six with HUS due to invasive Streptococcus pneumoniae infection. Mortality was 5.3%, including two out of six children with S. pneumoniae infection. The severity of thrombocytopenia and the presence of central nervous system involvement significantly correlated with mortality. In conclusion, childhood HUS is not rare in Switzerland. Contrasting other countries, E. coli O157:H7 play only a minor role in the etiology. Incomplete manifestation is not uncommon. PMID:19830454

Schifferli, Alexandra; von Vigier, Rodo O; Fontana, Matteo; Spart, Giuseppina; Schmid, Hans; Bianchetti, Mario G; Rudin, Christoph

2010-05-01

244

Occurrence of extended spectrum beta-lactamases producing alpha hemolytic Escherichia coli in neonatal diarrhea.  

PubMed

E. coli, often highly pathogenic in neonatal and immuno-compromised patients, are usually supposed susceptible to a variety of chemotherapeutic agents, however with the time and also due to the extensive use of chemotherapeutic agents irrespective of their susceptibility, have evolved drug resistant strains. Moreover, the production of extended spectrum beta-lactamases producing enteric pathogens is a serious issue. In this context the present study was conducted to find out occurrence of extended spectrum Beta-lactamases producing alpha hemolytic Escherichia coli in neonates, of less than one month of age, suffering from diarrhea. Fecal samples were collected from various private hospitals in Mathura and Agra districts of Uttar Pradesh, India. With the help of hospital nursing staffs sterilized stool samples were collected and processed for isolation of E. coli. The double disk diffusion method was applied to assess the ESBL production. E. coli organisms were isolated from 39 kids out of 120 samples. The assessment of isolates revealed alpha hemolytic nature of 23 isolates on 5% sheep blood agar. As usual when drug sensitivity was performed that revealed their multi drug resistance pattern which on further examination with double disk method showed 17 of them to be extended spectrum beta-lactamases producing E. coli. The presence of enterohemorrhagic extended spectrum beta-lactamases producing Escherichia coli in kids is a matter of concern and public health importance as it may be due to the transmission from hospital itself during the birth time or post birth admission period. PMID:24783787

Kumar, Amit; Verma, Amit Kumar; Malik, Subhash; Gupta, Manoj Kumar; Sharma, Arvind; Rahal, Anu

2014-01-01

245

X-linked Sideroblastic Anemia Due to Carboxyl-terminal ALAS2 Mutations That Cause Loss of Binding to the ?-Subunit of Succinyl-CoA Synthetase (SUCLA2)*  

PubMed Central

Mutations in the erythroid-specific aminolevulinic acid synthase gene (ALAS2) cause X-linked sideroblastic anemia (XLSA) by reducing mitochondrial enzymatic activity. Surprisingly, a patient with the classic XLSA phenotype had a novel exon 11 mutation encoding a recombinant enzyme (p.Met567Val) with normal activity, kinetics, and stability. Similarly, both an expressed adjacent XLSA mutation, p.Ser568Gly, and a mutation (p.Phe557Ter) lacking the 31 carboxyl-terminal residues also had normal or enhanced activity, kinetics, and stability. Because ALAS2 binds to the ? subunit of succinyl-CoA synthetase (SUCLA2), the mutant proteins were tested for their ability to bind to this protein. Wild type ALAS2 bound strongly to a SUCLA2 affinity column, but the adjacent XLSA mutant enzymes and the truncated mutant did not bind. In contrast, vitamin B6-responsive XLSA mutations p.Arg452Cys and p.Arg452His, with normal in vitro enzyme activity and stability, did not interfere with binding to SUCLA2 but instead had loss of positive cooperativity for succinyl-CoA binding, an increased Km for succinyl-CoA, and reduced vitamin B6 affinity. Consistent with the association of SUCLA2 binding with in vivo ALAS2 activity, the p.Met567GlufsX2 mutant protein that causes X-linked protoporphyria bound strongly to SUCLA2, highlighting the probable role of an ALAS2-succinyl-CoA synthetase complex in the regulation of erythroid heme biosynthesis. PMID:22740690

Bishop, David F.; Tchaikovskii, Vassili; Hoffbrand, A. Victor; Fraser, Marie E.; Margolis, Steven

2012-01-01

246

Iron-deficiency anemia in Castleman disease: implication of the interleukin 6/hepcidin pathway.  

PubMed

In addition to occasional autoimmune hemolytic anemia, unexplained iron-deficiency anemia has been reported in childhood Castleman disease (CD). The recent discovery of hepcidin has regenerated the research on iron metabolism. This hormone is a key regulator of iron homeostasis, mainly by inhibiting intestinal iron absorption. Liver expression of hepcidin increases in response to interleukin 6 (IL-6). With chronic overproduction of IL-6 as a hallmark, CD could be an interesting human model for studying the contribution of the IL-6/hepcidin pathway in the pathogenesis of anemia of chronic disease. We report here the case of a 16-year-old boy with chronic iron-deficiency anemia (plasma ferritin: 19 ?g/L; plasma iron: 2.2 ?mol/L; negative bone marrow Perls' Prussian blue stain), inflammatory syndrome (C-reactive protein: 108 mg/L), and growth retardation for the previous 2 years. Diagnostic workup revealed a large mesenteric mass corresponding to localized CD of mixed histologic type. Resection of the tumor resulted in complete resolution of iron-deficiency anemia and inflammatory syndrome. Parallel variations of plasma IL-6, C-reactive protein, and hepcidin concentrations, together with tumor immunohistochemistry, strongly suggested that IL-6 synthesized by the tumor caused both the inflammation and iron deficiency through enhancement of hepcidin production by the liver. The results of this unique case study (1) explain the mechanism of iron deficiency observed in some children with CD, (2) confirm in vivo the regulatory effect of IL-6 in human hepcidin production, and (3) suggest that iron deficiency is a causal link between IL-6 and anemia of chronic disease. PMID:21041280

Arlet, Jean-Benot; Hermine, Olivier; Darnige, Luc; Ostland, Vaughn; Westerman, Mark; Badoual, Ccile; Pouchot, Jacques; Capron, Loc

2010-12-01

247

MACROCYTIC ANEMIA OF PREGNANCY REVIEW OF LITERATURE AND REPORT OF A CASE TREATED WITH FOLIC AcID*  

E-print Network

The association of anemia with pregnancy is well recognized. In this country the anemia is commonly due to iron deficiencies and is hypochromic. In the tropics a macrocytic, hyperchromic anemia of pregnancy has attracted attention and has been the subject of many recent investigations. Its counterpart in the temperate climates, the macrocytic or so-called pernicious anemia of pregnancy, has been considered a relatively rare dyscrasia.', The macrocytic anemia of pregnancy was first recognized over a century ago when Channing2 reported ten fatal cases. In 1919 Osler7 differentiated the so-called pernicious anemia of pregnancy from typical Addisonian anemia by pointing out that when recovery from the former disease took place it was permanent and the woman might escape it in subsequent pregnancies. In macrocytic anemia of pregnancy the peripheral blood picture may vgry from one identical with that of true pernicous anemia to one lacking all characteristic features of this anemia.1 13 On the other hand, examination of the bone marrow reveals pictures identical with those found in true Addisonian pernicious anemia and clearly indicates that macrocytic anemia of pregnancy has for its immediate cause arrested maturation of the megaloblasts. The two features which may be relied upon for the certain diagnosis of macrocytic anemia of pregnancy are the appearance of megaloblasts in the peripheral blood and the finding of a megaloblastic change in the bone marrow.1 If the peripheral blood picture is not diagnostic, bone marrow biopsy by means of sternal puncture is necessary or some cases will be missed. The following features serve to differentiate the macrocytic anemia of pregnancy from the true Addisonian pernicious anemia: the presence of free hydrochloric acid in gastric juice either without or after histamine injection, a lower frequency and the degree of macrocytosis and

Sidney E

248

Molecular Pathogenesis of Fanconi Anemia  

Microsoft Academic Search

Fanconi anemia (FA) is a rare inherited disorder characterized clinically by aplastic anemia, developmental defects, and a susceptibility to cancer. Eleven complementation groups have been identified (FA-A, -B, -C, -D1, -D2, -E, -F, -G, -I, -J, and -L), and the genes responsible for 9 groups (FANCA, B, C, D1, D2, E, F, G, and L) have been cloned. The proteins

Natalie Collins; Gary M. Kupfer

2005-01-01

249

Selective C3 deficiency due to C3 nephritic factor in an apparently healthy girl  

Microsoft Academic Search

SummaryRoutine laboratory investigations performed on the serum of an 8-year-old girl examined because of a moderate degree of iron-deficiency\\u000a anemia showed a markedly reduced C3 level. More detailed complement studies revealed a selective C3 deficiency, as indicated\\u000a by the almost undetectable C3 concentration tested by both hemolytic and immunochemical assays and by the normal or slightly\\u000a reduced levels of all

FRANCESCO TEDESCO; Pier Angelo Tovo; Giorgio Tamaro; Marina Basaglia; Sandra Perticarari; Maria Antonietta Villa

1985-01-01

250

Recurrent Syncope Due to Refractory Cerebral Venous Sinus Thrombosis and Transient Elevations of Intracranial Pressure  

PubMed Central

Chronic paroxysmal intracranial hypertension leading to syncope is a phenomenon not reported previously in patients with refractory cerebral venous sinus thrombosis. We report a case of paroxysmal intracranial hypertension leading to syncopal episodes in a patient with idiopathic autoimmune hemolytic anemia and venous sinus thrombosis. This case demonstrates that intermittent elevations in intracranial pressure can lead to syncope in patients with venous sinus thrombosis and emphasizes the importance of considering this potentially treatable etiology of syncopal episodes. PMID:24381706

Larimer, P.; McDermott, M.W.; Scott, B.J.; Shih, T.T.; Poisson, S.N.

2014-01-01

251

Direct Hyperbilirubinemia Complicating ABO Hemolytic Disease of the Newborn  

Microsoft Academic Search

A retrospective study of the diagnostic implications of conjugated hyperbilirubinemia com plicating ABO hemolytic disease of the newborn (HDN) was done by studying the records of 264 infants with ABO-HDN. Direct hyperbilirubinemia was found to complicate ABO-HDN in 3 per cent of the infants, all being full term. Eighty-seven per cent were female and familial occurrence was noted in half

Yakov Sivan; Paul Merlob; Jacob Nutman; Salomon H. Reisner

1983-01-01

252

Pulmonary Hemorrhage Complicating a Typical Hemolytic-Uremic Syndrome  

Microsoft Academic Search

We describe a case of pulmonary bleeding and subsequent acute respiratory distress syndrome (ARDS) in a 20-month-old female suffering from a typical postdiarrheal hemolytic-uremic syndrome (HUS). Acute renal failure was treated early by peritoneal dialysis. It is of interest to underline that thrombocytopenia or any coagulative impairment was absent when this complication occurred, and spontaneous diuresis recovery was ongoing. All

M. Piastra; A. Ruggiero; A. Langer; E. Caresta; A. Chiaretti; S. Pulitan; G. Polidori; R. Riccardi

2004-01-01

253

Hemolytic venoms from marine cnidarian jellyfish - an overview  

PubMed Central

Cnidarian jellyfish are viewed as an emergent problem in several coastal zones throughout the world. Recurrent outbreaks pose a serious threat to tourists and bathers, as well as to sea-workers, involving health and economical aspects. As a rule, cnidarian stinging as a consequence of nematocyst firing induces merely local symptoms but cardiovascular or neurological complications can also occur. Hemolysis is a frequent effect of cnidarian stinging; this dangerous condition is known to be caused by several venoms and can sometimes be lethal. At present, the bulk of data concerning hemolytic cnidarian venoms comes from the study of benthic species, such as sea anemones and soft corals, but hemolytic factors were found in venoms of several siphonophore, cubozoan and scyphozoan jellyfish, which are mainly involved in the envenomation of bathers and sea-workers. Therefore, the aim of this paper is to review the scientific literature concerning the hemolytic venoms from cnidarian jellyfish taking into consideration their importance in human pathology as well as health implications and possible therapeutic measures. PMID:25386336

Mariottini, Gian Luigi

2014-01-01

254

Hemolytic activity in extracts of the diatom Nitzschia.  

PubMed

The few reports about diatom toxins are related to central nervous system toxicity, induced by domoic acid. In the present work Nitzschia sp. (Bacillariophyceae) was studied. The cells were cultured in f/2 medium, under 4000 lux and 14/10 hr light/dark cycle. After massive growth (5 x 10(6) cells/ml) the diatom cells were filtered, and an extract was prepared and partitioned in two fractions (polar and apolar). After cell harvesting by filtration, the diatom cells were shaken in artificial sea water to extract the water-soluble extracellular matrix (mucilage). An extract was prepared with the washed cells (free of mucilage), and polar and apolar fractions were obtained. Hemolytic assays were performed using 4.0 and 0.5% erythrocyte suspensions. Both the diatom polar and apolar fractions showed hemolytic activity. The membrane phospholipid sphingomyelin was tested as an acceptor for the hemolysins in the polar and apolar fractions. The mucilage did not exhibit hemolytic activity. PMID:9080587

Rangel, M; Malpezzi, E L; Susini, S M; de Freitas, J C

1997-02-01

255

Fanconi anemia and ubiquitination.  

PubMed

Fanconi anemia (FA) is a rare recessive hereditary disease characterized clinically by congenital defects, progressive bone-marrow failure, and cancer predisposition. Cells from FA patients exhibit hypersensitivity to DNA cross-linking agents, such as mitomycin C (MMC). To date, at least 12 FA genes have been found deleted or mutated in FA cells, and 10 FA gene products form a core complex involved in FA/BRCA2 DNA repair pathway?FA pathway. The ubiquitin E3 ligase FANCL, an important factor of FA core complex, co-functions with a new ubiquitin conjugating enzyme UBE2T to catalyze the monoubiquitination of FANCD2. FANCD2-Ub binds BRCA2 to form a new complex located in chromatin foci and then take part in DNA repair process. The deubiquitylating enzyme USP1 removes the mono-ubiquitin from FANCD2-Ub following completion of the repair process, then restores the blocked cell cycle to normal order by shutting off the FA pathway. In a word, the FANCD2 activity adjusted exquisitely by ubiquitination and/or deubiquitination in vivo may co-regulate the FA pathway involving in variant DNA repair pathway. PMID:17643942

Zhang, Yingying; Zhou, Xiaowei; Huang, Peitang

2007-07-01

256

What Are the Signs and Symptoms of Anemia?  

MedlinePLUS

... Twitter. What Are the Signs and Symptoms of Anemia? The most common symptom of anemia is fatigue ( ... mild symptoms or none at all. Complications of Anemia Some people who have anemia may have arrhythmias ( ...

257

Malaria, erythrocytic infection, and anemia.  

PubMed

Malaria is a major world health problem. It results from infection of parasites belonging to the genus Plasmodium. Plasmodium falciparum and Plasmodium vivax cause the major human malarias, with P falciparum being the more virulent. During their blood stages of infection, both P falciparum and P vivax induce anemia. Severe malarial anemia caused by P falciparum is responsible for approximately a third of the deaths associated with disease. Malarial anemia appears to be multi-factorial. It involves increased removal of circulating erythrocytes as well as decreased production of erythrocytes in the bone marrow. The molecular mechanisms underlying malarial anemia are largely unknown. Over the last five years, malaria parasite ligands have been investigated for their remodeling of erythrocytes and possible roles in destruction of mature erythrocytes. Polymorphisms in cytokines have been associated with susceptibility to severe malarial anemia: these cytokines and malaria "toxins" likely function by perturbing erythropoiesis. Finally a number of co-infections increase susceptibility to malarial anemia, likely because they exacerbate inflammation caused by malaria. Because of the complexities involved, the study of severe malarial anemia may need a "systems approach" to yield comprehensive understanding of defects in both erythropoiesis and immunity associated with disease. New and emerging tools such as (i) mathematical modeling of the dynamics of host control of malarial infection, (ii) ex vivo perfusion of human spleen to measure both infected and uninfected erythrocyte retention, and (iii) in vitro development of erythroid progenitors to dissect responsiveness to cytokine imbalance or malaria toxins, may be especially useful to develop integrated mechanistic insights and therapies to control this major and fatal disease pathology. PMID:20008186

Haldar, Kasturi; Mohandas, Narla

2009-01-01

258

Peginesatide for the treatment of anemia in the nephrology setting.  

PubMed

Anemia is a major complication in patients with chronic kidney disease, as the damaged kidney is unable to produce enough erythropoietin. Peginesatide (formerly known as Hematide) is a synthetic, peptide-based erythropoiesis-stimulating agent linked to polyethylene glycol. Based on extensive preclinical and clinical data substantiating the efficacy and safety of this agent, it was approved in the U.S. in March 2012 for the treatment of anemia due to chronic kidney disease in adult patients on dialysis. Peginesatide (Omontys) was launched in the U.S. in April 2012. PMID:22745925

Graul, A I

2012-06-01

259

Novel Human Erythrovirus Associated with Transient Aplastic Anemia  

Microsoft Academic Search

Erythrovirus (formerly parvovirus) B19 causes a wide range of diseases in humans, including anemia due to aplastic crisis. Diagnosis of B19 infection relies on serology and the detection of viral DNA by PCR. These techniques are usually thought to detect all erythrovirus field isolates, since the B19 genome is known to undergo few genetic variations. We have detected an erythrovirus

QUANG TRI NGUYEN; CHRISTOPHE SIFER; VERONIQUE SCHNEIDER; XAVIER ALLAUME; ANNABELLE SERVANT; FRANCOISE BERNAUDIN; VERONIQUE AUGUSTE; ANTOINE GARBARG-CHENON; UFR Saint-Antoine

1999-01-01

260

HEMOGLOBIN PRODUCTION FACTORS IN THE HUMAN LIVER : ANEMIAS, HYPOPROTEINEMIA, CIRRHOSIS, PIGMENT ABNORMALITIES, AND PREGANCY.  

PubMed

Human liver tissue has been assayed to determine the amount of hemoglobin production factors in normal and abnormal states. Standardized dogs made anemic by blood removal have been used in this biological assay. Normal animal liver as control is rated as 100 per cent. Normal human liver tissue as compared with the normal animal control contains more of these hemoglobin production factors-a biological assay ratio of 120 to 160 per cent. Infections, acute and chronic, do not appear to modify these values, the concentration of hemoglobin-producing factors falling within the normal range. Pernicious anemia and aplastic anemia both show large liver stores of hemoglobin-producing factors-a biological assay ratio of 200 to 240 per cent. Therapy in pernicious anemia reduces these liver stores as new red cells are formed. Secondary anemia presents a low normal or subnormal liver store of hemoglobin-producing factors-an assay of 60 to 130 per cent. Hemochromatosis, erythroblastic anemia, and hemolytic icterus in spite of large iron deposits in the liver usually show a biological assay which is normal or close to normal. Polycythemia shows low reserve stores of hemoglobin-producing factors. Leukemias present a wide range of values discussed above. Hypoproteinemia almost always is associated with low reserve stores of hemoglobin-producing factors in the liver-biological assays of 60 to 80 per cent. Hypoproteinemia means a depletion of body protein reserve stores including the labile protein liver reserves-a strong indication that the prehemoglobin material (or globin) is related to these liver stores. Pregnancy, eclampsia, and lactation all may present subnormal liver stores of hemoglobin-producing factors. Exhaustion of protein stores lowers the barrier to infection and renders the liver very susceptible to many toxic substances. It should not be difficult to correct hypoproteinemia under these conditions and thus relieve the patient of a real hazard. PMID:19871236

Whipple, G H; Robscheit-Robbins, F S

1942-09-01

261

Sleep alterations and iron deficiency anemia in infancy  

PubMed Central

Iron-deficiency anemia (IDA) continues to be the most common single nutrient deficiency in the world. An estimated 20-25% of the worlds infants have IDA, with at least as many having iron deficiency without anemia. Infants are at particular risk due to rapid growth and limited dietary sources of iron. We found that infants with IDA showed different motor activity patterning in all sleep-waking states and several differences in sleep states organization. Sleep alterations were still apparent years after correction of anemia with iron treatment in the absence of subsequent IDA. We suggest that altered sleep patterns may represent an underlying mechanism that interferes with optimal brain functioning during sleep and wakefulness in former IDA children. PMID:20620103

Peirano, Patricio D.; Algarin, Cecilia R.; Chamorro, Rodrigo A.; Reyes, Sussanne C.; Duran, Samuel A.; Garrido, Marcelo I.; Lozoff, Betsy

2013-01-01

262

Delayed Anemia after Treatment with Injectable Artesunate in the Democratic Republic of the Congo: A Manageable Issue  

PubMed Central

Cases of delayed hemolytic anemia have been described after treatment with injectable artesunate, the current World Health Organization (WHO)recommended first-line drug for the treatment of severe malaria. A total of 350 patients (215 [61.4%] < 5 years of age and 135 [38.6%] ? 5 years of age) were followed-up after treatment with injectable artesunate for severe malaria in hospitals and health centers of the Democratic Republic of the Congo. Complete series of hemoglobin (Hb) measurements were available for 201 patients. A decrease in Hb levels between 2 and 5 g/dL was detected in 23 (11.4%) patients during the follow-up period. For five patients, Hb levels decreased below 5 g/dL during at least one follow-up visit. All cases of delayed anemia were clinically manageable and resolved within one month. PMID:25071004

Burri, Christian; Ferrari, Giovanfrancesco; Ntuku, Henry Maggi; Kitoto, Antoinette Tshefu; Duparc, Stephan; Hugo, Pierre; Mitembo, Didier Kalemwa; Lengeler, Christian

2014-01-01

263

Delayed anemia after treatment with injectable artesunate in the Democratic Republic of the Congo: a manageable issue.  

PubMed

Cases of delayed hemolytic anemia have been described after treatment with injectable artesunate, the current World Health Organization (WHO)-recommended first-line drug for the treatment of severe malaria. A total of 350 patients (215 [61.4%] < 5 years of age and 135 [38.6%] ? 5 years of age) were followed-up after treatment with injectable artesunate for severe malaria in hospitals and health centers of the Democratic Republic of the Congo. Complete series of hemoglobin (Hb) measurements were available for 201 patients. A decrease in Hb levels between 2 and 5 g/dL was detected in 23 (11.4%) patients during the follow-up period. For five patients, Hb levels decreased below 5 g/dL during at least one follow-up visit. All cases of delayed anemia were clinically manageable and resolved within one month. PMID:25071004

Burri, Christian; Ferrari, Giovanfrancesco; Ntuku, Henry Maggi; Kitoto, Antoinette Tshefu; Duparc, Stephan; Hugo, Pierre; Mitembo, Didier Kalemwa; Lengeler, Christian

2014-10-01

264

FastStats: Anemia or Iron Deficiency  

MedlinePLUS

... State and Territorial Data NCHS Home FastStats Home Anemia or Iron Deficiency Data are for the U.S. ... care Number of visits to emergency departments with anemia as the primary diagnosis: 209,000 Source: National ...

265

Genetics Home Reference: Congenital dyserythropoietic anemia  

MedlinePLUS

... literature OMIM Genetic disorder catalog Conditions > Congenital dyserythropoietic anemia (often shortened to CDA ) On this page: Description ... Reviewed July 2009 What is CDA? Congenital dyserythropoietic anemia (CDA) is an inherited blood disorder that affects ...

266

How Is Sickle Cell Anemia Diagnosed?  

MedlinePLUS

... the NHLBI on Twitter. How Is Sickle Cell Anemia Diagnosed? A simple blood test, done at any ... States, all States mandate testing for sickle cell anemia as part of their newborn screening programs. The ...

267

How Is Sickle Cell Anemia Treated?  

MedlinePLUS

... from the NHLBI on Twitter. How Is Sickle Cell Anemia Treated? Sickle cell anemia has no widely ... severity of the disease. Blood and Marrow Stem Cell Transplant A blood and marrow stem cell transplant ...

268

Who Is at Risk for Anemia?  

MedlinePLUS

... such as kidney disease, cancer, diabetes, rheumatoid arthritis, HIV/AIDS, inflammatory bowel disease (including Crohn's disease), liver disease, heart failure , and thyroid disease Long-term infections A family history of inherited anemia, such as sickle cell anemia ...

269

Heart failure and anemia: mechanisms and pathophysiology  

Microsoft Academic Search

Anemia is a common comorbidity in patients with heart failure and affects up to 50% of patients, depending on the definition\\u000a of anemia used and on the population studied. Presence of anemia and lower hemoglobin (Hgb) concentrations are powerful independent\\u000a predictors of adverse outcomes in heart failure. Even small reductions in Hgb are associated with worse outcomes. Correction\\u000a of anemia

Inder S. Anand

2008-01-01

270

Diagnosis of Atypical Hemolytic Uremic Syndrome and Response to Eculizumab Therapy  

PubMed Central

Atypical hemolytic uremic syndrome (aHUS) has a high mortality rate if not detected and treated early. While in the past, it was associated with renal failure in children, today, it has become increasingly identified among adults. Due to recent advances in the pathogenesis of aHUS and other major thrombotic microangiopathies (TMA), diagnosing it has become a lot easier. We present a case of a 62-year-old man who was initially thought to have thrombotic thrombocytopenic purpura (TTP), but after further evaluation was diagnosed with aHUS. We will discuss how to distinguish aHUS from other major TMA and the role of eculizumab in the management of aHUS.

Mathew, Jacob J; Denunzio, Troy M; Carmichael, Mark G

2014-01-01

271

Anemia in inflammatory bowel disease: a neglected issue with relevant effects.  

PubMed

Anemia, a common complication associated with inflammatory bowel disease (IBD), is frequently overlooked in the management of IBD patients. Unfortunately, it represents one of the major causes of both decreased quality of life and increased hospital admissions among this population. Anemia in IBD is pathogenically complex, with several factors contributing to its development. While iron deficiency is the most common cause, vitamin B12 and folic acid deficiencies, along with the effects of pro-inflammatory cytokines, hemolysis, drug therapies, and myelosuppression, have also been identified as the underlying etiology in a number of patients. Each of these etiological factors thus needs to be identified and corrected in order to effectively manage anemia in IBD. Because the diagnosis of anemia in IBD often presents a challenge, combinations of several hematimetric and biochemical parameters should be used. Recent studies underscore the importance of determining the ferritin index and hepcidin levels in order to distinguish between iron deficiency anemia, anemia due to chronic disease, or mixed anemia in IBD patients. With regard to treatment, the newly introduced intravenous iron formulations have several advantages over orally-administered iron compounds in treating iron deficiency in IBD. In special situations, erythropoietin supplementation and biological therapies should be considered. In conclusion, the management of anemia is a complex aspect of treating IBD patients, one that significantly influences the prognosis of the disease. As a consequence, its correction should be considered a specific, first-line therapeutic goal in the management of these patients. PMID:24707137

Guagnozzi, Danila; Lucendo, Alfredo J

2014-04-01

272

Anemia in inflammatory bowel disease: A neglected issue with relevant effects  

PubMed Central

Anemia, a common complication associated with inflammatory bowel disease (IBD), is frequently overlooked in the management of IBD patients. Unfortunately, it represents one of the major causes of both decreased quality of life and increased hospital admissions among this population. Anemia in IBD is pathogenically complex, with several factors contributing to its development. While iron deficiency is the most common cause, vitamin B12 and folic acid deficiencies, along with the effects of pro-inflammatory cytokines, hemolysis, drug therapies, and myelosuppression, have also been identified as the underlying etiology in a number of patients. Each of these etiological factors thus needs to be identified and corrected in order to effectively manage anemia in IBD. Because the diagnosis of anemia in IBD often presents a challenge, combinations of several hematimetric and biochemical parameters should be used. Recent studies underscore the importance of determining the ferritin index and hepcidin levels in order to distinguish between iron deficiency anemia, anemia due to chronic disease, or mixed anemia in IBD patients. With regard to treatment, the newly introduced intravenous iron formulations have several advantages over orally-administered iron compounds in treating iron deficiency in IBD. In special situations, erythropoietin supplementation and biological therapies should be considered. In conclusion, the management of anemia is a complex aspect of treating IBD patients, one that significantly influences the prognosis of the disease. As a consequence, its correction should be considered a specific, first-line therapeutic goal in the management of these patients. PMID:24707137

Guagnozzi, Danila; Lucendo, Alfredo J

2014-01-01

273

Erythropoietic stress and anemia in diabetes mellitus  

Microsoft Academic Search

Anemia is one of the world's most common preventable conditions, yet it is often overlooked, especially in people with diabetes mellitus. Diabetes-related chronic hyperglycemia can lead to a hypoxic environment in the renal interstitium, which results in impaired production of erythropoietin by the peritubular fibroblasts and subsequent anemia. Anemia in patients with diabetes mellitus might contribute to the pathogenesis and

Peter Winocour; Dhruv K. Singh; Ken Farrington

2009-01-01

274

Production of a bacteriolysin by a hemolytic Escherichia coli strain.  

PubMed Central

Nonhemolytic Escherichia coli were outnumbered by hemolytic E. coli within 24 h after being inoculated in a mixed culture at an initial ratio of 200 nonhemolytic to 1 hemolytic organism. The hemolytic strain was found to produce a cell-free, filterable substance which causes lysis of nonhemolytic E. coli B when grown in liquid cultures but not when grown on agar plates. The bacteriolysin is inactivated by boiling, by freezing and thawing, and by incubation with trypsin. The inability to inhibit growth on an agar plate, dependence on cell concentration for its effect, lysis of the sensitive cells, and appearance of phage particles in the cell lysates suggest that this substance is not like colicins or microcins previously described. After lysis of E. coli B, bacteriophage particles were visible in transmission electron micrographs of material pelleted by ultracentrifugation. However, no bacteriophage were observed in pellets from the bacteriolysin-containing supernatants before lysis of E. coli B. Failure to find bacteriophage in these preparations, and the fact that some bacteriolysin activity remains in the supernatant solution after centrifugation at 150,000 X g for 6.5 h, indicate that the bacteriolysin is not itself a bacteriophage. Exposure of E. coli B to UV light and mitomycin C did not induce production of a temperate phage. The properties of this system, in which a cell-free substance produced by one strain of bacteria causes lysis of another strain, appear to differ from those of the various types of bacteriocins and bacteriophages described to date. Images PMID:6350182

Jorgensen, S E; Mussen, H K; Mulcahy, P F; Wu, G K

1983-01-01

275

Production of a bacteriolysin by a hemolytic Escherichia coli strain.  

PubMed

Nonhemolytic Escherichia coli were outnumbered by hemolytic E. coli within 24 h after being inoculated in a mixed culture at an initial ratio of 200 nonhemolytic to 1 hemolytic organism. The hemolytic strain was found to produce a cell-free, filterable substance which causes lysis of nonhemolytic E. coli B when grown in liquid cultures but not when grown on agar plates. The bacteriolysin is inactivated by boiling, by freezing and thawing, and by incubation with trypsin. The inability to inhibit growth on an agar plate, dependence on cell concentration for its effect, lysis of the sensitive cells, and appearance of phage particles in the cell lysates suggest that this substance is not like colicins or microcins previously described. After lysis of E. coli B, bacteriophage particles were visible in transmission electron micrographs of material pelleted by ultracentrifugation. However, no bacteriophage were observed in pellets from the bacteriolysin-containing supernatants before lysis of E. coli B. Failure to find bacteriophage in these preparations, and the fact that some bacteriolysin activity remains in the supernatant solution after centrifugation at 150,000 X g for 6.5 h, indicate that the bacteriolysin is not itself a bacteriophage. Exposure of E. coli B to UV light and mitomycin C did not induce production of a temperate phage. The properties of this system, in which a cell-free substance produced by one strain of bacteria causes lysis of another strain, appear to differ from those of the various types of bacteriocins and bacteriophages described to date. PMID:6350182

Jorgensen, S E; Mussen, H K; Mulcahy, P F; Wu, G K

1983-09-01

276

Perioperative anemia management in colorectal cancer patients: A pragmatic approach  

PubMed Central

Anemia, usually due to iron deficiency, is highly prevalent among patients with colorectal cancer. Inflammatory cytokines lead to iron restricted erythropoiesis further decreasing iron availability and impairing iron utilization. Preoperative anemia predicts for decreased survival. Allogeneic blood transfusion is widely used to correct anemia and is associated with poorer surgical outcomes, increased post-operative nosocomial infections, longer hospital stays, increased rates of cancer recurrence and perioperative venous thromboembolism. Infections are more likely to occur in those with low preoperative serum ferritin level compared to those with normal levels. A multidisciplinary, multimodal, individualized strategy, collectively termed Patient Blood Management, minimizes or eliminates allogeneic blood transfusion. This includes restrictive transfusion policy, thromboprophylaxis and anemia management to improve outcomes. Normalization of preoperative hemoglobin levels is a World Health Organization recommendation. Iron repletion should be routinely ordered when indicated. Oral iron is poorly tolerated with low adherence based on published evidence. Intravenous iron is safe and effective but is frequently avoided due to misinformation and misinterpretation concerning the incidence and clinical nature of minor infusion reactions. Serious adverse events with intravenous iron are extremely rare. Newer formulations allow complete replacement dosing in 15-60 min markedly facilitating care. Erythropoiesis stimulating agents may improve response rates. A multidisciplinary, multimodal, individualized strategy, collectively termed Patient Blood Management used to minimize or eliminate allogeneic blood transfusion is indicated to improve outcomes. PMID:24587673

Munoz, Manuel; Gomez-Ramirez, Susana; Martin-Montanez, Elisa; Auerbach, Michael

2014-01-01

277

Cooley's Anemia: A Psychosocial Directory.  

ERIC Educational Resources Information Center

The directory is intended to aid patients and their families who are coping with the genetic disorder of Cooley's anemia. A brief review of the disease covers background, genetics, symptoms, effect on the patient, treatment, and current research. The next section looks at psychosocial needs at various times (time of diagnosis, infancy and toddler

National Center for Education in Maternal and Child Health, Washington, DC.

278

An anemia of Alzheimer's disease.  

PubMed

Lower hemoglobin is associated with cognitive impairment and Alzheimer's disease (AD). Since brain iron homeostasis is perturbed in AD, we investigated whether this is peripherally reflected in the hematological and related blood chemistry values from the Australian Imaging Biomarker and Lifestyle (AIBL) study (a community-based, cross-sectional cohort comprising 768 healthy controls (HC), 133 participants with mild cognitive impairment (MCI) and 211 participants with AD). We found that individuals with AD had significantly lower hemoglobin, mean cell hemoglobin concentrations, packed cell volume and higher erythrocyte sedimentation rates (adjusted for age, gender, APOE-?4 and site). In AD, plasma iron, transferrin, transferrin saturation and red cell folate levels exhibited a significant distortion of their customary relationship to hemoglobin levels. There was a strong association between anemia and AD (adjusted odds ratio (OR)=2.43, confidence interval (CI) (1.31, 4.54)). Moreover, AD emerged as a strong risk factor for anemia on step-down regression, even when controlling for all other available explanations for anemia (adjusted OR=3.41, 95% CI (1.68, 6.92)). These data indicated that AD is complicated by anemia, which may itself contribute to cognitive decline. PMID:24419041

Faux, N G; Rembach, A; Wiley, J; Ellis, K A; Ames, D; Fowler, C J; Martins, R N; Pertile, K K; Rumble, R L; Trounson, B; Masters, C L; Bush, A I

2014-11-01

279

Living with Sickle Cell Anemia  

MedlinePLUS

... specific stresses related to sickle cell anemia, including: Body-image problems caused by delayed sexual maturity. Coping with pain and fear of addiction from using strong pain medicines. Living with ... pain and damage to the body at any time.) Teen support groups and family ...

280

Treatment of Sickle Cell Anemia.  

National Technical Information Service (NTIS)

The patent application relates to the discovery that cyanate, such as a 0.01-1.0M potassium cyanate solution, is useful to prevent the sickling of the red blood cells of sickle cell anemia patients. It has also been discovered that red blood cells when ta...

A. Cerami, J. M. Manning

1971-01-01

281

MEGALOBLASTIC AND OTHER MACROCYTIC ANEMIA  

E-print Network

9/16/2013 1 MEGALOBLASTIC AND OTHER MACROCYTIC ANEMIA MACROCYTOSIS MCV > 100 fL MCHC ­ Normal False LABORATORY FINDINGS Peripheral Blood Macrocytic, Normochromic Leukocytes and Platelets Decreased Oval Macrocytes Hypersegmented Neutrophils LABORATORY FINDINGS Bone Marrow Hypercellular Decreased M:E ratio

282

Dangerous drug interactions leading to hemolytic uremic syndrome following lung transplantation  

Microsoft Academic Search

BACKGROUND: To report our experience of a rather uncommon drug interaction, resulting in hemolytic uremic syndrome (HUS). METHODS: Two consecutive cases of hemolytic uremic syndrome were diagnosed in our service. In both patients the use of macrolides in patients taking Tacrolimus, resulted in high levels of Tacrolimus. RESULTS: The first patient was a 48 years old female with Bilateral emphysema.

Haralabos Parissis; Kate Gould; John Dark

2010-01-01

283

Hemolytic activity of venom from crown-of-thorns starfish Acanthaster planci spines  

PubMed Central

Background The crown-of-thorns starfish Acanthaster planci is a venomous species from Taiwan whose venom provokes strong hemolytic activity. To understand the hemolytic properties of A. planci venom, samples were collected from A. planci spines in the Penghu Islands, dialyzed with distilled water, and lyophilized into A. planci spine venom (ASV) powder. Results Both crude venom and ASV cause 50% hemolysis at a concentration of 20?g/mL. The highest hemolytic activity of ASV was measured at pH7.0-7.4; ASV-dependent hemolysis was sharply reduced when the pH was lower than 3 or greater than 8. There was almost no hemolytic activity when the Cu2+ concentration was increased to 10mM. Furthermore, incubation at 100C for 30 to 60minutes sharply decreased the hemolytic activity of ASV. After treatment with the protease ?-chymotrypsin, the glycoside hydrolase cellulase, and the membrane component cholesterin, the hemolytic activity of ASV was significantly inhibited. Conclusions The results of this study provide fundamental information about A. planci spine venom. The hemolytic activity was affected by pH, temperature, metal ions, EDTA, cholesterin, proteases, and glycoside hydrolases. ASV hemolysis was inhibited by Cu2+, cholesterin, ?-chymotrypsin, and cellulose, factors that might prevent the hemolytic activity of venom and provide the medical treatment for sting. PMID:24063308

2013-01-01

284

[Anemia as a surgical risk factor].  

PubMed

Perioperative anemia is common in patients undergoing surgery and is associated with increased morbidity and mortality and a decreased quality of life. The main causes of anemia in the perioperative context are iron deficiency and chronic inflammation. Anemia can be aggravated by blood loss during surgery, and is most commonly treated with allogeneic transfusion. Moreover, blood transfusions are not without risks, once again increasing patient morbidity and mortality. Given these concerns, we propose to review the pathophysiology of anemia in the surgical environment, as well as its treatment through the consumption of iron-rich foods and by oral or intravenous iron therapy (iron sucrose and iron carboxymaltose). In chronic inflammatory anemia, we use erythropoiesis-stimulating agents (erythropoietin alpha) and, in cases of mixed anemia, the combination of both treatments. The objective is always to reduce the need for perioperative transfusions and speed the recovery from postoperative anemia, as well as decrease the patient morbidity and mortality rate. PMID:24314568

Moral Garca, Victoria; ngeles Gil de Bernab Sala, M; Nadia Diana, Kinast; Pericas, Bartolom Cantallops; Nebot, Alexia Galindo

2013-07-01

285

Hemolytic action and surface activity of triterpene saponins from Anchusa officinalis L. Part 21: On the costituents of Boraginaceae.  

PubMed

Relationship between chemical structure, hemolytic action and surface activity of five glucosides of oleanolic acid were studied. Monodesmosidic saponins are more hemolytic than bisdesmosidic. The hemolytic activity of monodesmosides decreased with the length and the branching of the glucosidic chain. Surface activity is major in bisdesmosides. This property increases with the length of the glucosidic chain in monodesmosides. Increase of hemolytic action is accompanied by a decrease of surface activity. PMID:7433502

Romussi, G; Cafaggi, S; Bignardi, G

1980-08-01

286

Maternal ?-Hemolytic Streptococcal Pharyngeal Exposure and Colonization in Pregnancy  

PubMed Central

Objectives. To report the pharyngeal colonization rate of ?-hemolytic streptococci and changes in the value of antistreptolysin O (ASO) and anti-DNase B serology titers during pregnancy. Methods. Healthy pregnant women were recruited and blood was drawn in each trimester. The upper limit of normal (ULN) values for ASO and anti-DNase B was calculated for each trimester. Throat swabs were collected for culture and positive cultures were further assessed for the identification of serogroup of the isolated ?-hemolytic streptococcus. Results. Out of a total of 126 pregnant women, 34.1% had positive throat cultures. Group C and group G strains were isolated in 18.2% of throat cultures while group F was detected in 13.5% of cases. The rate of colonization with GAS was 1.6%. There was an overall drop in ASO titer during pregnancy while anti-DNase B titers remained relatively unchanged. ULN values of 164IU, 157IU, and 156IU were calculated for ASO at the first, second, and third trimesters, respectively. Based on the ULN values, 28.6% of patients had recent streptococcal exposure. Conclusions. These results show that pregnant women act as a reservoir for spreading potentially immunogenic (groups C and G) and disease producing (group F) virulent strains of streptococci.

Brar, Anoop K.; Hathcock, Trupti; Cunningham, Madeleine W.; Eghtesady, Pirooz

2014-01-01

287

Hemolytic mechanism of dioscin proposed by molecular dynamics simulations.  

PubMed

Saponins are a class of compounds containing a triterpenoid or steroid core with some attached carbohydrate modules. Many saponins cause hemolysis. However, the hemolytic mechanism of saponins at the molecular level is not yet fully understood. In an attempt to explore this issue, we have studied dioscin-a saponin with high hemolytic activity-through extensive molecular dynamics (MD) simulations. Firstly, all-atom MD simulations of 8 ns duration were conducted to study the stability of the dioscin-cholesterol complex and the cholesterol-cholesterol complex in water and in decane, respectively. MM-GB/SA computations indicate that the dioscin-cholesterol complex is energetically more favorable than the cholesterol-cholesterol complex in a non-polar environment. Next, several coarse-grained MD simulations of 400 ns duration were conducted to directly observe the distribution of multiple dioscin molecules on a DPPC-POPC-PSM-CHOL lipid bilayer. Our results indicate that dioscin can penetrate into the lipid bilayer, accumulate in the lipid raft micro-domain, and then bind cholesterol. This leads to the destabilization of lipid raft and consequent membrane curvature, which may eventually result in the hemolysis of red cells. This possible mechanism of hemolysis can well explain some experimental observations on hemolysis. PMID:19513766

Lin, Fu; Wang, Renxiao

2010-01-01

288

Isolation of a Variant of Subtilosin A with Hemolytic Activity?  

PubMed Central

Bacillus subtilis produces an anionic bacteriocin called subtilosin A that possesses antibacterial activity against certain gram-positive bacteria. In this study, we uncovered a hemolytic mutant of B. subtilis that produces an altered form of subtilosin A. The mutant bacteriocin, named subtilosin A1, has a replacement of threonine at position 6 with isoleucine. In addition to the hemolytic activity, subtilosin A1 was found to exhibit enhanced antimicrobial activity against specific bacterial strains. The B. subtilis albB mutant that does not produce a putative immunity peptide was more sensitive to both subtilosin A and subtilosin A1. A spontaneous suppressor mutation of albB that restored resistance to subtilosin A and subtilosin A1 was obtained. The sbr (subtilosin resistance) mutation conferring the resistance is not linked to the sboA-alb locus. The sbr mutation does not increase the resistance of B. subtilis to other cell envelope-targeted antimicrobial agents, indicating that the mutation specifically confers the resistance to subtilosins. The findings suggest possible bioengineering approaches for obtaining anionic bacteriocins with enhanced and/or altered bactericidal activity. Furthermore, future identification of the subtilosin-resistant mutation could provide insights into the mechanism of subtilosin A activity. PMID:19633086

Huang, Tai; Geng, Hao; Miyyapuram, Venugopal R.; Sit, Clarissa S.; Vederas, John C.; Nakano, Michiko M.

2009-01-01

289

Isolation of a variant of subtilosin A with hemolytic activity.  

PubMed

Bacillus subtilis produces an anionic bacteriocin called subtilosin A that possesses antibacterial activity against certain gram-positive bacteria. In this study, we uncovered a hemolytic mutant of B. subtilis that produces an altered form of subtilosin A. The mutant bacteriocin, named subtilosin A1, has a replacement of threonine at position 6 with isoleucine. In addition to the hemolytic activity, subtilosin A1 was found to exhibit enhanced antimicrobial activity against specific bacterial strains. The B. subtilis albB mutant that does not produce a putative immunity peptide was more sensitive to both subtilosin A and subtilosin A1. A spontaneous suppressor mutation of albB that restored resistance to subtilosin A and subtilosin A1 was obtained. The sbr (subtilosin resistance) mutation conferring the resistance is not linked to the sboA-alb locus. The sbr mutation does not increase the resistance of B. subtilis to other cell envelope-targeted antimicrobial agents, indicating that the mutation specifically confers the resistance to subtilosins. The findings suggest possible bioengineering approaches for obtaining anionic bacteriocins with enhanced and/or altered bactericidal activity. Furthermore, future identification of the subtilosin-resistant mutation could provide insights into the mechanism of subtilosin A activity. PMID:19633086

Huang, Tai; Geng, Hao; Miyyapuram, Venugopal R; Sit, Clarissa S; Vederas, John C; Nakano, Michiko M

2009-09-01

290

Hematological parameters and prevalence of anemia among free-living elderly in south Brazil  

PubMed Central

Objective The aims of this study were to analyze the hematological parameters, the prevalence of anemia and the association between anemia and socioeconomic conditions in an elderly community-based population. Methods A population-based study was performed as part of the Multidimensional Study of the Elderly in Porto Alegre, Brazil (EMIPOA). An initial total of 1058 community residents aged 60 years and older were interviewed. Of these, 392 agreed to have a physical evaluation and a blood sample was taken from each. The hematological parameters analyzed in the blood samples included the hemoglobin concentration, mean cell volume (MCV), mean corpuscular hemoglobin concentration (MCHC) and red cell distribution width (RDW). The association between the variables and the diagnosis of anemia was assessed using the chi-squared test and a multiple logistic regression model. Results The overall prevalence of anemia was 12.8%. Anemia was present in 13.7% of women and in 10.4% of men. Normocytic normochromic anemia without anisocytosis was the most common type of anemia (46%). The assessment of erythrocyte morphology showed significant differences between anemic and non-anemic individuals (microcytosis = 12% vs. 1.5%, hypochromia = 40% vs. 8.8%, and anisocytosis = 26% vs. 7%). In the analysis of socioeconomic conditions, significant differences were found in respect to age and race. Conclusion The prevalence of anemia increases with age and is associated with race, microcytosis, hypochromia and anisocytosis. Anemia is not a condition that should be associated only with the aging process, as it may be due to pathological conditions that occur most frequently in this age group. As a result, a diagnosis of anemia warrants adequate clinical attention. PMID:23741189

Sgnaolin, Vanessa; Engroff, Paula; Ely, Luisa Scheer; Schneider, Rodolfo Herberto; Schwanke, Carla Helena Augustin; Gomes, Irenio; Morrone, Fernanda Bueno; de Carli, Geraldo Attilio

2013-01-01

291

Decreased Hematocrit-To-Viscosity Ratio and Increased Lactate Dehydrogenase Level in Patients with Sickle Cell Anemia and Recurrent Leg Ulcers  

PubMed Central

Leg ulcer is a disabling complication in patients with sickle cell anemia (SCA) but the exact pathophysiological mechanisms are unknown. The aim of this study was to identify the hematological and hemorheological alterations associated with recurrent leg ulcers. Sixty-two SCA patients who never experienced leg ulcers (ULC-) and 13 SCA patients with a positive history of recurrent leg ulcers (ULC+) - but with no leg ulcers at the time of the study were recruited. All patients were in steady state condition. Blood was sampled to perform hematological, biochemical (hemolytic markers) and hemorheological analyses (blood viscosity, red blood cell deformability and aggregation properties). The hematocrit-to-viscosity ratio (HVR), which reflects the red blood cell oxygen transport efficiency, was calculated for each subject. Patients from the ULC+ group were older than patients from the ULC- group. Anemia (red blood cell count, hematocrit and hemoglobin levels) was more pronounced in the ULC+ group. Lactate dehydrogenase level was higher in the ULC+ group than in the ULC- group. Neither blood viscosity, nor RBC aggregation properties differed between the two groups. HVR was lower and RBC deformability tended to be reduced in the ULC+ group. Our study confirmed increased hemolytic rate and anemia in SCA patients with leg ulcers recurrence. Furthermore, our data suggest that although systemic blood viscosity is not a major factor involved in the pathophysiology of this complication, decreased red blood cell oxygen transport efficiency (i.e., low hematocrit/viscosity ratio) may play a role. PMID:24223994

Connes, Philippe; Lamarre, Yann; Hardy-Dessources, Marie-Dominique; Lemonne, Nathalie; Waltz, Xavier; Mougenel, Danile; Mukisi-Mukaza, Martin; Lalanne-Mistrih, Marie-Laure; Tarer, Vanessa; Tressires, Benoit; Etienne-Julan, Maryse; Romana, Marc

2013-01-01

292

Decreased hematocrit-to-viscosity ratio and increased lactate dehydrogenase level in patients with sickle cell anemia and recurrent leg ulcers.  

PubMed

Leg ulcer is a disabling complication in patients with sickle cell anemia (SCA) but the exact pathophysiological mechanisms are unknown. The aim of this study was to identify the hematological and hemorheological alterations associated with recurrent leg ulcers. Sixty-two SCA patients who never experienced leg ulcers (ULC-) and 13 SCA patients with a positive history of recurrent leg ulcers (ULC+)--with no leg ulcers at the time of the study--were recruited. All patients were in steady state condition. Blood was sampled to perform hematological, biochemical (hemolytic markers) and hemorheological analyses (blood viscosity, red blood cell deformability and aggregation properties). The hematocrit-to-viscosity ratio (HVR), which reflects the red blood cell oxygen transport efficiency, was calculated for each subject. Patients from the ULC+ group were older than patients from the ULC- group. Anemia (red blood cell count, hematocrit and hemoglobin levels) was more pronounced in the ULC+ group. Lactate dehydrogenase level was higher in the ULC+ group than in the ULC- group. Neither blood viscosity, nor RBC aggregation properties differed between the two groups. HVR was lower and RBC deformability tended to be reduced in the ULC+ group. Our study confirmed increased hemolytic rate and anemia in SCA patients with leg ulcers recurrence. Furthermore, our data suggest that although systemic blood viscosity is not a major factor involved in the pathophysiology of this complication, decreased red blood cell oxygen transport efficiency (i.e., low hematocrit/viscosity ratio) may play a role. PMID:24223994

Connes, Philippe; Lamarre, Yann; Hardy-Dessources, Marie-Dominique; Lemonne, Nathalie; Waltz, Xavier; Mougenel, Danile; Mukisi-Mukaza, Martin; Lalanne-Mistrih, Marie-Laure; Tarer, Vanessa; Tressires, Benoit; Etienne-Julan, Maryse; Romana, Marc

2013-01-01

293

Strategies for Surveillance of Pediatric Hemolytic Uremic Syndrome: Foodborne Diseases Active Surveillance Network (FoodNet), 2000-2007  

PubMed Central

Background.?Postdiarrheal hemolytic uremic syndrome (HUS) is the most common cause of acute kidney failure among US children. The Foodborne Diseases Active Surveillance Network (FoodNet) conducts population-based surveillance of pediatric HUS to measure the incidence of disease and to validate surveillance trends in associated Shiga toxinproducing Escherichia coli (STEC) O157 infection. Methods.?We report the incidence of pediatric HUS, which is defined as HUS in children <18 years. We compare the results from provider-based surveillance and hospital discharge data review and examine the impact of different case definitions on the findings of the surveillance system. Results.?During 20002007, 627 pediatric HUS cases were reported. Fifty-two percent of cases were classified as confirmed (diarrhea, anemia, microangiopathic changes, low platelet count, and acute renal impairment). The average annual crude incidence rate for all reported cases of pediatric HUS was 0.78 per 100 000 children <18 years. Regardless of the case definition used, the year-to-year pattern of incidence appeared similar. More cases were captured by provider-based surveillance (76%) than by hospital discharge data review (68%); only 49% were identified by both methods. Conclusions.?The overall incidence of pediatric HUS was affected by key characteristics of the surveillance system, including the method of ascertainment and the case definitions. However, year-to-year patterns were similar for all methods examined, suggesting that several approaches to HUS surveillance can be used to track trends. PMID:22572665

Ong, Kanyin L.; Apostal, Mirasol; Comstock, Nicole; Hurd, Sharon; Webb, Tameka Hayes; Mickelson, Stephanie; Scheftel, Joni; Smith, Glenda; Shiferaw, Beletshachew; Boothe, Effie

2012-01-01

294

Epidemiology of anemia in older adults.  

PubMed

Anemia is a common, multifactorial condition among older adults. The World Health Organization (WHO) definition of anemia (hemoglobin concentration <12 g/dL in women and <13 g/dL in men) is most often used in epidemiologic studies of older adults. More than 10% of community-dwelling adults age 65 years and older has WHO-defined anemia. After age 50 years, prevalence of anemia increases with advancing age and exceeds 20% in those 85 years and older. In nursing homes, anemia is present in 48% to 63% of residents. Incidence of anemia in older adults is not well characterized. Among older adults with anemia, approximately one third have evidence of iron, folate, and/or vitamin B(12) deficiency, another third have renal insufficiency and/or chronic inflammation, and the remaining third have anemia that is unexplained. Several studies demonstrate that anemia is associated with poorer survival in older adults. This review details the distribution and consequences of anemia in older adults and identifies future epidemiologic research needs. PMID:18809090

Patel, Kushang V

2008-10-01

295

Fanconi anemia - learning from children  

PubMed Central

Fanconi Anemia (FA) is a rare autosomic recessive and X-linked disease with chromosomal instability after exposure to crosslinking agents as the hallmark. Clinical features of FA are somatic malformations, progressive bone marrow failure and cancer proneness, however there is wide clinical heterogeneity. The symptom most frequently and early associated with morbidity and mortality is progressive pancytopenia in the first decade of life although acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) can appear before aplastic anemia. Squamous cell carcinoma (SCC) of the head-neck, intestinal or genital tract has a very high incidence in FA and can appear at young age. This paper will focus on treatment of bone marrow failure in FA. PMID:22053284

Svahn, Johanna; Dufour, Carlo

2011-01-01

296

Anemia Among Hospitalized Children at a Multispecialty Hospital, Bangalore (Karnataka), India  

PubMed Central

Background: Due to the limited availability of data related to anemia in hospitalized children, this research was conducted to study the occurrence, morphological patterns, distribution in different age groups, sex, and severity of anemia among children aged 6 months-12 years. Setting: Inpatients in department of pediatrics at a multispecialty hospital, Bangalore. Study Design: Descriptive cross sectional study from Oct, 2011 to Sep, 2012. Materials and Methods: Ethical clearance was obtained from the ethical committee of the hospital as per 1964 Declaration of Helsinki. Unrestricted random sampling method was used to select the study group consisting of 882 children between the age of 6 months and 12 years. After obtaining the consent, data were obtained and statistically analyzed using statistical tools like mean, median, standard deviation, and Chi-square test. Results: Out of 882 children selected, 642 (72.79%) were anemic, out of which a majority of 629 (98%) children suffered from nonhemoglobinopathies and a meagre 13 (2%) suffered from hemoglobinopathies. Children in the age group of 6 months-1 year were most affected with nonhemoglobinopathies (33%). Moderate degree of anemia (hemoglobin = 7-9.9 g/dL) was the commonest grade of anemia (80%), while microcytic hypochromic anemia was commonest morphological type of anemia (48%). Among hemoglobinopathies, thalassemia major was the most common (69%, that is 9 out of 13 patients). Conclusion: The occurrence of anemia among children aged between 6 months and 12 years is high and nonhemoglobinopathies predominate over the hemoglobinopathies. PMID:24791237

Saba, Firdos; Poornima, Siddaraju; Balaji, Pishey Ashwathnarayan Rao; Varne, Smitha Ranoji Rao; Jayashree, Krishnamurthy

2014-01-01

297

MCPIP1 Deficiency in Mice Results in Severe Anemia Related to Autoimmune Mechanisms  

PubMed Central

Autoimmune gastritis is an organ-specific autoimmune disease of the stomach associated with pernicious anemia. The previous work from us and other groups identified MCPIP1 as an essential factor controlling inflammation and immune homeostasis. MCPIP1-/- developed severeanemia. However, the mechanisms underlying this phenotype remain unclear. In the present study, we found that MCPIP1 deficiency in mice resulted in severe anemia related to autoimmune mechanisms. Although MCPIP1 deficiency did not affect erythropoiesis per se, the erythropoiesis in MCPIP1-/- bone marrow erythroblasts was significantly attenuated due to iron and vitamin B12 (VB12) deficiency, which was mainly resulted from autoimmunity-associated gastritis and parietal cell loss. Consistently, exogenous supplement of iron and VB12 greatly improved the anemia phenotype of MCPIP1-/- mice. Finally, we have evidence suggesting that autoimmune hemolysis may also contribute to anemia phenotype of MCPIP1-/- mice. Taken together, our study suggests that MCPIP1 deficiency in mice leads to the development of autoimmune gastritis and pernicious anemia. Thus, MCPIP1-/- mice may be a good mouse model for investigating the pathogenesis of pernicious anemia and testing the efficacy of some potential drugs for treatment of this disease. PMID:24324805

Zhou, Zhou; Miao, Ruidong; Huang, Shengping; Elder, Brandon; Quinn, Tim; Papasian, Christopher J.; Zhang, Jifeng; Fan, Daping; Chen, Y. Eugene; Fu, Mingui

2013-01-01

298

Colonic lymphangiomatosis associated with anemia  

PubMed Central

Lymphangioma is an uncommon malformation of lymphatic system. Multiple colonic lymphangioma named as lymphangiomatosis is considered an extremely rare disease. Although lymphangioma is a benign tumor and most colonic lymphangiomas do not cause symptoms and do not require treatment, resection of lymphangioma is necessary in the presence of symptoms such as abdominal pain, bleeding, intussusceptions. We report a case of colonic lymphangiomatosis in a man who presented with abdominal discomfort and anemia, which was diagnosed and treated with endoscopic snare polypectomy. PMID:18837097

Chung, Woo Chul; Kim, Hye-Kang; Yoo, Jin Young; Lee, Jeong Rok; Lee, Kang-Moon; Paik, Chang Nyol; Jang, U-Im; Yang, Jin Mo

2008-01-01

299

[Anemia in chronic kidney disease].  

PubMed

Anemia is almost unavoidable in the last stages of chronic kidney disease. It is defined as a condition where hemoglobin concentration is below 2 standard deviations from the mean hemoglobin level of the general population, corrected for age and sex (typically, hemoglobin < 13 g/dL in adults and 12 g/dL in women). Although the cause is multi-factorial, the most known is inadequate erythropoietin production. Anemia has been associated with poor prognosis in patients with several conditions such as cancer, chronic kidney disease and congestive heart failure. Treatment with erythropoiesis-stimulating agents, such as erythropoietin, is a logical strategy that has enabled clinical improvement and reduced transfusion requirements for the patients; however, total correction of anemia with erythropoiesis-stimulating agents has demonstrated an increase in the risk of mortality or cardiovascular complications associated with these agents. In randomized trials, the achievement of normal or nearly normal hemoglobin levels is not associated with improved survival and reduced cardiovascular risk; however the ideal hemoglobin level with the use of erythropoiesis-stimulating agents seems to be problematic. More information is needed in order to obtain definite conclusions; in the meantime, using the lowest possible dose of erythropoietin seems to be the most prudent approach. PMID:25354060

Amador-Medina, Lauro Fabin

2014-01-01

300

Clinical Application of Immunofluorescence I. Grouping ?-Hemolytic Streptococci  

PubMed Central

Smith, Thomas B. (Armed Forces Institute of Pathology, Washington, D.C.). Clinical application of immunofluorescence. I. Grouping ?-hemolytic streptococci. J. Bacteriol. 89:198204. 1965.Procedures are described for the production of antistreptococcal serum in rabbits and for the preparation of group-specific conjugates for Lancefield groups A, C, and G. A modification of the conventional technique of absorption and inhibition to prevent cross-reactions with common antigens was used with excellent results. In addition, a promising new approach to eliminating cross-reactions of group A conjugate with antigens of groups C and G by dilution with group A-variant antiserum was tested. A complete method is introduced that enables the clinical laboratory to report whether group A streptococci are present in a given throat culture well within 24 hr after the physician collects the sample. Images PMID:14255663

Smith, Thomas B.

1965-01-01

301

Recurrent ocular involvement in pediatric atypical hemolytic uremic syndrome.  

PubMed

Atypical hemolytic uremic syndrome (HUS) is a subtype of thrombotic microangiopathy associated with complement alternative pathway dysregulation. It is clinically characterized by a relapsing course and a poor prognosis. Multiple organ systems are commonly affected by thrombotic microangiopathy in pediatric atypical HUS; however, ocular involvement is rarely reported. The case of an 11-year-old girl diagnosed as having atypical HUS who presented with bilateral central retinal vein occlusions with macular subhyaloid hemorrhage during her initial onset and ophthalmoplegia, diplopia, and optic disc edema during her relapsing episode 1 year later is described. All ocular manifestations occurred in the convalescence phase of atypical HUS. No other extrarenal complications were found and full recovery was achieved following typical treatment for atypical HUS (ie, plasma infusion, steroid, and supportive therapy). This is thought to be the first reported case of recurrent ocular involvement in pediatric atypical HUS. [J Pediatr Ophthalmol Strabismus 2014;51:e62-e65.]. PMID:25347082

Zheng, Xiaoyu; Gorovoy, Ian R; Mao, Jianhua; Jin, Ji; Chen, Xi; Cui, Qi N

2014-01-01

302

Anemia and Iron Deficiency in Developing Countries  

Microsoft Academic Search

Iron deficiency and anemia are major public health concerns throughout the world and are of special concern in many developing\\u000a countries where the incidence and severity of anemia in certain populations is very high. Pregnant women, women of childbearing\\u000a age, and young children are especially vulnerable to iron deficiency and iron-deficiency anemia (IDA) because of increased\\u000a iron needs during growth

Usha Ramakrishnan; Beth Imhoff-Kunsch

303

Anemia - Multiple Languages: MedlinePlus  

MedlinePLUS

... Arabic (???????) Bosnian (Bosanski) Chinese - Simplified (????) French (franais) Hindi (??????) Japanese (???) Korean (???) Russian ( ... PDF Health Information Translations Return to top French (franais) Anemia Anmie - franais (French) Bilingual PDF Health Information ...

304

Cost-effectiveness of continuous erythropoietin receptor activator in anemia  

PubMed Central

Background Erythropoiesis-stimulating agents (ESAs) are the mainstay of anemia therapy. Continuous erythropoietin receptor activator (CERA) is a highly effective, long-acting ESA developed for once-monthly dosing. A multitude of clinical studies has evaluated the safety and efficiency of this treatment option for patients with renal anemia. In times of permanent financial pressure on health care systems, the cost-effectiveness of CERA should be of particular importance for payers and clinicians. Objective To critically analyze, from the nephrologists point of view, the published literature focusing on the cost-effectiveness of CERA for anemia treatment. Methods The detailed literature search covered electronic databases including MEDLINE, PubMed, and Embase, as well as international conference abstract databases. Results Peer-reviewed literature analyzing the definite cost-effectiveness of CERA is scarce, and most of the available data originate from conference abstracts. Identified data are restricted to the treatment of anemia due to chronic kidney disease. Although the majority of studies suggest a considerable cost advantage for CERA, the published literature cannot easily be compared. While time and motion studies clearly indicate that a switch to CERA could minimize health care staff time in dialysis units, the results of studies comparing direct costs are more ambivalent, potentially reflecting the differences between health care systems and variability between centers. Conclusion Analyzed data are predominantly insufficient; they miss clear evidence and have to thus be interpreted with great caution. In this day and age of financial restraints, results from well-designed, head-to-head studies with clearly defined endpoints have to prove whether CERA therapy can achieve cost savings without compromising anemia management. PMID:25050070

Schmid, Holger

2014-01-01

305

Genetics Home Reference: Thiamine-responsive megaloblastic anemia syndrome  

MedlinePLUS

... OMIM Genetic disorder catalog Conditions > Thiamine-responsive megaloblastic anemia syndrome On this page: Description Genetic changes Inheritance ... Reviewed February 2009 What is thiamine-responsive megaloblastic anemia syndrome? Thiamine-responsive megaloblastic anemia syndrome is a ...

306

Genetics Home Reference: X-linked sideroblastic anemia  

MedlinePLUS

... OMIM Genetic disorder catalog Conditions > X-linked sideroblastic anemia On this page: Description Genetic changes Inheritance Diagnosis ... Reviewed April 2009 What is X-linked sideroblastic anemia? X-linked sideroblastic anemia is an inherited disorder ...

307

Genetics Home Reference: Iron-refractory iron deficiency anemia  

MedlinePLUS

... Genetic disorder catalog Conditions > Iron-refractory iron deficiency anemia On this page: Description Genetic changes Inheritance Diagnosis ... July 2014 What is iron-refractory iron deficiency anemia? Iron-refractory iron deficiency anemia is one of ...

308

Genetics Home Reference: X-linked sideroblastic anemia and ataxia  

MedlinePLUS

... OMIM Genetic disorder catalog Conditions > X-linked sideroblastic anemia and ataxia On this page: Description Genetic changes ... Reviewed April 2009 What is X-linked sideroblastic anemia and ataxia? X-linked sideroblastic anemia and ataxia ...

309

What Are the Signs and Symptoms of Sickle Cell Anemia?  

MedlinePLUS

... What Are the Signs and Symptoms of Sickle Cell Anemia? The signs and symptoms of sickle cell ... who have sickle cell anemia. Complications of Sickle Cell Anemia Sickle cell crises can affect many parts ...

310

Cancer-related anemia: its causes and characteristics.  

PubMed

Under normal circumstances, the circulating red blood cell mass is maintained at a level that is constant in each individual, although that level may vary by more than 10% among individuals of the same age and gender. At normal ambient oxygen tension, two factors determine the circulating red blood cell mass: red blood cell life span, which is finite and in humans approximates 120 days; and the rate of effective red blood cell production. To maintain a constant red blood cell mass, therefore, approximately 20 mL of red blood cells must be produced each day to replace those red blood cells lost from the circulation through senescence. Anemia, which may be defined functionally as lack of sufficient red blood cells to maintain adequate tissue oxygenation, develops when the demand for new red blood cells exceeds the capacity of the bone marrow to produce them. This may be due to excessive red blood cell destruction, impaired red blood cell production, bleeding, or any combination of these. Acquired anemia is always a consequence of another disorder, which must be identified to ensure that the corrective therapy is appropriate. In patients with solid tumors, multiple mechanisms for causing anemia have been identified: blood loss that is either intrinsic or iatrogenic; nutritional deficiencies involving primarily iron or folic acid; hemolysis (autoimmune, traumatic, or drug-induced); bone marrow failure due to tumor encroachment, myelofibrosis, or marrow necrosis; infection; inflammation; or simply the presence of a cancer elsewhere in the body. The three noted causes of marrow failure share a common denominator: impaired production of erythropoietin. For any degree of anemia, a patient with cancer produces much less erythropoietin than expected and, therefore, cannot compensate for impaired red blood cell production. Inflammation or infection can exacerbate this situation. Indeed, anemia in patients with cancer appears to behave much like that in patients with chronic renal failure who become anemic because of the inability of the kidneys to produce erythropoietin adequately. The cause of impaired erythropoietin production in patients with cancer who have anemia is not entirely understood, but may be due in part to the production of inflammatory cytokines in response to the tumor. Such cytokines also would be expected to blunt the ability of the bone marrow to respond to the available circulating erythropoietin.(ABSTRACT TRUNCATED AT 400 WORDS) PMID:8202724

Spivak, J L

1994-04-01

311

Sigma E Regulators Control Hemolytic Activity and Virulence in a Shrimp Pathogenic Vibrio harveyi  

E-print Network

Members of the genus Vibrio are important marine and aquaculture pathogens. Hemolytic activity has been identified as a virulence factor in many pathogenic vibrios including V. cholerae, V. parahaemolyticus, V. alginolyticus, ...

Rattanama, Pimonsri

312

Drag reducing polymers as simple indicators of hemolytic potential in biomechanical devices  

E-print Network

An experimental study was carried out to determine if drag reducing polymers can be simple indicators of hemolytic potential in biomechanical devices. Specifically, three different blood pumps, known as a left ventricle ...

Shieh, Sarah

2009-01-01

313

A Burkholderia cepacia complex non-ribosomal peptide-synthesized toxin is hemolytic and required for full virulence  

PubMed Central

Members of the Burkholderia cepacia complex (Bcc) have recently gained notoriety as significant bacterial pathogens due to their extreme levels of antibiotic resistance, their transmissibility in clinics, their persistence in bacteriostatic solutions, and their intracellular survival capabilities. As pathogens, the Bcc are known to elaborate a number of virulence factors including proteases, lipases and other exoproducts, as well as a number of secretion system associated effectors. Through random and directed mutagenesis studies, we have identified a Bcc gene cluster capable of expressing a toxin that is both hemolytic and required for full Bcc virulence. The Bcc toxin is synthesized via a non-ribosomal peptide synthetase mechanism, and appears to be related to the previously identified antifungal compound burkholdine or occidiofungin. Further testing shows mutations to this gene cluster cause a significant reduction in both hemolysis and Galleria mellonella mortality. Mutation to a glycosyltransferase gene putatively responsible for a structural-functional toxin variant causes only partial reduction in hemolysis. Molecular screening identifies the Bcc species containing this gene cluster, of which several strains produce hemolytic activity. PMID:22546908

Thomson, Euan L.S.; Dennis, Jonathan J.

2012-01-01

314

Aplastica Anemia And Viral Hepatitis  

PubMed Central

Acquired aplastic anemia (aAA) is a severe and rare disease, characterized by hematopoietic bone marrow failure and peripheral cytopenia. The pathophysiology is immune mediated in most cases, activated T1 lymphocytes have been identified as effector cells. The disease can be successfully treated with combined immunosuppressive therapy or allogeneic hematopoietic stem cell transplantation. Hepatitis-associated aplastic anemia (HAA) is a syndrome of bone marrow failure following the development of acute seronegative hepatitis. HAA syndrome most often affects young males who presented severe pancytopenia two to three months after an episode of acute hepatitis. The clinical course of hepatitis is more frequently benign but a fulminant severe course is also described. The bone marrow failure can be explosive and severe and it is usually fatal if untreated, no correlations have been observed between severity of hepatitis and AA. In none of the studies a specific virus could be identified and most cases are seronegative for known hepatitis viruses. The clinical characteristics and response to immunotherapy indicate a central role for immune-mediated mechanism in the pathogenesis of HAA. The initial target organ of the immune response is the liver as suggested by the time interval between hepatitis and the onset of bone marrow failure. Liver histology is characterized by T cell infiltrating the parenchyma as reported in acute hepatitis. Recently in HAA it has been demonstrated intrahepatic and blood lymphocytes with T cell repertoire similar to that of confirmed viral acute hepatitis. The expanded T cell clones return to a normal distribution after response to immunosuppressive treatment, suggesting the antigen or T cell clearance. Therapeutic options are the same as acquired aplastic anemia. PMID:21415960

Cudillo, Laura

2009-01-01

315

Plasma Fibrinogen Concentration in ABO-Hemolytic Disease of the Newborn  

Microsoft Academic Search

Plasma fibrinogen and total serum proteins were measured in infants affected by ABO-hemolytic disease and in normal infants cord blood and blood taken 48 h after birth. The average plasma fibrinogen concentrations in the blood of infants with ABO-hemolytic disease was 447.36 mg\\/dl as compared with 267.09 mg\\/dl (p < 0.005) in cord blood and 313.82 mg\\/dl (p < 0.005)

E. L. Romano; J. Linares; G. Surez

1982-01-01

316

THE QUESTION OF SENSITIZATION OF JOINTS WITH NON-HEMOLYTIC STREPTOCOCCI  

PubMed Central

It was impossible to demonstrate a condition of specific joint sensitization to non-hemolytic streptococci by first injecting the joints of rabbits with small doses of killed non-hemolytic streptococci, or with extracts of these organisms, and subsequently inoculating the rabbits intravenously with homologous living bacteria. Joints so treated were no more liable to involvement than were other untreated joints of the same animals. PMID:19868811

Swift, Homer F.; Boots, Ralph H.

1923-01-01

317

DISSOCIATION OF HEMOLYTIC AND LYMPHOCYTE-TRANSFORMING ACTIVITIES OF STREPTOLYSIN S PREPARATIONS  

PubMed Central

The ability of streptolysin S preparations to induce high percentages of transformation in human peripheral blood lymphocytes was confirmed in a series of apparently healthy donors. Transforming activity was not demonstrated in the two media used for streptolysin S production, nor in control preparations in which a strain each of Streptococcus viridans, Staphylococcus aureus (nonhemolytic), and Diplococcus pneumoniae was substituted for the beta hemolytic streptococcal strain used for streptolysin S production. The relation of the hemolytic activity to the lymphocyte transforming activity of streptolysin S preparations was studied by means of inactivation and fractionation experiments. Heating produced a loss in both activities, but more in the hemolytic than in the transforming activity. The transformation obtained with a heated preparation had a high degree of correlation with that obtained with the unheated preparation in a series of normal subjects and patients with various rheumatic diseases, whose lymphocytes were often less responsive to stimulation with streptolysin S preparations (both heated and unheated) than the lymphocytes of the normal subjects studied. Treatment of streptolysin S preparations with chymotrypsin, vegetable lecithin, or trypan blue (the latter in minute amounts) resulted in preparations with no detectable hemolytic activity but with undiminished lymphocyte transforming activity. Chromatographic fractionations on DEAE-Sephadex columns yielded fractions endowed with transforming but not with hemolytic activity, and other fractions endowed with hemolytic but not with transforming activity. The recovery of the hemolytic activity was not complete and quantitation of the recovery of the transforming activity was not attempted. These experiments indicate that the hemolytic and transforming activities of streptolysin S preparations are independent of each other, and specifically that they are the attributes of two different streptococcal products, one of which is streptolysin S. The other is a nonhemolytic streptococcal product present in streptolysin S preparations but previously unrecognized. Some implications of these findings are discussed. PMID:4387992

Taranta, Angelo; Cuppari, Girolamo; Quagliata, Franco

1969-01-01

318

Pathology Case Study: Macrocytic Anemia  

NSDL National Science Digital Library

This is a case study presented by the University of Pittsburgh Department of Pathology in which an older man suffering from chronic bronchitis and macrocytic anemia also developed persistent flu symptoms. Visitors view the microscopic and gross descriptions, including images, and have the opportunity to diagnose the patient. This is an excellent resource for students in the health sciences to familiarize themselves with using patient history and laboratory results to diagnose disease. It is also a helpful site for educators to use to introduce or test student learning in hematopathology.

Bahler, David; Kulich, Scott; Shekhter-Levin, Sofia

2008-05-05

319

9 CFR 311.34 - Anemia.  

Code of Federal Regulations, 2010 CFR

...Animal Products 2 2010-01-01 2010-01-01 false Anemia. 311.34 Section 311.34 Animals and Animal Products...DISEASED OR OTHERWISE ADULTERATED CARCASSES AND PARTS 311.34 Anemia. Carcasses of livestock too anemic to produce wholesome...

2010-01-01

320

The Student with Sickle Cell Anemia.  

ERIC Educational Resources Information Center

Sickle cell anemia is the most common and severe of inherited chronic blood disorders. In the United States, sickle cell anemia is most common among the Black population. Among the most commonly occurring symptoms are: an enlarged spleen, episodes of severe pain, easily contracted infections, skin ulcers, and frequent urination. (JN)

Tetrault, Sylvia M.

1981-01-01

321

Fanconi anemia in Ashkenazi Jews.  

PubMed

Fanconi anemia (FA) should be included among the genetic diseases that occur at high frequency in the Ashkenazi Jewish population. FA exhibits extensive genetic heterogeneity; there are currently 11 complementation groups reported, and 8 (i.e., FANCA, FANCC, FANCD1/BRCA2, FANCD2, FANCE, FANCF, FANCG, and FANCL) genes have been isolated. While patients may be from widely diverse ethnic groups, a single mutation in complementation group FA-C, c.711 + 4A > T (commonly known as IVS4 + 4A > T prior to current nomenclature rules) is unique to FA patients of Ashkenazi Jewish ancestry, and has a carrier frequency of greater than 1/100 in this population. In addition, a mutation (c.65G > A) in FANCA (FA-A is the most common complementation group in non-Jewish patients) and the mutation c.6174delT in FANCD1/BRCA2 are also unique to the Ashkenazi Jewish population. Therefore, the study of Fanconi anemia can lend insight into the types of cancer-predisposing genetic diseases specific to the Ashkenazi. PMID:15516848

Kutler, David I; Auerbach, Arleen D

2004-01-01

322

[Detection and Analysis of ABO Hemolytic Disease in Newborn].  

PubMed

This study was purposed to investigate the incidence and the model of ABO hemolytic disease in newborn (ABO-HDN) and the results of the three hemolysis test, so as to provide the evidences for clinical diagnosis and therapy. A total of 227 cases of maternal-fetal ABO incompatibility from January 2013 to October 2013 in the First Affiliated Hospital of Xiamen University were enrolled in the study. The ABO blood group of newborn and mother was detemined and three hemolysis tests (direct antiglobulin test, free antibody test, RBC antibody release test) were performed. The results indicated that in 227 cases of ABO incompatible pregnancies,186 cases were ABO-HDN (81.94%). There was no significant difference in the incidence between O-A and O-B incompatible pregnancies (P > 0.05). The positive ratio of direct antiglobulin test, free antibody test and RBC antibody release test were 59.14% (110/186), 84.78% (156/186) and 94.62% (176/186) respectively. It is concluded that the incidence of ABO-HDN is high. The main models of ABO-HDN were O-A and O-B. There was no significant difference in the incidence between O-A and O-B incompatible pregnancies. Three hemolysis tests are high sensitivity and are helpful in early diagnosis and early treatment of HDN. PMID:25338602

Lin, Zhao-Xia; Dong, Qing-Song

2014-09-01

323

Gemcitabine-associated thrombotic thrombocytopenic purpura and hemolytic uremic syndrome.  

PubMed

A patient being treated for metastatic adenocarcinoma of the pancreas presents to the clinic for a routine appointment. A complete blood count reveals hemoglobin of 6.5 g/dl and a platelet count of 30,000 K/mm3 thought to be from the last of many doses of gemcitabine. On assessment, the only complaint was fatigue with no evidence of bleeding or other abnormal physical findings other than pallor. Past medical history includes hypertension managed with three antihypertensive agents. Additional laboratory tests reveal elevated blood urea nitrogen (69 mg/dl), creatinine (2.76 mg/dl), and lactic dehydrogenase (LDH), was well as indirect bilirubin (2.1 mg/dl). The patient is admitted and transfused with packed red blood cells (pRBCs). The next day, the platelet count drops to 9,000 K/mm3 and the hemoglobin increases, appropriately, to 8.9 g/dl. Urinalysis is positive for hemoglobin (+ 3). The peripheral blood smear is positive for schistocytes (fragmented RBCs). A pheresis catheter is placed after the patient was evaluated by a hematologist and a nephrologist. A presumptive diagnosis of thrombotic thrombocytopenic purpura (TTP) with hemolytic uremic syndrome (HUS) was made. PMID:25158661

Held-Warmkessel, Jeanne

2014-09-01

324

The CXCR4/CXCR7/SDF-1 pathway contributes to the pathogenesis of Shiga toxin-associated hemolytic uremic syndrome in humans and mice  

PubMed Central

Hemolytic uremic syndrome (HUS) is a potentially life-threatening condition. It often occurs after gastrointestinal infection with E. coli O157:H7, which produces Shiga toxins (Stx) that cause hemolytic anemia, thrombocytopenia, and renal injury. Stx-mediated changes in endothelial phenotype have been linked to the pathogenesis of HUS. Here we report our studies investigating Stx-induced changes in gene expression and their contribution to the pathogenesis of HUS. Stx function by inactivating host ribosomes but can also alter gene expression at concentrations that minimally affect global protein synthesis. Gene expression profiling of human microvascular endothelium treated with Stx implicated a role for activation of CXCR4 and CXCR7 by their shared cognate chemokine ligand (stromal cellderived factor-1 [SDF-1]) in Stx-mediated pathophysiology. The changes in gene expression required a catalytically active Stx A subunit and were mediated by enhanced transcription and mRNA stability. Stx also enhanced the association of CXCR4, CXCR7, and SDF1 mRNAs with ribosomes. In a mouse model of Stx-mediated pathology, we noted changes in plasma and tissue content of CXCR4, CXCR7, and SDF-1 after Stx exposure. Furthermore, inhibition of the CXCR4/SDF-1 interaction decreased endothelial activation and organ injury and improved animal survival. Finally, in children infected with E. coli O157:H7, plasma SDF-1 levels were elevated in individuals who progressed to HUS. Collectively, these data implicate the CXCR4/CXCR7/SDF-1 pathway in Stx-mediated pathogenesis and suggest novel therapeutic strategies for prevention and/or treatment of complications associated with E. coli O157:H7 infection. PMID:22232208

Petruzziello-Pellegrini, Tania N.; Yuen, Darren A.; Page, Andrea V.; Patel, Sajedabanu; Soltyk, Anna M.; Matouk, Charles C.; Wong, Dennis K.; Turgeon, Paul J.; Fish, Jason E.; Ho, J.J. David; Steer, Brent M.; Khajoee, Vahid; Tigdi, Jayesh; Lee, Warren L.; Motto, David G.; Advani, Andrew; Gilbert, Richard E.; Karumanchi, S. Ananth; Robinson, Lisa A.; Tarr, Phillip I.; Liles, W. Conrad; Brunton, James L.; Marsden, Philip A.

2012-01-01

325

What is the optimal treatment for anemia in inflammatory bowel disease?  

PubMed

Anemia is common in inflammatory bowel disease (IBD), with a prevalence ranging from 8.8% to 73.7%. This wide range reflects the definitions used and the populations studied. Although many patients are reported to be asymptomatic, systematic studies have shown anemia to have a significant impact on quality of life. Consequently treatment should be instituted early. The commonest cause of anemia in IBD is iron deficiency, predominantly related to gastrointestinal blood loss. Anemia of chronic disease often occurs concomitantly, due to cytokine-mediated impaired erythropoiesis and dysregulated iron metabolism. Oral iron is a simple and effective method for treating iron deficiency, but requires long courses of treatment. It is also theoretically implicated with worsening intestinal inflammation, via the production of toxic reactive oxygen species. Intravenous iron avoids these concerns, especially with the development of ferric carboxymaltose, which allow up to 1000mg to be given rapidly. In patients failing to respond to intravenous iron, the anemia of chronic disease is most likely to be causative. In this setting evidence suggests that additional erythropoietin therapy can be effective. Blood transfusions should be avoided as part of routine management and reserved for patients with substantial acute gastro-intestinal bleeding, where there is a risk of hemodynamic compromise. This article discusses the underlying physiology of anemia in IBD, and presents the current evidence supporting treatment options available. PMID:22023204

Kent, Alexandra J; Blackwell, Victoria J; Travis, Simon P L

2012-07-01

326

Anemia  

MedlinePLUS

... your body. Some foods or medicines, including milk, antacids or stomach acid-lowering medicines, also can prevent ... Avoid these foods when eating iron-rich foods. Antacids and some other medicines that contain calcium also ...

327

Relationship of maternal knowledge of anemia with maternal and child anemia and health-related behaviors targeted at anemia among families in Indonesia  

PubMed Central

Objectives Our specific aim was to characterize maternal knowledge of anemia and its relationship to maternal and child anemia and to behaviors related to anemia reduction. Methods We examined the relationship between maternal knowledge of anemia and anemia in the mother and the youngest child, aged 659 mo, in 7,913 families from urban slums and 37,874 families from rural areas of Indonesia. Knowledge of anemia was defined based upon the mothers ability to correctly name at least one symptom of anemia and at least one treatment or strategy for reducing anemia. Hemoglobin was measured in both the mother and the child. Results In urban and rural areas, respectively, 35.8% and 36.9% of mothers had knowledge of anemia, 28.7% and 25.1% of mothers were anemic (hemoglobin <12 g/dL), and 62.3% and 54.0% of children were anemic (hemoglobin <11 g/dL). Maternal knowledge of anemia was associated with child anemia in urban and rural areas, respectively, (Odds Ratio [O.R.] 0.90, 95% Confidence Interval [C.I.] 0.79, 1.02, P = 0.10; O.R. 0.93, 95% C.I. 0.87, 0.98, P = 0.01) in multivariate logistic regression models adjusting for potential confounders. There was no significant association between maternal knowledge of anemia and maternal anemia. Maternal knowledge of anemia was significantly associated with iron supplementation during pregnancy and child consumption of fortified milk. There was no association of maternal knowledge of anemia with child deworming. Conclusions Maternal knowledge of anemia is associated with lower odds of anemia in children and with some health behaviors related to reducing anemia. PMID:22241619

Souganidis, Ellie S.; Sun, Kai; de Pee, Saskia; Kraemer, Klaus; Rah, Jee-Hyun; Moench-Pfanner, Regina; Sari, Mayang; Bloem, Martin W.; Semba, Richard D.

2014-01-01

328

Protrusio acetabuli in sickle-cell anemia  

SciTech Connect

Of 155 adults with sickle-cell anemia (SS, SC), radiographs of the pelvis or hip demonstrated protrusio acetabuli on at least one side in 14 (3 men and 11 women), as indicated by projection of the acetabular line medial to the ilio-ischial line. All 14 patients had bone changes attributable to sickle-cell anemia, including marrow hyperplasia and osteonecrosis; however, the severity of femoral or acetabular osteonecrosis did not appear directly related to the protrusion. The authors conclude that sickle-cell anemia can predispose to development of protrusio acetabuli.

Martinez, S.; Apple, J.S.; Baber, C.; Putman, C.E.; Rosse, W.F.

1984-04-01

329

High anemia prevalence in western China.  

PubMed

We assessed the prevalence of anemia among schoolchildren in western China as determined by seven cross-sectional surveys involving 12,768 children aged 8-12 years. Subjects were selected randomly from 283 primary schools in 41 economically disadvantaged counties of Ningxia, Qinghai, Shaanxi and Sichuan Provinces. Data were collected through questionnaires and hemoglobin levels were measured. The anemia prevalence was 34% using the WHO hemoglobin cutoff of < 120 g/l. Boarding students and girls were more likely to be anemic. The prevalence of anemia in schoolchildren was high. Iron deficiency is a significant nutrition issue in China. PMID:22299447

Luo, Renfu; Wang, Xiaobing; Zhang, Linxiu; Liu, Chengfang; Shi, Yaojiang; Miller, Grant; Rozelle, Scott; Yu, Elaine; Martorell, Reynaldo

2011-09-01

330

Iron-refractory iron deficiency anemia (IRIDA).  

PubMed

Iron deficiency anemia is a common global problem whose etiology is typically attributed to acquired inadequate dietary intake and/or chronic blood loss. However, in several kindreds multiple family members are affected with iron deficiency anemia that is unresponsive to oral iron supplementation and only partially responsive to parenteral iron therapy. The discovery that many of these cases harbor mutations in the TMPRSS6 gene led to the recognition that they represent a single clinical entity: iron-refractory iron deficiency anemia (IRIDA). This article reviews clinical features of IRIDA, recent genetic studies, and insights this disorder provides into the regulation of systemic iron homeostasis. PMID:25064705

Heeney, Matthew M; Finberg, Karin E

2014-08-01

331

[Metastatic prostate cancer complicated with chronic disseminated intravascular coagulopathy causing acute renal failure, mimicking thrombotic thrombocytopenic purpura and hemolytic uremic syndrome: pathomechanism, differential diagnosis and therapy related to a case].  

PubMed

Disseminated intravascular coagulopathy (DIC) is characterized as activation of the clotting system resulting in fibrin thrombi, gradually diminishing levels of clotting factors with increased risk of bleeding. Basically two types of DIC are distinguished: (1) chronic (compensated) - with alteration of laboratory values and (2) acute (non-compensated) - with severe clinical manifestations: bleeding, shock, acute renal failure (ARF), transient focal neurologic deficit, delirium or coma. Chronic DIC related to metastatic neoplasia is caused by pancreatic, gastric or prostatic carcinoma in most of the cases. Incidence rate of DIC is 13-30% in prostate cancer, among those only 0.4-1.65% of patients had clinical signs and symptoms of DIC. In other words, chronic DIC is developed in one of eight patients with prostate cancer. DIC is considered as a poor prognostic factor in prostatic carcinoma. The similar clinical and laboratory findings of TTP-HUS (thrombotic thrombocytopenic purpura - hemolytic uremic syndrome) and DIC makes it difficult to differentiate between them. A 71 years old male patient with known chronic obstructive pulmonary disease, benign prostatic hyperplasia, significant carotid artery stenosis, gastric ulcer and alcoholic liver disease was admitted to another hospital with melena. Gastroscopy revealed intact gastric mucosa and actually non-bleeding duodenal ulcer covered by clots. Laboratory results showed hyperkalemia, elevated kidney function tests, indirect hyperbilirubinemia, increased liver function tests, leukocytosis, anemia, thrombocytopenia and elevated international normalized ratio (INR). He was treated with saline infusions, four units of red blood cells and one unit of fresh frozen plasma transfusions. Four days later he was transported to our Institution with ARF. Physical examination revealed dyspnoe, petechiae, hemoptoe, oliguria, chest-wall pain and aggressive behavior. Thrombocytopenia, signs of MAHA (fragmentocytes and helmet cells in the peripheral blood), normal INR, elevated lactate dehydrogenase (LDH) and ARF suggested TTP-HUS. Hemodialysis and six plasmaferesis (PF) were carried out. After the fifth PF, skin manifestations of thrombotic microangiopathy occurred on the feet. Clotting analysis revealed elevated D-dimer (>5 ?g/mL), normal fibrinogen (3.2 g/L), a slightly raised INR (1.36) and activated partial prothrombin time (APTT) (45.8 sec), normal reticulocyte (57 G/L) and a slightly low platelet count (123 G/L), which proved to be chronic DIC. Therapeutic dose of low-molecular-weight heparin (LMWH) was started. Elevated prostate-specific antigen (PSA) (109.6 ng/mL) suggested prostatic carcinoma. Prostate biopsy revealed adenocarcinoma (Gleason: 4+4 for left lobe and 3+3 for right lobe). Elevated alkaline phosphatase suggested metastases in the bone, which were confirmed by bone scintigraphy. Combined androgen blockade (CAB) was started. After three months follow-up our patient's status is satisfactory. PSA is in the normal range (4.6 ng/mL). Thrombocytopenia of uncertain origin with normal or raised INR, APTT, elevated D-dimer, normal fibrinogen and reticulocyte count prove the diagnosis of chronic DIC. This process warrants searching for metastatic neoplasia. Due to the relatively low serum levels of circulating procoagulant factors (e.g. tissue factor), therapeutic dose of LMWH can be used with good efficiency in chronic DIC with low risk of bleeding. Severe DIC as a complication of metastatic prostate cancer can be treated by androgen deprivation therapy (ADT) or CAB in combination with ketokonazole and concomitant use of supportive treatment. Deme D, Ragn M, Kovcs L, Kalmr K, Varga E, Varga T, Rakonczai E. Metastatic prostate cancer complicated with chronic disseminated intravascular coagulopathy causing acute renal failure mimicking thrombotic thrombocytopenic purpura and hemolytic uremic syndrome: pathomechanism, differential diagnosis and therapy related to a case. PMID:21163766

Deme, Dniel; Ragn, Mrton; Kalmr, Katalin; Kovcs, Lajos; Varga, Erzsbet; Varga, Tnde; Rakonczai, Ervin

2010-12-01

332

Clinical management of aplastic anemia  

PubMed Central

Acquired aplastic anemia is a potentially fatal bone marrow failure disorder that is characterized by pancytopenia and a hypocellular bone marrow. Hematopoietic stem-cell transplantation or bone marrow transplantation (BMT) is the treatment of choice for young patients who have a matched sibling donor. Immunosuppression with either anti-thymocyte globulin and cyclosporine or high-dose cyclophosphamide is an effective therapy for patients who are not suitable BMT candidates owing to age or lack of a suitable donor. Results of BMT from unrelated and mismatched donors are improving, but presently this treatment option is best reserved for those patients who do not respond, relapse or develop secondary clonal disorders following immunosuppressive therapy. Efforts are currently underway to both improve immunosuppressive regimens and to expand the application of BMT. PMID:21495931

DeZern, Amy E; Brodsky, Robert A

2011-01-01

333

TNF-? signaling in Fanconi anemia.  

PubMed

Tumor necrosis factor-alpha (TNF-?) is a major pro-inflammatory cytokine involved in systemic inflammation and the acute phase reaction. Dysregulation of TNF production has been implicated in a variety of human diseases including Fanconi anemia (FA). FA is a genomic instability syndrome characterized by progressive bone marrow failure and cancer susceptibility. The patients with FA are often found overproducing TNF-?, which may directly affect hematopoietic stem cell (HSC) function by impairing HSC survival, homing and proliferation, or indirectly change the bone marrow microenvironment critical for HSC homeostasis and function, therefore contributing to disease progression in FA. In this brief review, we discuss the link between TNF-? signaling and FA pathway with emphasis on the implication of inflammation in the pathophysiology and abnormal hematopoiesis in FA. PMID:23890415

Du, Wei; Erden, Ozlem; Pang, Qishen

2014-01-01

334

Radiation resistance of a hemolytic micrococcus isolated from chicken meat  

SciTech Connect

The effects of environmental factors on a highly radiation-resistant hemolytic micrococcus isolated from chicken meat were studied. NaCl tolerance and gamma radiation resistance of the cells were growth phase-related. The cells were resistant to injury from drying or freezing/thawing. Under certain conditions, cells in the frozen state required approximately 5 Mrad to inactivate 90% of the population; 0.2 Mrad injured an equivalent proportion. Survival curve of the cells heated at 60/sup 0/C showed a unique pattern which was in three distinct phases. Heat-stressed cells were much more sensitive to radiation inactivation than unheated cells. When suspended in fresh m-Plate Count Broth (PCB), the injured cells repaired without multiplication during incubation at 32/sup 0/C. The repair process in this bacterium, however, was slower compared to thermally injured organisms studied by other workers. An improved replica-plating technique, was devised for isolation of radiation-sensitive mutants of pigmented bacteria. A simple method to demonstrate radiation-inducible radiation resistance in microbial cells was developed. The new method required neither washing/centrifugation nor procedures for cell enumeration. Mutagenesis treatment of radiation-resistant micrococcal bacterium with N-methyl-N'-nitro-N-nitrosoguanidine (NTG) followed by FPR and screening steps resulted in isolation of two radiation-sensitive mutants. The more sensitive mutant strain, designated as 702, was seven times as sensitive to gamma or UC radiation as the wild type. No apparent difference was observed between 702 and the wild type in (1) cell morphology, colonial morphology, and pigment production or (2) tolerance to NaCl, drying/storage, freezing/thawing, and heating. Sodium dodecyl sulfate treatment (for curing) of wild type did not result in isolation of a radiation-sensitive mutant.

Tan, S.T.

1982-01-01

335

Anemia in children with chronic kidney disease.  

PubMed

Anemia in children with chronic kidney disease (CKD) is common secondary to inadequate erythropoietin production, iron deficiency, blood loss, inflammation, secondary hyperparathyroidism, uremic toxins, and nutritional deficiencies. Anemia has a variety of deleterious consequences, including associations with increased mortality and left ventricular hypertrophy. Recombinant human erythropoietin is effective in treating anemia in children with CKD, and recent studies show that darbepoetin alpha is an attractive alternative because it requires less frequent injections. Iron deficiency is a major cause of anemia that is resistant to erythropoietin or darbepoetin alpha. Although oral iron is effective in some patients, many children, especially those receiving hemodialysis, require intravenous iron to replenish their iron stores. Both acute dosing and chronic dosing of intravenous iron are effective in pediatric patients. PMID:16198278

Greenbaum, Larry A

2005-10-01

336

Anemia caused by low iron - children  

MedlinePLUS

Anemia - iron deficiency - children ... able to absorb iron well, even though the child is eating enough iron Slow blood loss over ... bleeding in the digestive tract Iron deficiency in children can also be related to lead poisoning .

337

Sickle Cell Anemia: New Approaches To Therapy.  

National Technical Information Service (NTIS)

This citation summarizes a one-page announcement of technology available for utilization. Patients with sickle cell anemia experience unpredictable episodes of severe, sometimes disabling pain in the joints, abdomen, or spine, episodes that may last from ...

1984-01-01

338

[Equine infectious anemia--a review].  

PubMed

This article combines essential facts of equine infectious anemia. Beside etiology and epidemiology, emphasis is put on the clinical course and laboratory diagnosis. Finally, control measures and prophylactic issues are discussed. PMID:25080822

Haas, Ludwig

2014-01-01

339

Gametophyte development in Anemia mexicana Klotzsch  

E-print Network

GAMETOPHYTE DEVELOPMENT IN ANEMIA MEXICANA KLOTZSCH A Thesis by JOAN ELIZABETH NESTER Submitted to the Graduate College of Texas A&M University in partial fulfillment of the requirement for the degree of MASTER OF SCIENCE August 1979 Major... Subject: Botany GAMETOPHYTE DEVELOPMENT IN ANEMIA MEXICANA KLOTZSCH A Thesis by JOAN ELIZABETH NESTER Approved as sty e and content by: rl, udge(~u Chatrman of Committee ember e ber Head o Department August 1979 ABSTRACT Gametophyte Development...

Nester, Joan Elizabeth

2012-06-07

340

Fanconis anemia in monozygotic twins  

Microsoft Academic Search

Fanconis anemia is one of the inherited causes of bone marrow failure. It is inherited in autosomal recessive fashion. It\\u000a presents as aplastic anemia usually at the age of 78 yr. Leukemias and solid tumours are complications in those who manage\\u000a to survive beyond two decades. Though it has been seen in siblings, reports in monozygotic twins have been very

Fulton Dsouza; M. K. Usha; S. D. Subba Rao

2007-01-01

341

Advancements in anemias related to chronic conditions.  

PubMed

Anemia of chronic disease (ACD), the most frequent anemia among hospitalized patients, occurs in chronic inflammatory disorders, such as chronic infections, cancer and autoimmune diseases. Different causes contribute to ACD including diversion of iron traffic, diminished erythropoiesis, blunted response to erythropoietin, erythrophagocytosis, hematologic malignancies and solid tumors. A particular case of ACD is represented by anemia of chronic kidney disease (CKD). ACD is characterized by hyposideremia and altered iron transport. Cytokines are implicated in the ACD by reducing erythropoiesis and increasing iron sequestration in the reticuloendothelial system. The regulation of iron absorption across the epithelium of the proximal small intestine is essential for maintaining body iron concentrations within a physiologically defined range. Hepcidin controls cellular iron efflux by binding to the iron export protein ferroportin, causing ferroportin to be phosphorylated and degraded in lysosomes. Finally, hepcidin inhibits iron release from the reticulo-endothelial system. Increased expression of hepcidin leads to decreased iron absorption and iron deficient anemia. Hepcidin, therefore, is a negative regulator of iron transport in plasma. Causes of anemia in patients with CKD are multifactorial, but the most well-known cause is inadequate erythropoietin production. In these patients, anemia increases the risk of either cardiovascular disease or renal failure. PMID:20618092

Guidi, Gian Cesare; Lechi Santonastaso, Clara

2010-09-01

342

Family structure and child anemia in Mexico.  

PubMed

Utilizing longitudinal data from the nationally-representative Mexico Family Life Survey, this study assesses the association between family structure and iron-deficient anemia among children ages 3-12 in Mexico. The longitudinal models (n=4649), which control for baseline anemia status and allow for consideration of family structure transitions, suggest that children living in stable-cohabiting and single-mother families and those who have recently experienced a parental union dissolution have higher odds of anemia than those in stable-married, father-present family structures. Interaction effects indicate that unmarried family contexts have stronger associations with anemia in older children (over age five); and, that the negative effects of parental union dissolution are exacerbated in poorer households. Resident maternal grandparents have a significant beneficial effect on child anemia independent of parental family structure. These results highlight the importance of family structure for child micronutrient deficiencies and suggest that understanding social processes within households may be critical to preventing child anemia in Mexico. PMID:23294876

Schmeer, Kammi K

2013-10-01

343

Hepcidin in anemia of chronic heart failure  

PubMed Central

Anemia is a common finding among patients with chronic heart failure. Although co-morbidities, such as kidney failure, might contribute to the pathogenesis of anemia, many patients with heart failure do not have any other obvious etiology for their anemia. We investigated whether anemia in heart failure is associated with an elevation in hepcidin concentration. We used time-of-flight mass spectrometry to measure hepcidin concentration in urine and serum samples of patients with heart failure and in control subjects. We found that the concentration of hepcidin was lower in urine samples of patients with heart failure compared to those of control subjects. Serum hepcidin was also reduced in heart failure but was not significantly lower than that in controls. There were no significant differences between hepcidin levels in patients with heart failure and anemia compared to patients with heart failure and normal hemoglobin. We concluded that hepcidin probably does not play a major role in pathogenesis of anemia in patients with chronic heart failure. PMID:21080339

Divakaran, Vijay; Mehta, Sachin; Yao, David; Hassan, Saamir; Simpson, Steven; Wiegerinck, Erwin; Swinkels, Dorine W.; Mann, Douglas L.; Afshar-Kharghan, Vahid

2010-01-01

344

Intravenous Immunoglobulin G Treatment in ABO Hemolytic Disease of the Newborn, is it Myth or Real?  

PubMed

Intravenous Immunoglobulin G (IVIG) therapy has been used as a component of the treatment of hemolytic disease of the newborn. There is still no consensus on its use in ABO hemolytic disease of the newborn routinely. The aim of this study is to determine whether administration of IVIG to newborns with ABO incompatibility is necessary. One hundred and seventeen patients with ABO hemolytic disease and positive Coombs test were enrolled into the study. The subjects were healthy except jaundice. Infants were divided into two groups: Group I (n=71) received one dose of IVIG (1g/kg) and LED phototherapy whereas Group II (n=46) received only LED phototherapy. One patient received erythrocyte transfusion in Group I, no exchange transfusion was performed in both groups. Mean duration of phototherapy was 3.11.3days in Group I and 2.270.7days in Group II (p<0.05). Mean duration of hospital stay was 5.342.2days in Group I and 3.531.3days in Group II (p<0.05). Mean duration of phototherapy was 4.01.5days and 2.731.1days in double and single doses of IVIG respectively, and this was statistically significant (p<0.05). IVIG therapy didn't decrease neither phototherapy nor hospitalization duration in infants with ABO hemolytic disease. Meticulus follow-up of infants with ABO hemolytic disease and LED phototherapy decreases morbidity. IVIG failed to show preventing hemolysis in ABO hemolytic disease. PMID:24554813

Beken, Serdar; Hirfanoglu, Ibrahim; Turkyilmaz, Canan; Altuntas, Nilgun; Unal, Sezin; Turan, Ozden; Onal, Esra; Ergenekon, Ebru; Koc, Esin; Atalay, Yildiz

2014-03-01

345

In vitro cytotoxic effect of alpha-hemolytic Escherichia coli on human blood granulocytes.  

PubMed Central

The cytotoxic effect of Escherichia coli bacteria on human blood granulocytes was measured by recording numbers of nonlysed cells and percentages of viable cells after in vitro incubation with bacteria in the presence of plasma. A total of 179 strains from various sources of infection were tested. Of 117 alpha-hemolytic strains, 59 were cytotoxic. Five nonhemolytic mutant strains, derived from alpha-hemolytic cytotoxic strains, were nontoxic. None of the 62 nonhemolytic strains were toxic. Four spontaneously occurring alpha-hemolytic, nontoxic mutant strains were isolated from cytotoxic ones. Cytotoxicity of bacteria reached a maximum after log-phase growth at 30 to 37 degrees C for 2.5 h, and the toxic capacity was equal after growth in various media, including human urine and plasma. The cytotoxic effect increased with the length of exposure of granulocytes to bacteria and with increasing numbers of bacteria per granulocyte. Cytotoxic strains showed different degrees of toxicity, highly cytotoxic strains lysing about 90% of the granulocytes and killing about one-half of nonlysed cells in 1 h. Bacteria killed by heat, formaldehyde, or UV light were nontoxic. Alpha-hemolytic strains of O groups 2, 4, 6, 25, and 75 originating from various infections in humans were more frequently cytotoxic than alpha-hemolytic strains of other O groups derived from human infections. Culture supernatants containing free alpha-hemolysin were highly cytotoxic to human blood granulocytes, monocytes, and lymphocytes in vitro, whether supernatants originated from cytotoxic or noncytotoxic bacteria. Cytotoxicity to phagocytes, which is mediated by or closely linked genetically to alpha-hemolysin, may be a mechanism by which alpha-hemolytic strains of E. coli strengthen their ability to establish and maintain infections. PMID:6376357

Gadeberg, O V; Orskov, I

1984-01-01

346

Anemia after renal transplantation: an underestimated problem.  

PubMed

In end-stage renal disease patients anemia is known to be an independent risk factor for cardiovascular disease and death. In a monocenter retrospective analysis, we investigated 207 stable patients (68 women/139 men) who underwent a first renal transplantation. Immunosuppressive therapy was performed with either cyclosporine plus mycophenolate mofetil, tacrolimus plus mycophenolate mofetil, or rapamycin plus mycophenolate mofetil; 43.5% of the patients were treated with steroids. Seventy-eight patients (37.7%) displayed anemia, including 8.7% with a severe disorder displaying an average hemoglobin (Hb) level of <6.8 mmo/L in men and <6.2 mmol/L in women. In 8.2% of the cases, we observed moderate anemia (Hb 6.8-7.4 mmol/L in men and 6.2-6.8 mmol/L in women), and in 20.8% (29 men and 14 women), mild anemia (Hb <8.06 mmol/L in men and <7.45 mmol/L in women). Erythropoietin was administered in 55.5% of patients with severe anemia, 53% with moderate anemia, and 11.6% with mild anemia. Serum creatinine level was a significant predictor of anemia (B -0.004; SE 0.001; P < .01). Among patients with creatinine >200 micromol/L, 63% were anemic compared with 22% of those with a serum creatinine level <200 micromol/L (P < .05). No correlation was observed with immunosuppressive medication or treatment with angiotensin-converting enzyme inhibitors/angiotensin-II receptor antagonists. During a 3-year follow-up, both mortality and graft failure rates were significantly greater among anemic patients nonanemic patients (mortality 3.3% vs 0.5%, P < .001; graft failure 4.3% vs 0%, P < .001). We found an unexpectedly high incidence of anemia in patients with well-functioning grafts. Anemia as a risk factor for mortality and graft failure should be treated more intensively among renal transplant patients. PMID:19100418

Ott, U; Busch, M; Steiner, T; Wolf, G

2008-12-01

347

Alloantibodies to a paternally derived RBC KEL antigen lead to hemolytic disease of the fetus/newborn in a murine model.  

PubMed

Exposure to nonself red blood cell (RBC) antigens, either from transfusion or pregnancy, may result in alloimmunization and incompatible RBC clearance. First described as a pregnancy complication 80 years ago, hemolytic disease of the fetus and newborn (HDFN) is caused by alloimmunization to paternally derived RBC antigens. Despite the morbidity/mortality of HDFN, women at risk for RBC alloimmunization have few therapeutic options. Given that alloantibodies to antigens in the KEL family are among the most clinically significant, we developed a murine model with RBC-specific expression of the human KEL antigen to evaluate the impact of maternal/fetal KEL incompatibility. After exposure to fetal KEL RBCs during successive pregnancies with KEL-positive males, 21 of 21 wild-type female mice developed anti-KEL alloantibodies; intrauterine fetal anemia and/or demise occurred in a subset of KEL-positive pups born to wild type, but not agammaglobulinemic mothers. Similar to previous observations in humans, pregnancy-associated alloantibodies were detrimental in a transfusion setting, and transfusion-associated alloantibodies were detrimental in a pregnancy setting. This is the first pregnancy-associated HDFN model described to date, which will serve as a platform to develop targeted therapies to prevent and/or mitigate the dangers of RBC alloantibodies to fetuses and newborns. PMID:23801629

Stowell, Sean R; Henry, Kate L; Smith, Nicole H; Hudson, Krystalyn E; Halverson, Greg R; Park, Jaekeun C; Bennett, Ashley M; Girard-Pierce, Kathryn R; Arthur, C Maridith; Bunting, Silvia T; Zimring, James C; Hendrickson, Jeanne E

2013-08-22

348

Alloantibodies to a paternally derived RBC KEL antigen lead to hemolytic disease of the fetus/newborn in a murine model  

PubMed Central

Exposure to nonself red blood cell (RBC) antigens, either from transfusion or pregnancy, may result in alloimmunization and incompatible RBC clearance. First described as a pregnancy complication 80 years ago, hemolytic disease of the fetus and newborn (HDFN) is caused by alloimmunization to paternally derived RBC antigens. Despite the morbidity/mortality of HDFN, women at risk for RBC alloimmunization have few therapeutic options. Given that alloantibodies to antigens in the KEL family are among the most clinically significant, we developed a murine model with RBC-specific expression of the human KEL antigen to evaluate the impact of maternal/fetal KEL incompatibility. After exposure to fetal KEL RBCs during successive pregnancies with KEL-positive males, 21 of 21 wild-type female mice developed anti-KEL alloantibodies; intrauterine fetal anemia and/or demise occurred in a subset of KEL-positive pups born to wild type, but not agammaglobulinemic mothers. Similar to previous observations in humans, pregnancy-associated alloantibodies were detrimental in a transfusion setting, and transfusion-associated alloantibodies were detrimental in a pregnancy setting. This is the first pregnancy-associated HDFN model described to date, which will serve as a platform to develop targeted therapies to prevent and/or mitigate the dangers of RBC alloantibodies to fetuses and newborns. PMID:23801629

Stowell, Sean R.; Henry, Kate L.; Smith, Nicole H.; Hudson, Krystalyn E.; Halverson, Greg R.; Park, Jaekeun C.; Bennett, Ashley M.; Girard-Pierce, Kathryn R.; Arthur, C. Maridith; Bunting, Silvia T.; Zimring, James C.

2013-01-01

349

Aplastic anemia: presence in human bone marrow of cells that suppress myelopoiesis.  

PubMed Central

Bone marrow from a patient with aplastic anemia was shown by multiple criteria to have a block in early myeloid differentiation. This block was overcome in vitro by elimination of marrow lymphocytes. Furthermore, this differentiation block was transferred in vitro to normal marrow by coculturing with the patient's marrow. We suggest that some cases of aplastic anemia may be due to an immunologically based suppression of marrow cell differentiation rather than to a defect in stem cells or their necessary inductive environment. Images PMID:1085449

Kagan, W A; Ascensao, J A; Pahwa, R N; Hansen, J A; Goldstein, G; Valera, E B; Incefy, G S; Moore, M A; Good, R A

1976-01-01

350

Normal erythropoiesis but severe polyposis and bleeding anemia in Smad4-deficient mice.  

PubMed

The tumor suppressor Smad4 mediates signaling by the transforming growth factor beta (TGF-beta) superfamily of ligands. Previous studies showed that several TGF-beta family members exert important functions in hematopoiesis. Here, we studied the role of Smad4 in adult murine hematopoiesis using the inducible Mx-Cre/loxP system. Mice with homozygous Smad4 deletion (Smad4(Delta/Delta)) developed severe anemia 6 to 8 weeks after induction (mean hemoglobin level 70 g/L). The anemia was not transplantable, as wild-type mice reconstituted with Smad4(Delta/Delta) bone marrow cells had normal peripheral blood counts. These mice did not develop an inflammatory disease typical for mice deficient in TGF-beta receptors I and II, suggesting that the suppression of inflammation by TGF-beta is Smad4 independent. The same results were obtained when Smad4 alleles were deleted selectively in hematopoietic cells using the VavCre transgenic mice. In contrast, lethally irradiated Smad4(Delta/Delta) mice that received wild-type bone marrow cells developed anemia similar to Smad4(Delta/Delta) mice that did not receive a transplant. Liver iron stores were decreased and blood was present in stool, indicating that the anemia was due to blood loss. Multiple polyps in stomach and colon represent a likely source of the bleeding. We conclude that Smad4 is not required for adult erythropoiesis and that anemia is solely the consequence of blood loss. PMID:17638848

Pan, Dejing; Schomber, Tibor; Kalberer, Christian P; Terracciano, Luigi M; Hafen, Katrin; Krenger, Werner; Hao-Shen, Hui; Deng, Chuxia; Skoda, Radek C

2007-10-15

351

Bed bugs reproductive life cycle in the clothes of a patient suffering from Alzheimer's disease results in iron deficiency anemia.  

PubMed

We report the case of an 82-year-old patient, hospitalized for malaise. Her clothes were infested by numerous insects and the entomological analysis identified them as being Cimex lectularius (bed bugs). The history of the patient highlighted severe cognitive impairment. The biological assessment initially showed a profound microcytic, aregenerative, iron deficiency anemia. A vitamin B12 deficiency due to pernicious anemia (positive intrinsic factor antibodies) was also highlighted, but this was not enough to explain the anemia without macrocytosis. Laboratory tests, endoscopy and a CT scan eliminated a tumor etiology responsible for occult bleeding. The patient had a mild itchy rash which was linked to the massive colonization by the bed bugs. The C. lectularius bite is most often considered benign because it is not a vector of infectious agents. Far from trivial, a massive human colonization by bed bugs may cause such a hematic depletion that severe microcytic anemia may result. PMID:23673315

Sabou, Marcela; Imperiale, Delphine Gallo; Andrs, Emmanuel; Abou-Bacar, Ahmed; Foegl, Jacinthe; Lavigne, Thierry; Kaltenbach, Georges; Candolfi, Ermanno

2013-01-01

352

What Are the Signs and Symptoms of Aplastic Anemia?  

MedlinePLUS

... What Are the Signs and Symptoms of Aplastic Anemia? Lower than normal numbers of red blood cells, ... most of the signs and symptoms of aplastic anemia. Signs and Symptoms of Low Blood Cell Counts ...

353

For Parents of Children with Diamond Blackfan Anemia  

MedlinePLUS

... Disorders For Parents of Children with Diamond Blackfan Anemia Parenting Corner Q&A When your child is ... Starlight Childrens Foundation www.starlight.org Diamond Blackfan Anemia Foundation (DBAF) http://www.dbafoundation.org/ DBA Nurse ...

354

What Are the Signs and Symptoms of Fanconi Anemia?  

MedlinePLUS

... What Are the Signs and Symptoms of Fanconi Anemia? Major Signs and Symptoms Your doctor may suspect ... sisters also should be tested for the disorder. Anemia The most common symptom of all types of ...

355

Escherichia coli O 157:H7-associated hemolytic-uremic syndrome after ingestion of contaminated hamburgers.  

PubMed

We conducted a retrospective analysis of 37 children with Escherichia coli O157:H7-associated hemolytic-uremic syndrome. The infection was traced to contaminated hamburgers at a fast-food restaurant chain. Within 5 days of the first confirmed case, the Washington State Department of Health identified the source and interrupted transmission of infection. Ninety-five percent of the children initially had severe hemorrhagic colitis. Nineteen patients (51%) had significant extrarenal abnormalities, including pancreatitis, colonic necrosis, glucose intolerance, coma, stroke, seizures, myocardial dysfunction, pericardial effusions, adult respiratory disease syndrome, and pleural effusions. Three deaths occurred, each in children with severe multisystem disease. At follow-up two children have significant impairment of renal function (glomerular filtration rate < 80 ml/min/per 1.73 Hm2); both of these children have a normal serum creatinine concentration. Hemolytic-uremic syndrome is the most common cause of acute renal failure in children, and this experience emphasizes the systemic nature of this disease. Clinicians should anticipate that multisystem involvement may occur in these patients, necessitating acute intervention or chronic follow-up. This outbreak of Hemolytic-uremic syndrome also highlights the microbiologic hazards of inadequately prepared food and emphasizes the importance of public health intervention in controlling Hemolytic-uremic syndrome. PMID:7931869

Brandt, J R; Fouser, L S; Watkins, S L; Zelikovic, I; Tarr, P I; Nazar-Stewart, V; Avner, E D

1994-10-01

356

Experimental reproduction of hemolytic disease of the newborn in lower monkeys  

Microsoft Academic Search

Summary The article describes the author's experiments with artificial induction in lower monkeys (Papiohamadryas) of a hemolytic disease of newborn. The experiments were made on monkey couples sires and dams incompatible in the isoantigenic respect. An increase in the immunologic incompatibility between the fetus and the maternal body was achieved by immunization of females with blood erythrocytes from

L. S. Volkova; M. Sh. Verbitskii; A. V. Andreeva

1966-01-01

357

FETAL AND ADULT HEMOGLOBINS IN THE BLOOD OF INFANTS AFFECTED WITH HEMOLYTIC DISEASE OF THE NEWBORN  

Microsoft Academic Search

Hb by the Rh agglutinin-lysin system (Jonxis6) should be an increase in the proportion of adult Hb in the blood of infants affected with hemolytic dis- ease, and this proportion should be even greater if, as Jonxis believes, the affected infant develops adult Hb in utero as a protective mechanism. As pointed out by Baar,' the conclusions of Jonxis are

ERIC PONDER; PHILIP LEVINE

1950-01-01

358

Immunologic Basis and Immunoprophylaxis of RhD Induced Hemolytic Disease of the Newborn (HDN)  

Microsoft Academic Search

RhD antigen is the most immunogenic and clinically significant antigen of red blood cells after ABO system. It has historically been associated with hemolytic disease of the newborn (HDN) which is now routinely prevented by the administration of polyclonal anti-D immunoglobulin. This management of HDN has proven to be one of the most successful cases of prophylactic treatment based on

Roya Payam; Khaja Pasha; Fazel Shokri

359

Characterization of Maternal Isoagglutinins in ABO Hemolytic Disease of the Newborn  

Microsoft Academic Search

diagnosis of ABO hemolytic disease of the newborn (ABO HDN). The majority of the tests currently used in most hospital clinical laboratories for this purpose make use of certain serologic properties that differentiate the isoagglutinins into two groups. Although both groups probably arise as the result of antigenic stimulation, the early literature has termed them \\

Susis W. FONG; ARLENE NUCKTON; H. H. FUDENBERG

1966-01-01

360

Radionuclide studies of the kidney in children with hemolytic-uremic syndrome  

SciTech Connect

Twenty-six children with hemolytic-uremic syndrome (HUS) had radionuclide studies while oliguric or anuric in order to assess prognosis. Renographic abnormalities were compared with clinical and biochemical parameters and eventual outcome. Presence of an anephric pattern failed to predict development of irreversible renal damage. The authors conclude that radionuclide renography is of no value in children with HUS.

Campos, A.; Kim, Y.; Miller, K.; Maner, S.M.; Loken, M.K.; Michael, A.F.

1982-12-01

361

Asbestos Hemolysis' Chrysotilc fibers rsert a marked hemolytic activity OII suspensions of \\vnshed sheq  

E-print Network

Asbestos Hemolysis' Chrysotilc fibers rsert a marked hemolytic activity OII suspensions of \\vnshed of chrysotile asbestos is dependent on the openness of the fibrrs as chnractrrized by the air permeability>- repeated trratmcnt with ret1 blood cells. The nlechanism of asbestos helnolysis cannot yet 1x1

Ahmad, Sajjad

362

Comparing micellar, hemolytic, and antibacterial properties of di-and tricarboxyl dendritic amphiphiles  

E-print Network

amphiphiles Bhadreshkumar B. Maisuria a, , Marcelo L. Actis a,à , Shauntrece N. Hardrict a,§ , Joseph O April 2011 Keywords: Dendritic amphiphiles Staphylococcus aureus MRSA Critical micelle concentrations Hemolytic activities a b s t r a c t Homologous dicarboxyl dendritic amphiphiles--RCONHC(CH3)(CH2CH2COOH)2

Falkinham, Joseph

363

The Hemolytic Enterotoxin HBL Is Broadly Distributed among Species of the Bacillus cereus Group  

Microsoft Academic Search

The prevalence of the hemolytic enterotoxin complex HBL was determined in all species of the Bacillus cereus group with the exception of Bacillus anthracis. hblA, encoding the binding subunit B, was detected by PCR and Southern analysis and was confirmed by partial sequencing of 18 strains. The sequences formed two clusters, one including B. cereus and Bacillus thuringiensis strains and

BIRGIT M. PRU; RICHARD DIETRICH; BIRGIT NIBLER; ERWIN MARTLBAUER; SIEGFRIED SCHERER

1999-01-01

364

Treatment of iron deficiency anemia associated with gastrointestinal tract diseases.  

PubMed

The gastrointestinal (GI) tract is a common site of bleeding that may lead to iron deficiency anemia (IDA). Treatment of IDA depends on severity and acuity of patients' signs and symptoms. While red blood cell transfusions may be required in hemodynamically unstable patients, transfusions should be avoided in chronically anemic patients due to their potential side effects and cost. Iron studies need to be performed after episodes of GI bleeding and stores need to be replenished before anemia develops. Oral iron preparations are efficacious but poorly tolerated due to non-absorbed iron-mediated GI side effects. However, oral iron dose may be reduced with no effect on its efficacy while decreasing side effects and patient discontinuation rates. Parenteral iron therapy replenishes iron stores quicker and is better tolerated than oral therapy. Serious hypersensitive reactions are very rare with new intravenous preparations. While data on worsening of inflammatory bowel disease (IBD) activity by oral iron therapy are not conclusive, parenteral iron therapy still seems to be advantageous in the treatment of IDA in patients with IBD, because oral iron may not be sufficient to overcome the chronic blood loss and GI side effects of oral iron which may mimic IBD exacerbation. Finally, we believe the choice of oral vs parenteral iron therapy in patients with IBD should primarily depend on acuity and severity of patients' signs and symptoms. PMID:20533591

Bayraktar, Ulas D; Bayraktar, Soley

2010-06-14

365

Probing vasoocclusion phenomena in sickle cell anemia via mesoscopic simulations.  

PubMed

Vasoocclusion crisis is a key hallmark of sickle cell anemia. Although early studies suggest that this crisis is caused by blockage of a single elongated cell, recent experiments have revealed that vasoocclusion is a complex process triggered by adhesive interactions among different cell groups in multiple stages. However, the quantification of the biophysical characteristics of sickle cell anemia remains an open issue. Based on dissipative particle dynamics, we develop a multiscale model for the sickle red blood cells (SS-RBCs), accounting for diversity in both shapes and cell rigidities, to investigate the precise mechanism of vasoocclusion. First, we investigate the adhesive dynamics of a single SS-RBC in shear flow and static conditions, and find that the different cell groups (SS2: young-deformable SS-RBCs, ISCs: rigid-irreversible SS-RBCs) exhibit heterogeneous adhesive behavior due to the diverse cell morphologies and membrane rigidities. We quantify the observed adhesion behavior (in static conditions) in terms of a balance of free energies due to cell adhesion and deformation, and propose a power law that relates the free-energy increase as a function of the contact area. We further simulate postcapillary flow of SS-RBC suspensions with different cell fractions. The more adhesive SS2 cells interact with the vascular endothelium and trap ISC cells, resulting in vasoocclusion in vessels less than 12-14 ?m depending on the hematocrit. Under inflammation, adherent leukocytes may also trap ISC cells, resulting in vasoocclusion in even larger vessels. PMID:23798393

Lei, Huan; Karniadakis, George E

2013-07-01

366

21 CFR 500.27 - Methylene blue-containing drugs for use in animals.  

Code of Federal Regulations, 2010 CFR

...methylene blue cause Heinz body hemolytic anemia in cats when used according to label...animals. (ii) The Heinz body hemolytic anemia reaction to methylene blue has also...Heinz bodies) and associated hemolytic anemia is unclear. (2) The...

2010-04-01

367

76 FR 22620 - Triflusulfuron-Methyl; Pesticide Tolerances  

Federal Register 2010, 2011, 2012, 2013

...changes consistent with mild hemolytic anemia were observed in the rat and the...immunotoxicity in the available studies. Hemolytic anemia, an effect associated with exposure to...although it is not clear that the hemolytic anemia observed with...

2011-04-22

368

Aplastic anemia in a petrochemical factory worker.  

PubMed Central

A petrochemical worker with aplastic anemia was referred to our hospital. He worked in a petroleum resin-producing factory and had been exposed to low-level benzene while packaging the powder resin and pouring lime into a deactivation tank. According to the yearly environmental survey of the working area, the airborne benzene level was approximately 0.28 ppm. Exposure to benzene, a common chemical used widely in industry, may progressively lead to pancytopenia, aplastic anemia, and leukemia. The hematotoxicity of benzene is related to the amount and duration of exposure. Most risk predictions for benzene exposures have been based on rubber workers who were exposed to high concentrations. In the petroleum industry, the concentration of benzene is relatively low, and there are disputes over the toxicity of low-level benzene because of a lack of evidence. In this paper we report the case of aplastic anemia induced by low-level benzene exposure. Images Figure 1 PMID:10504154

Baak, Y M; Ahn, B Y; Chang, H S; Kim, J H; Kim, K A; Lim, Y

1999-01-01

369

Congential dyserythropoietic anemia--type IV.  

PubMed

Congenital dyserythropoietic anemia is characterized by ineffective erythropoiesis and increased numbers of multinucleated red cell precursors in the marrow. This syndrome has been subclassified on the basis of morphologic differences in the red cell precursors. Type I is characterized by megaloblastoid erythropoiesis and macrocytosis; Type II, by normoblastic multinuclearity and normocytosis; and Type III, by frequent giant multinucleated erythroblasts and macrocytes. Type II is further distinguished from the other types by serologic and ultrastructural abnormalities. The patient presented in this report does not fit any of the above categories; her red cells are similar to Type II congenital dyserythropoietic anemia cells, but no characteristic ultrastructural or serologic abnormalities are present. It is suggested that this patient may represent an additional variant of congenital dyserythropoietic anemia, Type IV. PMID:1097617

Benjamin, J T; Rosse, W F; Daldorf, F G; McMillan, C W

1975-08-01

370

Hemophagocytosis causes a consumptive anemia of inflammation  

PubMed Central

Cytopenias of uncertain etiology are commonly observed in patients during severe inflammation. Hemophagocytosis, the histological appearance of blood-eating macrophages, is seen in the disorder hemophagocytic lymphohistiocytosis and other inflammatory contexts. Although it is hypothesized that these phenomena are linked, the mechanisms facilitating acute inflammation-associated cytopenias are unknown. We report that interferon ? (IFN-?) is a critical driver of the acute anemia observed during diverse microbial infections in mice. Furthermore, systemic exposure to physiologically relevant levels of IFN-? is sufficient to cause acute cytopenias and hemophagocytosis. Demonstrating the significance of hemophagocytosis, we found that IFN-? acts directly on macrophages in vivo to alter endocytosis and provoke blood cell uptake, leading to severe anemia. These findings define a unique pathological process of broad clinical and immunological significance, which we term the consumptive anemia of inflammation. PMID:21624938

Zoller, Erin E.; Lykens, Jennifer E.; Terrell, Catherine E.; Aliberti, Julio; Filipovich, Alexandra H.; Henson, Peter M.

2011-01-01

371

[Iron-deficiency anemia and gastrointestinal bleeding].  

PubMed

The physiology of iron homeostasis, clinical presentation, diagnosis, differential diagnosis and therapeutic options in iron-deficiency anemia are discussed. Iron deficiency is the most common haematological disorder encountered in general practice and iron-deficiency anemia is the most frequently occurring anemia throughout the world. Blood loss is a major cause of iron-deficiency anemia. Gastrointestinal bleeding is the most common cause of iron deficiency in adult men and is second only to menstrual blood loss as a cause in women. Iron-deficiency anemia is not a disease itself but a manifestation of an underlying disease, searching for the latter is therefore crucial and may be of far greater importance to the ultimate well-being of the patient than repleting iron stores. The symptoms and signs of iron deficiency are partially explained by the presence of anemia. However, there also appears to be a direct effect of iron deficiency on the central nervous system. The most important screening investigations for iron deficiency in clinical practice are the haemoglobin, the haematocrit and the mean corpuscular volume (MCV). The single most important measure of iron status is the serum ferritin, values below the lower limit of normal being specific for iron deficiency. In inflammation, hepatopathy and haemolysis serum ferritin is also released leading to falsely elevated values, therefore an analysis of the C-reactive protein (CRP) should always accompany the analysis of serum ferritin. Repleting iron stores is usually done with oral iron therapy, the available preparations are comparable with respect to efficacy, side effects and costs. The main indications for parenteral iron therapy are intolerance to oral iron, intestinal malabsorption and poor compliance to an oral regimen. The iron sucrose preparation should bepreferentially used for that purpose, the total dose is calculated from the amount of iron needed to restore the haemoglobin deficit plus an additional amount to replenish iron stores. PMID:16739893

Rfer, A; Criblez, D; Wuillemin, W A

2006-05-01

372

Anemia in hospitalized patients with pulmonary tuberculosis*  

PubMed Central

OBJECTIVE: To describe the prevalence of anemia and of its types in hospitalized patients with pulmonary tuberculosis. METHODS: This was a descriptive, longitudinal study involving pulmonary tuberculosis inpatients at one of two tuberculosis referral hospitals in the city of Rio de Janeiro, Brazil. We evaluated body mass index (BMI), triceps skinfold thickness (TST), arm muscle area (AMA), ESR, mean corpuscular volume, and red blood cell distribution width (RDW), as well as the levels of C-reactive protein, hemoglobin, transferrin, and ferritin. RESULTS: We included 166 patients, 126 (75.9%) of whom were male. The mean age was 39.0 10.7 years. Not all data were available for all patients: 18.7% were HIV positive; 64.7% were alcoholic; the prevalences of anemia of chronic disease and iron deficiency anemia were, respectively, 75.9% and 2.4%; and 68.7% had low body weight (mean BMI = 18.21 kg/m2). On the basis of TST and AMA, 126 (78.7%) of 160 patients and 138 (87.9%) of 157 patients, respectively, were considered malnourished. Anemia was found to be associated with the following: male gender (p = 0.03); low weight (p = 0.0004); low mean corpuscular volume (p = 0.03);high RDW (p = 0; 0003); high ferritin (p = 0.0005); and high ESR (p = 0.004). We also found significant differences between anemic and non-anemic patients in terms of BMI (p = 0.04), DCT (p = 0.003), and ESR (p < 0.001). CONCLUSIONS: In this sample, high proportions of pulmonary tuberculosis patients were classified as underweight and malnourished, and there was a high prevalence of anemia of chronic disease. In addition, anemia was associated with high ESR and malnutrition. PMID:25210963

Oliveira, Marina Gribel; Delogo, Karina Neves; de Oliveira, Hedi Marinho de Melo Gomes; Ruffino-Netto, Antonio; Kritski, Afranio Lineu; Oliveira, Martha Maria

2014-01-01

373

Risk factors associated with anemia, iron deficiency and iron deficiency anemia in rural Nepali pregnant women.  

PubMed

We conducted a cross sectional study to investigate risk factors associated with severe anemia [hemoglobin (Hb) < 8.0 g dl(-1)] and poor iron status among Nepali pregnant women. Socio-demographic, anthropometric, health and dietary data were collected from 3,531 women living in the southeastern plains of Nepal. Stool samples were analyzed for intestinal helminthes. Dark adaptation was assessed using the Night Vision Threshold Test (NVTT). Hb levels were measured in all subjects to detect anemia and the soluble transferrin receptor (sTfR) was measured among a subsample of 479 women. The iron status categories were: 1) normal (Hb> or = 11.0 g/dl and sTfR < or = 8.5 mg/l); 2) anemia without iron deficiency (Hb<11.0 g/dl and sTfR < or = 8.5 mg/l); 3) iron deficiency without anemia (Hb > or = 11.0 g/dl and sTfR>8.5 mg/l); and 4) iron deficiency anemia (IDA): (Hb<11.0 g/dl and sTfR>8.5 mg/l). Factors associated with severe anemia and poor iron status were determined using logistic regression. Hookworm infection increased the risk for developing severe anemia [adjusted odds ratio (AOR): 4.26; 95% CI 1.67-10.89; p<0.01] and IDA [relative risk ratio (RRR): 2.18; 95% CI 1.14-4.16; p<0.05]. Impaired dark adaptation was a common risk factor for iron deficiency with and without anemia. Intake of iron supplements as tablets and/or tonic was protective against severe anemia, anemia without iron deficiency and IDA. Dietary heme iron was significantly associated with iron deficiency without anemia (RRR: 0.1; 95% CI 0.02-0.47; p<0.01). These results indicate the risk factors varied by classification and multiple approaches are needed to reduce anemia and associated nutrient deficiencies. PMID:23077854

Makhoul, Zeina; Taren, Douglas; Duncan, Burris; Pandey, Pooja; Thomson, Cynthia; Winzerling, Joy; Muramoto, Myra; Shrestha, Ram

2012-05-01

374

Sigma E Regulators Control Hemolytic Activity and Virulence in a Shrimp Pathogenic Vibrio harveyi  

PubMed Central

Members of the genus Vibrio are important marine and aquaculture pathogens. Hemolytic activity has been identified as a virulence factor in many pathogenic vibrios including V. cholerae, V. parahaemolyticus, V. alginolyticus, V. harveyi and V. vulnificus. We have used transposon mutagenesis to identify genes involved in the hemolytic activity of shrimp-pathogenic V. harveyi strain PSU3316. Out of 1,764 mutants screened, five mutants showed reduced hemolytic activity on sheep blood agar and exhibited virulence attenuation in shrimp (Litopenaeus vannamei). Mutants were identified by comparing transposon junction sequences to a draft of assembly of the PSU3316 genome. Surprisingly none of the disrupted open reading frames or gene neighborhoods contained genes annotated as hemolysins. The gene encoding RseB, a negative regulator of the sigma factor (?E), was interrupted in 2 out of 5 transposon mutants, in addition, the transcription factor CytR, a threonine synthetase, and an efflux-associated cytoplasmic protein were also identified. Knockout mutations introduced into the rpoE operon at the rseB gene exhibited low hemolytic activity in sheep blood agar, and were 3-to 7-fold attenuated for colonization in shrimp. Comparison of whole cell extracted proteins in the rseB mutant (PSU4030) to the wild-type by 2-D gel electrophoresis revealed 6 differentially expressed proteins, including two down-regulated porins (OmpC-like and OmpN) and an upregulated protease (DegQ) which have been associated with ?E in other organisms. Our study is the first report linking hemolytic activity to the ?E regulators in pathogenic Vibrio species and suggests expression of this virulence-linked phenotype is governed by multiple regulatory pathways within the V. harveyi. PMID:22384269

Rattanama, Pimonsri; Thompson, Janelle R.; Kongkerd, Natthawan; Srinitiwarawong, Kanchana; Vuddhakul, Varaporn; Mekalanos, John J.

2012-01-01

375

Assessment of phytochemicals, antioxidant, anti-lipid peroxidation and anti-hemolytic activity of extract and various fractions of Maytenus royleanus leaves  

PubMed Central

Background Maytenus royleanus is traditionally used in gastro-intestinal disorders. The aim of this study was to evaluate the methanol extract of leaves and its derived fractions for various antioxidant assays and for its potential against lipid peroxidation and hemolytic activity. Methods Various parameters including scavenging of free-radicals (DPPH, ABTS, hydroxyl and superoxide radical), hydrogen peroxide scavenging, Fe3+ to Fe2+ reducing capacity, total antioxidant capacity, anti-lipid peroxidation and anti-hemolytic activity were investigated. Methanol extract and its derived fractions were also subjected for chemical constituents. LC-MS was also performed on the methanol extract. Results Qualitative analysis of methanol extract exhibited the presence of alkaloids, anthraquinones, cardiac glycosides, coumarins, flavonoids, saponins, phlobatannins, tannins and terpenoids. LC-MS chromatogram indicated the composition of diverse compounds including flavonoids, phenolics and phytoestrogens. Methanol extract, its ethyl acetate and n-butanol fractions constituted the highest amount of total phenolic and flavonoid contents and showed a strong correlation coefficient with the IC50 values for the scavenging of DPPH, hydrogen peroxide radicals, superoxide radicals, anti-lipid peroxidation and anti-hemolytic efficacy. Moreover, n-butanol fraction showed the highest scavenging activity for ABTS radicals and for reduction of Fe3+ to Fe2+. Conclusions Present results suggested the therapeutic potential of Maytenus royleanus leaves, in particular, methanol extract, ethyl acetate and n-butanol fraction as therapeutic agent against free-radical associated damages. The protective potential of the extract and or fraction may be attributed due to the high concentration of phenolic, flavonoid, tannins and terpenoids. PMID:23800043

2013-01-01

376

The burden of anemia among women in India  

Microsoft Academic Search

Objective: This research investigates the prevalence and determinants of anemia among women in Andhra Pradesh. We examined differences in anemia related to social class, urban\\/rural location and nutrition status body mass index (BMI). We hypothesized that rural women would have higher prevalence of anemia compared to urban women, particularly among the lower income groups, and that women with low body

M E Bentley; P L Griffiths

2003-01-01

377

The pathogenesis of the anemia of anaplasmosis  

E-print Network

. Even though it ~e e t ~ a tmmCXca ot ecyCaxem ~ ~ yaw ~ ewaW ea deva~ of the anemia of natural and experimental anaIQawsssis, bemo- globineada end ~binmria usua11g do not occur. Several plasma yroteins designated ~chins have been shown to g have... to the narrows of the con- /f trol cattle. Studies of ~scion smears made from the marrow specimens of the 15 infeote4 cattle when c~ to the 5 non-infected control cat- l tie supported the above findings. / / It is obvious Chat the mechanism of the anemia...

Foote, Lon E

2012-06-07

378

Genetic modulation of sickle cell anemia  

SciTech Connect

Sickle cell anemia, a common disorder associated with reduced life span of the red blood cell and vasoocclusive events, is caused by a mutation in the {Beta}-hemoglobin gene. Yet, despite this genetic homogeneity, the phenotype of the disease is heterogeneous. This suggests the modulating influence of associated inherited traits. Some of these may influence the accumulation of fetal hemoglobin, a hemoglobin type that interferes with the polymerization of sickle hemoglobin. Another inherited trait determines the accumulation of {alpha}-globin chains. This review focuses on potential genetic regulators of the phenotype of sickle cell anemia. 125 refs., 6 figs., 3 tabs.

Steinberg, M.H. [Univ. of Mississippi School of Medicine, Jackson, MS (United States)

1995-05-01

379

The risk assessment study for hemolytic disease of the fetus and newborn in a University Hospital in Turkey.  

PubMed

Maternal red-cell alloimmunization occurs when a woman's immune system is sensitized to foreign red-blood cell surface antigens, leading to the production of alloantibodies. The resulting antibodies often cross the placenta during pregnancies in sensitized women and, if the fetus is positive for red-blood-cell surface antigens, this will lead to hemolysis of fetal red-blood cells and anemia. The most severe cases of hemolytic disease in the fetus and newborn baby are caused by anti-D, anti-c, anti-E and anti-K antibodies. There are limited data available on immunization rates in pregnant women from Turkey. The aim of the present study was to provide data on the frequency and nature of maternal RBC alloimmunization in pregnant women in a tertiary care hospital. In this study, we retrospectively evaluated the indirect antiglobulin test results of Rh-negative pregnant women performed in our Blood Bank between 2006 and 2012. Indirect antiglobulin test positive women also underwent confirmatory antibody screening and identification. During the study period, 4840 women admitted to our antenatal clinics. With regards to the major blood group systems (ABO and Rh), the most common phenotype was O positive (38.67%). There were 4097 D-antigen-positive women (84.65%) and 743 women with D-antigen-negative phenotype (15.35%). The prevalence of alloimmunization was found to be 8.74% in D-antigen negative group. Despite prophylactic use of Rh immunglobulins, anti-D is still a common antibody identified as the major cause of alloimmunization in our study (anti-D antibody 68.57%, non-D antibody 31.42%). While alloimmunization rate to D antigen was 6.46%, non-D alloimmunization rate was 2.69% among Rh-negative pregnant women. Moreover, detailed identification facilities for antibodies other than anti-D are not available in most of centers across Turkey. However, large-scale studies on pregnant women need to be done in order to collect sufficient evidence to formulate guidelines and to define indications for alloantibody screening and identification. PMID:23619329

Altuntas, Nilgn; Yenicesu, Idil; Himmetoglu, Ozdemir; Kulali, Ferit; Kazanci, Ebru; Unal, Sezin; Aktas, Selma; Hirfanoglu, Ibrahim; Onal, Esra; Turkyilmaz, Canan; Ergenekon, Ebru; Koc, Esin; Atalay, Y?ld?z

2013-06-01

380

Blood smear  

MedlinePLUS

... of target cells may be due to: Decreased osmotic fragility Deficiency of an enzyme called lecithin cholesterol acyl ... due to: Autoimmune hemolytic anemia Hereditary spherocytosis Increased osmotic fragility The presence of elliptocytes may be a sign ...

381

Practical approach to the diagnosis and treatment of anemia associated with CKD in elderly.  

PubMed

Anemia is a frequent complication of chronic kidney disease (CKD). Inadequate production of erythropoietin by the failing kidneys leads to decreased stimulation of the bone marrow to produce red blood cells (RBCs). Anemia of CKD develops early and worsens with progressive renal insufficiency. Although over 40% of patients with CKD are anemic, anemia in this population is under-recognized and undertreated. Of considerable importance, anemia is a risk factor for cardiovascular disease and is associated with higher rates of hospitalization and mortality. Despite the availability of erythropoiesis-stimulating proteins (ESPs) to stimulate RBC production in CKD patients, approximately three fourths of patients initiating dialysis have a hemoglobin <11 g/dL. The recognition of anemia of CKD begins with an estimation of glomerular filtration rate (GFR), which can be far lower than a normal serum creatinine might suggest, especially in the elderly and in those with poor nutrition and muscle mass. If GFR is <60 mL/min/1.73 m(2), hemoglobin should be checked. The anemia is diagnosed when the hemoglobin is <12 g/dL in a man or a postmenopausal woman, or <11 g/dL in a premenopausal woman. The cause of anemia should be investigated in these individuals; this can range from erythropoietin deficiency due to CKD, to deficiency of vitamin B(12) and/or folate, iron deficiency, blood loss, inflammation, malignancy, and aluminum intoxication. After other causes of anemia have been excluded, CKD is the most likely etiology, and it should be treated with an ESP. Currently, epoetin alfa and darbepoetin alfa are the only 2 ESPs approved for use in the United States. Extended dosing of ESP has potential advantages for the patient and may also improve resource utilization. Consequently, both agents have been tested for dosing at extended intervals. Adequate iron stores--defined as transferrin saturation >20% and ferritin >100 mg--as well as ESP administration are needed to produce an appropriate increase in hemoglobin. Poor response to treatment with ESP can be due to many factors, including presence of iron deficiency, inflammation, continued blood loss, and hemoglobinopathy. PMID:17098634

Agarwal, Anil K

2006-11-01

382

Equine infectious anemia and equine infectious anemia virus in 2013: a review.  

PubMed

A detailed description of equine infectious anemia virus and host responses to it are presented. Current control and eradication of the infection are discussed with suggestions for improvements to increase their effectiveness. PMID:24183747

Cook, R F; Leroux, C; Issel, C J

2013-11-29

383

Descriptive epidemiology of marine anemia in seapen-reared salmon in southern British Columbia.  

PubMed

Marine anemia, also known as plasmacytoid leukemia, is a recently described disease of farmed Pacific salmon in British Columbia. Most of what is known about the disease has been generated through laboratory studies or field investigations of severely affected farms. The goals of this study were to determine the range of the spatial and temporal distribution of naturally occurring marine anemia, identify potential risk factors, and provide an initial description of the impact of the disease on commercial salmon farms in British Columbia. Data were obtained from mail surveys, farm visits, and reviews of clinical and laboratory records. An attempt was made to evaluate negative, as well as mildly, moderately, and severely affected sites. The results showed marine anemia to be widely distributed throughout the major salmon farming regions in British Columbia. The disease was most commonly diagnosed in August and September, when water temperatures were at their seasonal peaks. A wide variety of lineage's and fish sources were associated with the disease. The average mortality rate attributed to marine anemia was 6% (range 2.5% to 11%). The peak occurrence of the disease was associated with a peak in the occurrence of other infectious and inflammatory diseases. The broad demographic distribution of marine anemia, coupled with its endemic nature, indicated that the disease is unlikely to be due to the recent introduction of a new pathogen and that causal factors are widespread in southern British Columbia. It is concluded that the significance of diagnosing marine anemia is not that it is predictive of an impending epidemic of mortality, but that it is an indicator of the general pattern of disease on a farm. PMID:8809395

Stephen, C; Ribble, C S; Kent, M L

1996-07-01

384

Anemia in patients with coronary artery disease.  

PubMed

The pathophysiology of impaired hemodynamic and nonhemodynamic responses to anemia in patients with coronary artery disease is discussed. In animals, experimentally induced coronary artery disease significantly inhibits the hemodynamic response to surgical blood loss; anecdotal evidence in humans corroborates these findings. Erythropoietic response to surgical blood loss may also be blunted in patients with coronary artery disease. Regardless of whether anemia is the result of a preexisting condition or surgical blood loss, its presence worsens outcomes in patients with coronary artery disease who undergo cardiac surgery. The combination of coronary artery disease and anemia has resulted in acute myocardial infarction as well. Finally, anemia after noncardiac surgery is associated with an increased risk of myocardial ischemia, potentially creating a cycle in which blood loss and myocardial ischemia exacerbate each other. Oral iron replacement therapy after elective cardiac surgery increases adverse events without significantly improving hematocrit and hemoglobin levels or iron stores. Allogeneic blood transfusions are less than ideal, and autologous blood transfusion with erythropoietin administration is only possible before elective procedures. New procedures and medications have reduced the blood loss associated with percutaneous coronary intervention, and minimization of blood loss during percutaneous coronary intervention has potentially major clinical and economic implications. PMID:12908376

Nappi, Jean

2003-07-15

385

Hb F in sickle cell anemia  

Microsoft Academic Search

We have reviewed the methodology for an accurate quantitation of Hb F in the blood of patients with sickle cell anemia, values observed in hundreds of patients of different (racial or ethnic) backgrounds and with differences in severity of the disease, and the various factors that affect the level of Hb F. The latter include sex, age, genetic background or

A. D. Adekile; T. H. J. Huisman

1993-01-01

386

A short review of malabsorption and anemia.  

PubMed

Anemia is a frequent finding in most diseases which cause malabsorption. The most frequent etiology is the combination of iron and vitamin B12 deficiency. Celiac disease is frequently diagnosed in patients referred for evaluation of iron deficiency anemia (IDA), being reported in 1.8%-14.6% of patients. Therefore, duodenal biopsies should be taken during endoscopy if no obvious cause of iron deficiency (ID) can be found. Cobalamin deficiency occurs frequently among elderly patients, but it is often unrecognized because the clinical manifestations are subtle; it is caused primarily by food-cobalamin malabsorption and pernicious anemia. The classic treatment of cobalamin deficiency has been parenteral administration of the vitamin. Recent data suggest that alternative routes of cobalamin administration (oral and nasal) may be useful in some cases. Anemia is a frequent complication of gastrectomy, and has been often described after bariatric surgery. It has been shown that banding procedures which maintain digestive continuity with the antrum and duodenum are associated with low rates of ID. Helicobacter pylori (H. pylori) infection may be considered as a risk factor for IDA, mainly in groups with high demands for iron, such as some children and adolescents. Further controlled trials are needed before making solid recommendations about H. pylori eradication in these cases. PMID:19787827

Fernndez-Baares, Fernando; Monzn, Helena; Forn, Montserrat

2009-10-01

387

The maternal side of Fanconi Anemia.  

PubMed

Fanconi anemia is characterized by a higher sensitivity to DNA crosslinking agents, including aldehydes. In this issue of Molecular Cell, Oberbeck etal. (2014) reveal that detoxification of aldehydes by pregnant mothers contributes to limit the severity of the disease. PMID:25238193

Ruiz, Sergio; Fernandez-Capetillo, Oscar

2014-09-18

388

ANEMIA OF DISORDERED IRON METABOLISM AND HEME  

E-print Network

Total Iron Concentration 40-50 mg Hemoglobin = 0.5 mg iron/ml blood Transferrin = Transport Protein;9/16/2013 4 IRON DEFICIENCY ANEMIA CAUSES Dietary Deficiency Blood Loss Hemodialysis Malabsorption IDA infections, chronic inflammatory disorders, or neoplastic disorders Cytokines are mediators Inhibit EPO

389

Group G Beta-Hemolytic Streptococcal Bacteremia Characterized by 16S Ribosomal RNA Gene Sequencing  

PubMed Central

Little is known about the relative importance of the four species of Lancefield group G beta-hemolytic streptococci in causing bacteremia and the factors that determine the outcome for patients with group G beta-hemolytic streptococcal bacteremia. From 1997 to 2000, 75 group G beta-hemolytic streptococcal strains were isolated from the blood cultures of 66 patients. Sequencing of the 16S rRNA genes of the group G beta-hemolytic streptococci showed that all 75 isolates were Streptococcus dysgalactiae subspecies equisimilis. The API system (20 STREP) and Vitek system (GPI) successfully identified 65 (98.5%) and 62 (93.9%) isolates, respectively, as S. dysgalactiae subspecies equisimilis with >95% confidence, whereas the ATB Expression system (ID32 STREP) only successfully identified 49 isolates (74.2%) as S. dysgalactiae subspecies equisimilis with >95% confidence. The median age of the patients was 76 years (range, 33 to 99 years). Fifty-six patients (85%) were over 60 years old. All patients had underlying diseases. No source of the bacteremia was identified (primary bacteremia) in 34 patients (52%), whereas 17 (26%) had cellulitis and 8 (12%) had bed sore or wound infections. Fifty-eight patients (88%) had community-acquired group G streptococcal bacteremia. Sixty-two patients (94%) had group G Streptococcus recovered in one blood culture, whereas 4 patients (6%) had it recovered in multiple blood cultures. Fifty-nine patients (89%) had group G Streptococcus as the only bacterium recovered in their blood cultures, whereas in 7 patients other bacteria were recovered concomitantly with the group G Streptococcus in the blood cultures (Staphylococcus aureus in 3, Clostridium perfringens in 2, Citrobacter freundii in 1, and Bacteroides fragilis in 1). Overall, 10 patients (15%) died. Male sex, diagnosis other than cellulitis, hospital-acquired bacteremia, and multiple positive blood cultures were associated with mortality {P < 0.005 (relative risk [RR] = 7.6), P < 0.05 (RR = 3.7), P < 0.005 (RR = 5.6), and P < 0.05 (RR = 5.6), respectively}. Unlike group C beta-hemolytic streptococcal bacteremia, group G beta-hemolytic streptococcal bacteremia is not a zoonotic infection in Hong Kong. PMID:11526143

Woo, Patrick C. Y.; Fung, Ami M. Y.; Lau, Susanna K. P.; Wong, Samson S. Y.; Yuen, Kwok-Yung

2001-01-01

390

CD34+ gene expression profiling of individual children with very severe aplastic anemia indicates a pathogenic role of integrin receptors and the proapoptotic death ligand TRAIL  

PubMed Central

Background Very severe aplastic anemia is characterized by a hypoplastic bone marrow due to destruction of CD34+ stem cells by autoreactive T cells. Investigation of the pathomechanism by patient-specific gene expression analysis of the attacked stem cells has previously been impractical because of the scarcity of these cells at diagnosis. Design and Methods Employing unbiased RNA amplification, patient-specific gene expression profiling was carried out for CD34+ cells from patients newly diagnosed with very severe aplastic anemia (n=13), refractory anemia (n=8) and healthy controls (n=10). These data were compared to profiles of myelodysplastic disease (n=55), including refractory anemia (n=18). To identify possible targets of autoimmune attack, presence of autoreactive antibodies was tested in pre-therapeutic sera of patients with very severe aplastic anemia (n=19). Results CD34+ gene expression profiling distinguished between healthy controls, children with aplastic or refractory anemia and clonal disease. Interferon stimulated genes such as the apoptosis inducing death ligand TRAIL were strongly up-regulated in CD34+ cells of patients with aplastic anemia, in particular in patients responding to immunosuppressive treatment. In contrast, mRNA expression of integrin GPVI and the integrin complexes GPIa/IIa, GPIIb/IIIa, GPIB/GPIX/GPV was significantly down-regulated and corresponding antibodies were detected in 7 of 11 profiled patients and in 11 of 19 aplastic anemia patients. Conclusions As a potential diagnostic tool, patient-specific gene expression profiling of CD34+ stem cells made it possible to make the difficult differential diagnosis of most patients with aplastic and refractory anemia. Profiling indicated a prognostic correlation of TRAIL expression and patient benefit from immunosuppressive therapy. Downregulation of integrin expression and concurrent presence of autoreactive anti-integrin-antibodies suggested a previously unrecognized pathological role of integrins in aplastic anemia. PMID:22315490

Fischer, Ute; Ruckert, Christian; Hubner, Bernd; Eckermann, Olaf; Binder, Vera; Bakchoul, Tamam; Schuster, Friedhelm R.; Merk, Sylvia; Klein, Hans-Ulrich; Fuhrer, Monika; Dugas, Martin; Borkhardt, Arndt

2012-01-01

391

Investigating the effect of increasing charge density on the hemolytic activity of synthetic antimicrobial polymers.  

PubMed

The current study is aimed at investigating the effect of fine-tuning the cationic character of synthetic mimics of antimicrobial peptides (SMAMPs) on the hemolytic and antibacterial activities. A series of novel norbornene monomers that carry one, two, or three Boc-protected amine functionalities was prepared. Ring-opening metathesis polymerization (ROMP) of the monomers, followed by deprotection of the amine groups resulted in cationic antimicrobial polynorbornenes that carry one, two, and three charges per monomer repeat unit. Increasing the number of amine groups on the most hydrophobic polymer reduced its hemolytic activity significantly. To understand the membrane activity of these polymers, we conducted dye leakage experiments on lipid vesicles that mimic bacteria and red blood cell membranes, and these results showed a strong correlation with the hemolysis data. PMID:18816096

Al-Badri, Zoha M; Som, Abhigyan; Lyon, Sarah; Nelson, Christopher F; Nsslein, Klaus; Tew, Gregory N

2008-10-01

392

Synthesis of new sugar-based surfactants and evaluation of their hemolytic activities.  

PubMed

The synthesis of four sugar-based surfactants derived from glucose and (R)-12-hydroxystearic acid is described. The surfactants have a hydroxy group in the hydrophobic part, which is either free or acylated using acetyl chloride, hexanoyl chloride, or myristoyl chloride. Three of the synthesized surfactants are water-soluble and are evaluated with respect to their CMCs and hemolytic activities. The fourth surfactant has limited water solubility and is not further included in the study. The investigated surfactants are all hemolytic close to their respective CMC indicating that their use in parenteral formulations may be limited. Nevertheless, surfactants having the proposed structure appear as promising alternatives to existing solubilizing agents for pharmaceutical applications. PMID:16626152

Neimert-Andersson, Kristina; Sauer, Sven; Panknin, Olaf; Borg, Tessie; Sderlind, Erik; Somfai, Peter

2006-04-28

393

Severe Malarial Anemia: Innate Immunity and Pathogenesis  

PubMed Central

Greater than 80% of malaria-related mortality occurs in sub-Saharan Africa due to infections with Plasmodium falciparum. The majority of P. falciparum-related mortality occurs in immune-nave infants and young children, accounting for 18% of all deaths before five years of age. Clinical manifestations of severe falciparum malaria vary according to transmission intensity and typically present as one or more life-threatening complications, including: hyperparasitemia; hypoglycemia; cerebral malaria; severe malarial anemia (SMA); and respiratory distress. In holoendemic transmission areas, SMA is the primary clinical manifestation of severe childhood malaria, with cerebral malaria occurring only in rare cases. Mortality rates from SMA can exceed 30% in pediatric populations residing in holoendemic transmission areas. Since the vast majority of the morbidity and mortality occurs in immune-nave African children less than five years of age, with SMA as the primary manifestation of severe disease, this review will focus primarily on the innate immune mechanisms that govern malaria pathogenesis in this group of individuals. The pathophysiological processes that contribute to SMA involve direct and indirect destruction of parasitized and non-parasitized red blood cells (RBCs), inefficient and/or suppression of erythropoiesis, and dyserythropoiesis. While all of these causal etiologies may contribute to reduced hemoglobin (Hb) concentrations in malaria-infected individuals, data from our laboratory and others suggest that SMA in immune-nave children is characterized by a reduced erythropoietic response. One important cause of impaired erythroid responses in children with SMA is dysregulation in the innate immune response. Phagocytosis of malarial pigment hemozoin (Hz) by monocytes, macrophages, and neutrophils is a central factor for promoting dysregulation in innate inflammatory mediators. As such, the role of P. falciparum-derived Hz (PfHz) in mediating suppression of erythropoiesis through its ability to cause dysregulation in pro- and anti-inflammatory cytokines, growth factors, chemokines, and effector molecules is discussed in detail. An improved understanding of the etiological basis of suppression of erythropoietic responses in children with SMA may offer the much needed therapeutic alternatives for control of this global disease burden. PMID:22110393

Perkins, Douglas J.; Were, Tom; Davenport, Gregory C.; Kempaiah, Prakasha; Hittner, James B.; Ong'echa, John Michael

2011-01-01

394

D-penicillamine therapy in AB0 hemolytic disease of the newborn infant  

Microsoft Academic Search

This study comprises 120 full-term infants with AB0 hemolytic disease admitted to the neonatal department during a period of 60 months from 1970 to 1975. During the first 30 months newborns (n=61) received no D-penicillamine therapy, whereas all infants (n=59) received this treatment (300400 mg\\/kg\\/day, divided into 4 equal doses, for 25 days) during the last 30 months. The patients

L. Lakatos; B. Kvr; Gy. Oroszln; Zsuzsa Vekerdy

1976-01-01

395

Paternal leukocyte alloimmunization as a treatment for hemolytic disease of the newborn in a rabbit model  

Microsoft Academic Search

Objective: The purpose of this study was to evaluate maternal alloimmunization to paternal leukocytes as a treatment for hemolytic disease of the fetus\\/newborn in a rabbit model. Study Design: Twelve does and paired red blood cell-incompatible bucks underwent the experimental protocol. Fetal hematologic parameters that were obtained by ultrasound-guided intracardiac sampling were compared from unaffected, compatible litters; from affected, incompatible

Paul W. Whitecar; Rod Farb; Lalitha Subramanyam; Karen Dorman; Rukmini B. Balu; Kenneth J. Moise Jr

2002-01-01

396

Hemolytic-Uremic Syndrome Following Bone Marrow Transplantation in Adults for Hematologic Malignancies  

Microsoft Academic Search

One hundred and sixty eight adult patients with B-cell non-Hodgkin's lymphoma (NHL) and other hematologic ma- lignancies who underwent autologous or allogeneic bone marrow transplantation (BMT) were investigated for the subsequent development of hemolytic-uremic syndrome (HUS). All patients were conditioned with cyclophosphamide and total body irradiation. When examined at 3-month intervals for the first year post-BMT, all patients had uniform

Susan N. Rabinowe; Robert J. Soiffer; Nancy J. Tarbell; Donna Neuberg; Arnold S. Freedman; Julian Seifter; Kelly W. Blake; John G. Gribben; Kenneth C. Anderson; Tak Takvorian; Jerome Ritz; Lee M. Nadler

1991-01-01

397

Complete Genome Assembly of Streptococcus pyogenes ATCC 19615, a Group A ?-Hemolytic Reference Strain  

PubMed Central

We present the complete genome assembly of Streptococcus pyogenes ATCC 19615 (Rosenbach) as submitted to GenBank under accession number CP008926. This group A nonmotile ?-hemolytic clinical isolate is used for quality control in a variety of commercially available tests. The assembled genome is 1.84Mb (38.5% G+C content) and contains 1,788 coding regions. PMID:25258274

Minogue, T. D.; Daligault, H. A.; Davenport, K. W.; Bishop-Lilly, K. A.; Broomall, S. M.; Bruce, D. C.; Chain, P. S.; Chertkov, O.; Coyne, S. R.; Freitas, T.; Frey, K. G.; Gibbons, H. S.; Jaissle, J.; Redden, C. L.; Rosenzweig, C. N.; Xu, Y.

2014-01-01

398

Complete Genome Assembly of Streptococcus pyogenes ATCC 19615, a Group A ?-Hemolytic Reference Strain.  

PubMed

We present the complete genome assembly of Streptococcus pyogenes ATCC 19615 (Rosenbach) as submitted to GenBank under accession number CP008926. This group A nonmotile ?-hemolytic clinical isolate is used for quality control in a variety of commercially available tests. The assembled genome is 1.84Mb (38.5% G+C content) and contains 1,788 coding regions. PMID:25258274

Minogue, T D; Daligault, H A; Davenport, K W; Bishop-Lilly, K A; Broomall, S M; Bruce, D C; Chain, P S; Chertkov, O; Coyne, S R; Freitas, T; Frey, K G; Gibbons, H S; Jaissle, J; Redden, C L; Rosenzweig, C N; Xu, Y; Johnson, S L

2014-01-01

399

Anti-Factor H Autoantibodies Associated with Atypical Hemolytic Uremic Syndrome  

Microsoft Academic Search

Several studies have demonstrated genetic predisposition in non-shigatoxin-associated hemolytic uremic syndrome (HUS), involving regulatory proteins of the complement alternative pathway: Factor H (FH) and membrane co-factor protein (CD46). Regarding the observations of thrombotic thrombocytopenic purpura patients, in whom a von Willebrand factor protease (ADAMST-13) deficiency may be inherited or acquired secondary to IgG antibodies, it was speculated that HUS might

Marie-Agnes Dragon-Durey; Chantal Loirat; Sylvie Cloarec; Marie-Alice Macher; Jacques Blouin; Hubert Nivet; Laurence Weiss; Wolf Herman Fridman; Veronique Fremeaux-Bacchi

2005-01-01

400

Multiple cavitations in posterior reversible leukoencephalopathy syndrome associated with hemolytic-uremic syndrome  

Microsoft Academic Search

We describe a 4-year-old boy with posterior reversible leukoencephalopathy syndrome associated with hemolytic-uremic syndrome. He exhibited bloody stool by Escherichia coli O157: H7 infection with acute renal failure. He subsequently presented high blood pressure, followed by visual disturbance and loss of consciousness. Brain MRI revealed bilateral occipital high intensities by T2-weighted images and high value by apparent diffusion coefficient map,

Katsunori Fujii; Kaoru Matsuo; Tomozumi Takatani; Hideki Uchikawa; Yoichi Kohno

401

Bacteremia caused by hemolytic, high-level gentamicin-resistant Enterococcus faecalis.  

PubMed Central

Between 1 January 1984 and 31 December 1987, 206 enterococcal blood isolates at the University of Wisconsin Hospital and Clinics were analyzed for high-level aminoglycoside resistance (hereafter high-level aminoglycoside resistance is simply referred to as "resistance") and hemolysin production. Of 190 Enterococcus faecalis isolates, 68 (35.8%) were resistant to gentamicin. Of these 68 strains, 67 (98.5%) contained a gene coding for the bifunctional aminoglycoside-modifying 6'-aminoglycoside acetyltransferase-2"-aminoglycoside phosphotransferase [AAC(6')-APH(2")] enzyme. Of 190 isolates, 85 (44.7%) were hemolytic and contained a gene coding for component A of the enterococcal hemolysin. Sixty-two of 68 (91.2%) gentamicin-resistant isolates but only 23 of 122 (18.8%) gentamicin-susceptible isolates were hemolytic (P less than 0.001). Twelve of the hemolytic, gentamicin-resistant E. faecalis blood isolates, but only 2 of 9 nonhemolytic or gentamicin-susceptible isolates, had identical chromosomal DNA restriction endonuclease digestion patterns, suggesting a common derivation for these strains. A historical cohort study from 1 July 1985 to 31 March 1987 identified by regression analysis postsurgical intensive care unit status (odds ratio [OR], 5.0; 95% confidence interval [CI], 1.1 to 22.8) and prior treatment with an expanded- or broad-spectrum cephalosporin (OR, 3.0; 95% CI, 0.9 to 10.1) as risk factors for gentamicin-resistant E. faecalis bacteremia. Patients with hemolytic, gentamicin-resistant E. faecalis bacteremia had a fivefold-increased risk for death within 3 weeks of their bacteremia compared with patients with nonhemolytic, gentamicin-susceptible strains (95% CI, 1.0 to 25.4). Images PMID:1929336

Huycke, M M; Spiegel, C A; Gilmore, M S

1991-01-01

402

Increased carriage of resistant non-pneumococcal ?-hemolytic streptococci after antibiotic therapy  

Microsoft Academic Search

Objective: We compared colonization and resistance rates of non-pneumococcal ?-hemolytic streptococci (AHS) and Streptococcus pneumoniae in children receiving antibiotic therapy for acute otitis media. Study design: Between December 1997 and September 1998, children 6 months to 6 years of age, diagnosed with acute otitis media were randomly assigned to receive amoxicillin\\/clavulanate (Augmentin) 45 mg\\/kg\\/d in 2 divided doses for 10

Faryal Ghaffar; Ian R. Friedland; Kathy Katz; Luz Stella Muniz; Jeanette L. Smith; Phyllis Davis; Jason Reynolds; George H. McCracken

1999-01-01

403

Plasmapheresis in a very young infant with atypical hemolytic uremic syndrome  

Microsoft Academic Search

Atypical hemolytic uremic syndrome (HUS) is a heterogeneous group of disorders, the pathogenesis of which is unclear. Plasma\\u000a transfusions and plasmapheresis are widely used modes of therapy for adults with this life-threatening syndrome. There is\\u000a very limited experience in using plasmapheresis therapy in children and infants with atypical HUS. Plasmapheresis, which is\\u000a considered a relatively safe procedure in adults and

Daniella Magen; Ana Oliven; Yael Shechter; Ronit Elhasid; Gad Bar-Joseph; Israel Zelikovic

2001-01-01

404

Pore formation, polymerization, hemolytic and leukotoxic effects of a new Enterobacter cloacae toxin neutralized by antiserum.  

PubMed

A new toxin of Enterobacter cloacae was purified and studied by SDS-PAGE electrophoresis with the purpose of investigating its ability to generate polymers and their molecular mass. Monomer of 13.3 kDa and structures of multimeric mass were detected. The toxin of 66 kDa was the most abundant form of toxin. This polymer and the monomer were selected to examine blood cells damage. Membrane pores caused by both toxin forms seemed to be of similar dimension (estimated in 3.6 nm by experiments with osmotic protectors) and were able to lyse erythrocytes and leukocytes. The results obtained indicate that polymerization and pore formation are involved in the molecular events that participate in the cytotoxic effects of E. cloacae toxin. Immunization of rabbits with 13.3kDa toxin generated antibody response capable of inhibiting oxidative stress as well as hemolytic and leukotoxic effects. Immunoblotting indicated that monomer and polymer reacted with antihemolysin serum. The importance of E. cloacae toxin "in vivo" was studied in animals by means of assays performed in peritoneum of rats, inoculated with the hemolytic strain (C1) and a non-hemolytic variant (C4). Both strains stimulated infiltration of leukocytes in peritoneum, but C1 caused cell death and lysis wheras assays with C4 maintained the viability of leukocytes even within 5 h after extraction of samples. PMID:15881838

Paraje, Mara Gabriela; Eraso, Alberto Jorge; Albesa, Ins

2005-01-01

405

The in vitro hemolytic effect of diltiazem on erythrocytes exposed to varying osmolarity.  

PubMed

The hemolytic effect of diltiazem (a calcium channel blocker) on red blood cells (RBCs) exposed to varying osmolarity was investigated. Previous work on the in vitro hemolytic effect of verapamil shed some light on the potential for some drugs to induce hemolysis at moderate-to-high doses and in pre-existing osmotic stress. The current experimental approach used a modified red cell hemolysis assay with concentrations of diltiazem ranging from 50-1500 ?M compared to drug free controls. The time-course of hemolytic effects was also investigated. In conditions representing decreasing osmolarity (dilution from 140 to 0 mM NaCl) there was a significant increase in erythrocyte hemolysis that was also dependent on diltiazem concentration (ANOVA, p<0.05). The red cells also showed a significantly increased rate of hemolysis over 5 h with increasing concentration of diltiazem (ANOVA, p<0.05). Overall the data suggested that diltiazem can cause hemolysis of RBCs in a predictable time- and concentration-dependent manner, and that diltiazem increases the fragility of the erythrocytes further during hypotonic osmotic stress. The mechanism of diltiazem-dependent hemolysis could involve various ion transport pathways (i.e. Ca pump, Ca Channels) and subsequent effects on cell volume control or membrane fragility. PMID:20486888

Watts, T J

2010-10-01

406

Anemia after bariatric surgery: more than just iron deficiency.  

PubMed

Bariatric surgery for morbid obesity is rapidly gaining popularity. Restrictive and/or malabsorptive surgical interventions result in dramatic weight loss with significantly decreased obesity-related morbidity and mortality. Anemia, which may affect as many as two-thirds of these patients, is of concern and generally thought to be caused by iron deficiency. Although iron deficiency in this population may be frequent given pouch hypoacidity, defunctionalized small bowel, and red meat intolerance, it may not account for all anemias seen. First, there is increasing evidence that obesity creates a state of chronic inflammation. Both iron deficiency anemia and anemia of chronic inflammation present with low serum iron levels. Most studies reporting anemia after bariatric surgery lack serum ferritin determinations so that the relative contribution of inflammation to anemia cannot be assessed. Second, a significant number of anemias after bariatric surgery remain unexplained and may be attributable to less frequently seen micronutrient deficiencies such as copper, fatsoluble vitamins A and E, or an imbalance in zinc intake. Third, although deficiencies of folate and vitamin B(12) are infrequent, study observation periods may be too short to detect anemia attributable to vitamin B(12) deficiency because vitamin B(12) storage depletion takes many years. This review is intended to increase awareness of the mechanisms of anemia above and beyond iron deficiency in the bariatric patient and provide healthcare providers with tools for a more thoughtful approach to anemia in this patient population. PMID:19321896

von Drygalski, Annette; Andris, Deborah A

2009-01-01

407

Cost-effectiveness of Anemia Screening in Vulnerable Groups: A Systematic Review  

PubMed Central

Background: Anemia is the most common blood disorder observed in vulnerable groups and affects their efficiency in their everyday activities. Possible complications of the disease may be reduced or prevented by screening of patients. Screening programs impose certain costs upon the health system, which may offset their positive effects. Whether the positive impacts of screening outweigh its costs is a subject of debate among policy-makers. In this research, we have conducted a systematic review of the cost-effectiveness of anemia screening. Methods: The Pubmed, Science Direct, SCOPUS, EMBASE, and CINAHL databases were searched for relevant results dating between 1962-2010 using key words. The references of the related articles were gone over manually. In the end, Persian databases were also examined for results. Results: Using data from the four mentioned databases, a total of 722 articles were elected, which, after evaluation, were narrowed down to 4. Of these, 3 focused on newborns and infants. Disparity existed among obtained results, such that no two articles were similar, and this made making comparisons between them cumbersome and sometimes even impossible. Only one study evaluated cost-effectiveness of anemia screening in vulnerable target groups. Conclusions: Research findings show that there is not enough evidence of cost-effectiveness of screening for decision-making. Bearing in mind the importance of the matter to health policy-makers, due to high prevalence of iron-deficiency anemia in low- and middle-income countries, conduction of research in this field seems necessary. PMID:25104991

Nosratnejad, Shirin; Barfar, Eshagh; Hosseini, Hamed; Barooti, Esmat; Rashidian, Arash

2014-01-01

408

Aplastic anemia: immunosuppressive therapy in 2010  

PubMed Central

Acquired aplastic anemia (AA) is the typical bone marrow failure syndrome characterized by an empty bone marrow; an immune-mediated pathophysiology has been demonstrated by experimental works as well as by clinical observations. Immunusuppressive therapy (IST) is a key treatment strategy for aplastic anemia; since 20 years the standard IST for AA patients has been anti-thymocyte globuline (ATG) plus cyclosporine A (CyA), which results in response rates ranging between 50% and 70%, and even higher overall survival. However, primary and secondary failures after IST remain frequent, and to date all attempts aiming to overcome this problem have been unfruitful. Here we review the state of the art of IST for AA in 2010, focusing on possible strategies to improve current treatments. We also discuss very recent data which question the equality of different ATG preparations, leading to a possible reconsideration of the current standards of care for AA patients. PMID:22053283

Risitano, Antonio M.; Perna, Fabiana

2011-01-01

409

Exacerbation of microcytic anemia associated with cessation of anti-retroviral therapy in an HIV-1-infected patient with beta thalassemia.  

PubMed

We report a patient with Japanese minor ? thalassemia and HIV-1 infection. The patient showed prolonged anemia, which was originally attributed to chronic parvovirus B19 infection. Twelve years later, the patient presented with exacerbation of microcytic anemia following cessation of anti-retroviral therapy; the exacerbation resolved when anti-retroviral therapy was resumed. Sequencing of the ? globin gene revealed heterozygosity for a four-nucleotides deletion at codon 41/42 and minor ? thalassemia was confirmed. Because HIV-1-infected patients frequently show anemia due to nutritional deficiencies, opportunistic infections, AIDS-related malignancies, drug treatment and a direct effect of HIV-1 on the bone marrow, it is likely to overlook other causes of anemia. Thalassemia should be considered in the differential diagnosis of anemia even in HIV-1 infected patients, when microcytic anemia without iron deficiency is observed. Our case suggested that active HIV infection may have worsened ? thalassemia, and early introduction of anti-retroviral therapy is beneficial for the recovery of anemia. PMID:24613601

Furukawa, Yoshitaka; Hashiguchi, Teruto; Minami, Rumi; Yamamoto, Masahiro; Takashima, Hiroshi

2014-06-01

410

[Aplastic anemia after acute viral hepatitis].  

PubMed

The authors describe 4 patients with grave aplastic anemia that developed after acute virus hepatitis. In two cases aplasia occurred at the icteric period of hepatitis, in one during convalescence, and in one 5 months after the recovery from hepatitis. The counter electrophoresis technique failed to reveal the Australian antigen in all the 4 cases. Ninety per cent of patients out of over 200 reported cases of aplastic anemia that developed after acute virus hepatitis died. Of the 4 cases followed up by the authors, 3 patients died. One of the female patients was subjected to splenectomy 3 weeks after the occurrence of grave aplasia with fatty bone marrow with a purpose of immunodepression. Splenectomy entailed a considerable decrease in hemorrhagic diathesis. Later on the patient was treated with caprine antilymphocytic globulin. At present the patient is in a state of remission. The problems of the pathogenesis of aplastic anemia following acute virus hepatitis and potentialities of the disease treatment are under discussion. PMID:4049269

Idel'son, L I; Guse?nova, L A; Pogorel'skaia, E P; Aprosina, Z G; Novokreshchennykh, I I

1985-01-01

411

Anemia in heart failure: an overview of current concepts.  

PubMed

Chronic heart failure is a substantial public health problem. Anemia is an important comorbidity frequently observed in patients with the disease and, in heart failure, anemia has only recently started to attract systematic epidemiological and therapeutical research endeavor. This article describes the many aspects of anemia in chronic heart failure, starting with the ongoing discussion of how to define anemia, which has important consequences for the estimation of its prevalence and incidence. Further, we discuss prognostic implications of anemia in patients with chronic or acute heart failure, the etiology of anemia in heart failure and treatment possibilities. Such therapeutic avenues embrace intravenous iron preparations and subcutaneous administration of erythropoietin and its derivatives, all of which have been extensively studied over the last several years. Finally, this article describes the potential costs incurred by treating anemic patients with heart failure. PMID:21174515

von Haehling, Stephan; Jankowska, Ewa A; Ponikowski, Piotr; Anker, Stefan D

2011-01-01

412

Diamond-Blackfan anemia: genotype-phenotype correlations in Italian patients with RPL5 and RPL11 mutations  

PubMed Central

Background Diamond-Blackfan anemia is a rare, pure red blood cell aplasia of childhood due to an intrinsic defect in erythropoietic progenitors. About 40% of patients display various malformations. Anemia is corrected by steroid treatment in more than 50% of cases; non-responders need chronic transfusions or stem cell transplantation. Defects in the RPS19 gene, encoding the ribosomal protein S19, are the main known cause of Diamond-Blackfan anemia and account for more than 25% of cases. Mutations in RPS24, RPS17, and RPL35A described in a minority of patients show that Diamond-Blackfan anemia is a disorder of ribosome biogenesis. Two new genes (RPL5, RPL11), encoding for ribosomal proteins of the large subunit, have been reported to be involved in a considerable percentage of patients. Design and Methods In this genotype-phenotype analysis we screened the coding sequence and intron-exon boundaries of RPS14, RPS16, RPS24, RPL5, RPL11, and RPL35A in 92 Italian patients with Diamond-Blackfan anemia who were negative for RPS19 mutations. Results About 20% of the patients screened had mutations in RPL5 or RPL11, and only 1.6% in RPS24. All but three mutations that we report here are new mutations. No mutations were found in RPS14, RPS16, or RPL35A. Remarkably, we observed a higher percentage of somatic malformations in patients with RPL5 and RPL11 mutations. A close association was evident between RPL5 mutations and craniofacial malformations, and between hand malformations and RPL11 mutations. Conclusions Mutations in four ribosomal proteins account for around 50% of all cases of Diamond-Blackfan anemia in Italian patients. Genotype-phenotype data suggest that mutation screening should begin with RPL5 and RPL11 in patients with Diamond-Blackfan anemia with malformations. PMID:19773262

Quarello, Paola; Garelli, Emanuela; Carando, Adriana; Brusco, Alfredo; Calabrese, Roberto; Dufour, Carlo; Longoni, Daniela; Misuraca, Aldo; Vinti, Luciana; Aspesi, Anna; Biondini, Laura; Loreni, Fabrizio; Dianzani, Irma; Ramenghi, Ugo

2010-01-01

413

21 CFR 862.1365 - Glutathione test system.  

Code of Federal Regulations, 2010 CFR

...Glutathione measurements are used in the diagnosis and treatment of certain drug-induced hemolytic (erythrocyte destroying) anemias due to an inherited enzyme deficiency. (b) Classification. Class I (general controls). The device is exempt...

2010-04-01

414

Pharmacodynamic model for chemotherapy-induced anemia in rats  

Microsoft Academic Search

Anticancer agents often cause bone marrow toxicity resulting in progressive anemia which may influence the therapeutic effects\\u000a of erythropoietic-stimulating agents. The objective of this study was to develop a pharmacodynamic (PD) model to describe\\u000a chemotherapy-induced anemia in rats. Anemia was induced in male Wistar rats with a single intravenous (i.v.) injection of\\u000a 60mg\\/kg carboplatin. Hematological responses including reticulocytes, red blood

Sukyung Woo; Wojciech Krzyzanski; William J. Jusko

2008-01-01

415

Iron deficiency anemia--bridging the knowledge and practice gap.  

PubMed

Despite its high prevalence, anemia often does not receive proper clinical attention, and detection, evaluation, and management of iron deficiency anemia and iron-restricted erythropoiesis can possibly be an unmet medical need. A multidisciplinary panel of clinicians with expertise in anemia management convened and reviewed recent published data on prevalence, etiology, and health implications of anemia as well as current therapeutic options and available guidelines on management of anemia across various patient populations and made recommendations on the detection, diagnostic approach, and management of anemia. The available evidence confirms that the prevalence of anemia is high across all populations, especially in hospitalized patients. Anemia is associated with worse clinical outcomes including longer length of hospital stay, diminished quality of life, and increased risk of morbidity and mortality, and it is a modifiable risk factor of allogeneic blood transfusion with its own inherent risks. Iron deficiency is usually present in anemic patients. An algorithm for detection and management of anemia was discussed, which incorporated iron study (with primary emphasis on transferrin saturation), serum creatinine and glomerular filtration rate, and vitamin B12 and folic acid measurements. Management strategies included iron therapy (oral or intravenous), erythropoiesis-stimulating agents, and referral as needed. PMID:24931617

Shander, Aryeh; Goodnough, Lawrence T; Javidroozi, Mazyar; Auerbach, Michael; Carson, Jeffrey; Ershler, William B; Ghiglione, Mary; Glaspy, John; Lew, Indu

2014-07-01

416

21 CFR 250.201 - Preparations for the treatment of pernicious anemia.  

Code of Federal Regulations, 2010 CFR

...Preparations for the treatment of pernicious anemia. 250.201 Section 250.201 Food...Preparations for the treatment of pernicious anemia. (a) The ninth announcement of the Anti-anemia Preparations Advisory Board of the...

2010-04-01

417

[Successful use of "juzen-taiho-to", a kampo medicine, for the treatment of perioperative anemia and hypoalbuminemia].  

PubMed

An 88-year-old woman suffering from femoral neck fracture was transported to the emergency room of a hospital. The patient and her family refused transfusion, despite anemia, stating their affiliation with Jehova's Witnesses. Surgery was performed under general anesthesia, and the following day, anemia (hemoglobin, 7.5 g x dl(-1)) and hypoalbuminemia (albumin, 2.7 g x dl(-1)) were observed, in addition to anorexia and general fatigue. The patient underwent nutritional treatment with a kampo medicine (Juzen-taiho-to), which was administered as a medication due to difficulties with swallowing the powdered form. On the 18th day after admission, anemia (hemoglobin, 8.9 g x dl(-1)) and hypoalbuminemia (3.6 g x dl(-1)) improved, as did anorexia and general fatigue. It is thought that the components Shimotsu-to, a component known to improve anemia, and Shikunshi-to, a vital energy supplementing component, were the main ingredients that conferred the improvements in anemia and hypoalbuminemia. These findings suggest that Chinese herbal medicine for the nutritional treatment of the elderly has minimal side effects. PMID:25199335

Tanaka, Tomohiro; Komasawa, Nobuyasu; Kataiwa, Maiko; Hashimoto, Tsutomu; Ohue, Mutsumi; Minami, Toshiaki

2014-08-01

418

Neonatal hyperbilirubinemia due to ABO incompatibility: does blood group matter?  

PubMed

Newborn infants with maternal-fetal ABO incompatibility are at a greater risk for developing subsequent significant hyperbilirubinemia, and therefore, prediction of probable risk factors, such as the degree of hemolysis, gains importance. In this study, we aimed to evaluate the effect of fetal-neonatal blood group on the severity of hemolysis and jaundice due to maternal-fetal ABO incompatibility. In a retrospective analysis of 166 cases with ABO hemolytic disease of the newborn, risk factors for the severity of jaundice were compared in infants with blood group A or B. Both groups had similar demographic parameters such as birth weight, gender and day of admission. Similarly, there were no statistically significant differences in hematological parameters, such as initial hemoglobin levels, initial and final indirect bilirubin levels, frequency of positive direct Coombs test and hemolytic findings on peripheral blood smear, duration of phototherapy, number of exchange transfusions, and intravenous immunoglobulin (IVIG) therapy (p>0.05). We conclude that blood type has no effect on the severity of the hemolytic jaundice in ABO incompatibility. PMID:24382531

Akgl, Sinem; Korkmaz, Ay?e; Yi?it, Sule; Yurdakk, Murat

2013-01-01

419

Iron, anemia and hepcidin in malaria  

PubMed Central

Malaria and iron have a complex but important relationship. Plasmodium proliferation requires iron, both during the clinically silent liver stage of growth and in the disease-associated phase of erythrocyte infection. Precisely how the protozoan acquires its iron from its mammalian host remains unclear, but iron chelators can inhibit pathogen growth in vitro and in animal models. In humans, iron deficiency appears to protect against severe malaria, while iron supplementation increases risks of infection and disease. Malaria itself causes profound disturbances in physiological iron distribution and utilization, through mechanisms that include hemolysis, release of heme, dyserythropoiesis, anemia, deposition of iron in macrophages, and inhibition of dietary iron absorption. These effects have significant consequences. Malarial anemia is a major global health problem, especially in children, that remains incompletely understood and is not straightforward to treat. Furthermore, the changes in iron metabolism during a malaria infection may modulate susceptibility to co-infections. The release of heme and accumulation of iron in granulocytes may explain increased vulnerability to non-typhoidal Salmonella during malaria. The redistribution of iron away from hepatocytes and into macrophages may confer host resistance to superinfection, whereby blood-stage parasitemia prevents the development of a second liver-stage Plasmodium infection in the same organism. Key to understanding the pathophysiology of iron metabolism in malaria is the activity of the iron regulatory hormone hepcidin. Hepcidin is upregulated during blood-stage parasitemia and likely mediates much of the iron redistribution that accompanies disease. Understanding the regulation and role of hepcidin may offer new opportunities to combat malaria and formulate better approaches to treat anemia in the developing world. PMID:24910614

Spottiswoode, Natasha; Duffy, Patrick E.; Drakesmith, Hal

2014-01-01

420

Diagnosis and management of iron deficiency anemia.  

PubMed

Iron deficiency anemia (IDA) is a common hematologic condition, affecting a substantial proportion of the world's women and young children. Optimal management of IDA requires an accurate diagnosis, identification and correction of the underlying cause, provision of medicinal iron therapy, and confirmation of treatment success. There are limited data to support current treatment approaches regarding oral iron preparation, dosing, monitoring, and duration of therapy. New intravenous iron agents have improved safety profiles, which may foster their increased utilization in the treatment of patients with IDA. Clinical trials focused on improving current treatment standards for IDA are sorely needed. PMID:25064710

Powers, Jacquelyn M; Buchanan, George R

2014-08-01

421

Aplastic Anemia in Adolescents and Young Adults  

PubMed Central

Adolescent and young adult patient presentations of aplastic anemia require a particular perspective on both diagnosis and treatment. This unique age group necessitates a thorough diagnostic evaluation to ensure the etiology, acquired or inherited, is sufficiently determined. The treatment options include human leukocyte antigen-identical sibling hematopoietic cell transplantation or immunosuppressive therapy, and both require attention to the specific medical and social needs of these adolescents and young adults. Longitudinal surveillance throughout life for the development of late complications of the disease and treatment is mandatory. PMID:25228559

DeZern, Amy E.; Guinan, Eva C.

2014-01-01

422

Microradiographic Study of Odontologic Tissues in Cooley's Anemia  

Microsoft Academic Search

SYNOPSIS IN INTERLINGUA STUDIO MICRORADIOGRAPHIC DE Tissu ODONTOLOGIC IN ANEMIA DE COOLEY.Le presente studio esseva effectuate pro determinar le effectos de anemia de Cooley super le configuration del mineralisation e le morphologia del dentes e de lor structuras de supporto. Sectiones mollite esseva obtenite ab specimens includitein bioplastico. Examines microradiographic revelava que le dentina esseva mal mineralisate e que inusual

Narendar N. Soni; Frank E. Barbee; Angella D. Ferguson; Barbara A. Parrish

1966-01-01

423

Etiology of Strokes in Children with Sickle Cell Anemia  

ERIC Educational Resources Information Center

The most devastating complication of sickle cell anemia is cerebral infarction, affecting [approximately]30% of all individuals with sickle cell anemia. Despite being one of the most common causes of stroke in infants and children, the mechanism of cerebral infarction in this population has not been extensively studied and is poorly understood.

DeBaun, Michael R.; Derdeyn, Colin P.; McKinstry, Robert C., III

2006-01-01

424

Screening for Anemia in Children: AAP RecommendationsA Critique  

Microsoft Academic Search

The American Academy of Pediatrics (AAP) recommends screening for anemia between the ages of 9 to 12 months with additional screening between the ages of 1 and 5 years for patients at risk. The screen- ing may be universal or selective depending on the prev- alence of iron deficiency anemia in the population. Im- proved infant rearing practicesincluding wider availability,

Mudra Kohli-Kumar

2001-01-01

425

Spectrum of anemia associated with chronic liver disease  

PubMed Central

Anemia of diverse etiology is a common complication of chronic liver diseases. The causes of anemia include acute or chronic gastrointestinal hemorrhage, and hypersplenism secondary to portal hypertension. Severe hepatocellular disease predisposes to hemorrhage because of impaired blood coagulation caused by deficiency of blood coagulation factors synthesized by hepatocytes, and/or thrombocytopenia. Aplastic anemia, which is characterized by pancytopenia and hypocellular bone marrow, may follow the development of hepatitis. Its presentation includes progressive anemia and hemorrhagic manifestations. Hematological complications of combination therapy for chronic viral hepatitis include clinically significant anemia, secondary to treatment with ribavirin and/or interferon. Ribavirin-induced hemolysis can be reversed by reducing the dose of the drug or discontinuing it altogether. Interferons may contribute to anemia by inducing bone marrow suppression. Alcohol ingestion is implicated in the pathogenesis of chronic liver disease and may contribute to associated anemia. In patients with chronic liver disease, anemia may be exacerbated by deficiency of folic acid and/or vitamin B12 that can occur secondary to inadequate dietary intake or malabsorption. PMID:19787828

Gonzalez-Casas, Rosario; Jones, E Anthony; Moreno-Otero, Ricardo

2009-01-01

426

Spontaneous Resolution of Severe Aplastic Anemia following Thymic Hemorrhage  

Microsoft Academic Search

Over the last 7 years we have seen more than 200 severe aplastic anemia patients at this centre. Three of them developed an unusual complication in the form of thymic hemorrhage. Following this complication, all 3 patients recovered partially from their aplastic anemia, without any need for further immunosuppression. These cases show possible ways to manipulate the thymus gland as

Kanjaksha Ghosh; Manisha Madkaikar; Farah Jijina

2008-01-01

427

Acute psychosis: a presentation of cyanocobalamin deficiency megaloblastic anemia.  

PubMed

Cyanocobalamin deficiency is not rare in India. Patients present with megaloblastic anemia, pancytopenia and sometimes neuropsychiatric manifestations. Subacute combined degeneration of the cord, peripheral neuropathy, dementia, psychotic depression and paranoid schizophrenia are well reported. We are reporting a case of cyanocobalamine deficiency anemia who presented with acute psychosis which readily reversed on cyanocobalamin replacement. PMID:21886392

Tripathi, A K; Verma, S P; Himanshu, D

2010-09-01

428

The effect of macrocytosis on rat erythrocyte deformability during recovery from phenylhydrazine-induced anemia.  

PubMed

To investigate the role of red blood cell (RBC) geometry in determining the filterability of stress-induced macrocytes, measurements of RBC volume, diameter, and passage time through 3 micron and 5 micron filters were made on RBCs from control rats and from phenylhydrazine-treated rats during a 28-day recovery period following the peak hemolytic response to the anemia induced by phenylhydrazine (PHZ). Mean cell volumes (MCV) were calculated from volume distribution curves; RBC diameters were obtained from peripheral blood smears; surface area (SA) and mean cylindrical diameter (MCD) were calculated using a biconcave erythrocyte model. At the time of the peak macroreticulocyte response to PHZ, MCD and MCV were significantly increased compared to controls (3.07 vs 2.57 microns, and 102.1 vs 59.7 cubic microns, respectively), the ratio SA/MCV was significantly reduced (1.405 vs 1.670), and RBC filterability through both 3 and 5 micron cylindrical pores was significantly reduced. During the 28-day recovery period, MCV, MCD, SA/MCV, and filterability all returned toward the control values, MCD was inversely correlated with filterability through both 3 micron (r = -0.861, p less than .01) and 5 micron (r = -0.767, p less than .01) pores, and MCD fell below 3.6 microns in 97.5% of the animals despite the persistence of large macrocytic subpopulations. These results emphasize the correlation between RBC geometry and filterability, and demonstrate that macrocytes with favorable geometry can persist in the circulation for extended periods without remodeling or reduction in size. PMID:2361163

Norton, J M

1990-01-01

429

Prevalence of 25-hydroxyvitamin D deficiency in subgroups of elderly persons with anemia: association with anemia of inflammation.  

PubMed

Anemia and vitamin D deficiency are conditions that both result in significant morbidity and increase with age. The potential relationship between them remains poorly understood, particularly in the elderly. We used the Third National Health and Nutrition Examination Survey to examine the association of vitamin D deficiency with anemia subtypes in persons aged ? 60 years. Vitamin D deficiency was defined as serum levels < 20 ng/mL, and anemia was defined according to World Health Organization criteria. Vitamin D deficiency was associated with anemia prevalence independent of age, sex, or race/ethnicity (odds ratio, 1.47; 95% confidence interval, 1.06-2.05; P = .02) and varied significantly by anemia subtype (P overall = .003). The prevalence of vitamin D deficiency was 33.3% in the nonanemic population, 56% in anemia of inflammation (AI; P = .008), and 33.0% in unexplained anemia (P = .55). Non-Hispanic blacks had a 7-fold increased risk of AI compared with whites, and this was partially attenuated after adjusting for vitamin D deficiency. These data show that vitamin D deficiency is associated with specific subtypes of anemia in the elderly, especially in those with AI. Vitamin D may suppress inflammatory pathways, and studies to determine whether vitamin D supplementation ameliorates AI are warranted. PMID:21239700

Perlstein, Todd S; Pande, Reena; Berliner, Nancy; Vanasse, Gary J

2011-03-10

430

Molecular pathogenesis of Fanconi anemia: recent progress.  

PubMed

A rare genetic disease, Fanconi anemia (FA), now attracts broader attention from cancer biologists and basic researchers in the DNA repair and ubiquitin biology fields as well as from hematologists. FA is a chromosome instability syndrome characterized by childhood-onset aplastic anemia, cancer or leukemia susceptibility, and cellular hypersensitivity to DNA crosslinking agents. Identification of 11 genes for FA has led to progress in the molecular understanding of this disease. FA proteins, including a ubiquitin ligase (FANCL), a monoubiquitinated protein (FANCD2), a helicase (FANCJ/BACH1/BRIP1), and a breast/ovarian cancer susceptibility protein (FANCD1/BRCA2), appear to cooperate in a pathway leading to the recognition and repair of damaged DNA. Molecular interactions among FA proteins and responsible proteins for other chromosome instability syndromes (BLM, NBS1, MRE11, ATM, and ATR) have also been found. Furthermore, inactivation of FA genes has been observed in a wide variety of human cancers in the general population. These findings have broad implications for predicting the sensitivity and resistance of tumors to widely used anticancer DNA crosslinking agents (cisplatin, mitomycin C, and melphalan). Here, we summarize recent progress in the molecular biology of FA and discuss roles of the FA proteins in DNA repair and cancer biology. PMID:16493006

Taniguchi, Toshiyasu; D'Andrea, Alan D

2006-06-01

431

Diamond-Blackfan anemia, ribosome and erythropoiesis  

PubMed Central

Diamond-Blackfan anemia is a rare inherited bone marrow failure syndrome (5 to 7 cases/million live births) characterized by an are generative, usually macrocytic anemia with an absence or less than 5% of erythroid precursors (erythroblastopenia) in an otherwise normal bone marrow. The platelet and the white cell counts are usually normal but neutropenia, thrombopenia or thrombocytosis have been noted at diagnosis. In 40 to 50% of DBA patients, congenital abnormalities mostly in the cephalic area and in thumbs and upper limbs have been described. Recent analysis did show a phenotype/genotype correlation. Congenital erythroblastopenia of DBA is the first human disease identified to result from defects in ribosomal biogenesis. The first ribosomal gene involved in DBA, ribosomal protein (RP) gene S19 (RPS19 gene), was identified in 1999. Subsequently, mutations in 12 other RP genes out of a total of 78 RP genes have been identified in DBA. All RP gene mutations described to date are heterozygous and dominant inheritance has been documented in 40 to 45% of affected individuals. As RP mutations are yet to be identified in approximately 50% of DBA cases, it is likely that other yet to be identified genes involved in ribosomal biogenesis or other pathways may be responsible for DBA phenotype. PMID:20655265

Costa, L. Da; Moniz, H.; Simansour, M.; Tchernia, G.; Mohandas, N.; Leblanc, T.

2010-01-01

432

In search of the chemical basis of the hemolytic potential of silicas.  

PubMed

The membranolytic activity of silica particles toward red blood cells (RBCs) has been known for a long time and is sometimes associated with silica pathogenicity. However, the molecular mechanism and the reasons why hemolysis differs according to the silica form are still obscure. A panel of 15 crystalline (pure and commercial) and amorphous (pyrogenic, precipitated from aqueous solutions, vitreous) silica samples differing in size, origin, morphology, and surface chemical composition were selected and specifically prepared. Silica particles were grouped into six groups to compare their potential in disrupting RBC membranes so that one single property differed in each group, while other features were constant. Free radical production and crystallinity were not strict determinants of hemolytic activity. Particle curvature and morphology modulated the hemolytic effect, but silanols and siloxane bridges at the surface were the main actors. Hemolysis was unrelated to the overall concentration of silanols as fully rehydrated surfaces (such as those obtained from aqueous solution) were inert, and one pyrogenic silica also lost its membranolytic potential upon progressive dehydration. Overall results are consistent with a model whereby hemolysis is determined by a defined surface distribution of dissociated/undissociated silanols and siloxane groups strongly interacting with specific epitopes on the RBC membrane. PMID:23819533

Pavan, Cristina; Tomatis, Maura; Ghiazza, Mara; Rabolli, Virginie; Bolis, Vera; Lison, Dominique; Fubini, Bice

2013-08-19

433

Purification and characterization of salmolysin, an extracellular hemolytic toxin from Aeromonas salmonicida.  

PubMed Central

An extracellular hemolytic toxin of Aeromonas salmonicida, termed salmolysin, was purified 945-fold by ammonium sulfate precipitation, anion-exchange chromatography on DEAE-cellulose, and gel filtration chromatography on Sephadex G-100 and Sepharose 2B. Salmolysin appeared homogeneous upon cellulose acetate membrane electrophoresis and immunodiffusion analysis. The molecular weight of the toxin was estimated to be approximately 200,000 by the sedimentation equilibrium method. The UV absorption spectrum showed a maximum at 275 nm and a minimum at 262 nm. The isoelectric point was found to be at pI 5.4. Carbohydrate and protein analyses and other biochemical data indicated that salmolysin is a glycoprotein, containing approximately 62% carbohydrates. The toxin is a heat-labile substance and is stable at a neutral pH value. Ferrous ion inhibited the activity, whereas metal-chelating agents did not affect the activity. Sulfhydryl reagents did not inhibit the toxin, whereas reducing agents, such as L-cysteine and reduced glutathione, inhibited the toxin to a certain extent. Salmolysin was inactivated by a nonionic detergent but was stimulated by an anionic detergent, sodium deoxycholate, at a low concentration. The toxin was also inactivated by subtilisin and trypsin but was not inhibited by papain and pepsin. Salmolysin, with a remarkable hemolytic activity against salmonid erythrocytes, was lethal to rainbow trout when it was injected intramuscularly. Images PMID:3136147

Nomura, S; Fujino, M; Yamakawa, M; Kawahara, E

1988-01-01

434

Isolation and characterization of genetic variability in bacteria with ?-hemolytic and antifungal activity isolated from the rhizosphere of Medicago truncatula plants.  

PubMed

In the present study, we analyzed the frequency of hemolytic and antifungal activities in bacterial isolates from the rhizosphere of Medicago truncatula plants. Of the 2000 bacterial colonies, 96 showed ?-hemolytic activities (frequency, 4.8 x 10(-2)). Hemolytic isolates were analyzed for their genetic diversity by using random amplification of polymorphic DNA, yielding 88 haplotypes. The similarity coefficient of Nei and Li showed a polymorphic diversity ranging from 0.3 to 1. Additionally, 8 of the hemolytic isolates showed antifungal activity toward plant pathogens, Diaporthe phaseolorum, Colletotrichum acutatum, Rhizoctonia solani, and Fusarium oxysporum. The 16S ribosomal sequencing analysis showed that antagonistic bacterial isolates corresponded to Bacillus subtilis (UM15, UM33, UM42, UM49, UM52, and UM91), Bacillus pumilus (UM24), and Bacillus licheniformis (UM88). The present results revealed a higher genetic diversity among hemolytic isolates compared to that of isolates with antifungal action. PMID:25062484

Hernndez-Salmern, J E; Prieto-Barajas, C M; Valencia-Cantero, E; Moreno-Hagelsieb, G; Santoyo, G

2014-01-01

435

Selective C3 deficiency due to C3 nephritic factor in an apparently healthy girl.  

PubMed

Routine laboratory investigations performed on the serum of an 8-year-old girl examined because of a moderate degree of iron-deficiency anemia showed a markedly reduced C3 level. More detailed complement studies revealed a selective C3 deficiency, as indicated by the almost undetectable C3 concentration tested by both hemolytic and immunochemical assays and by the normal or slightly reduced levels of all the other complement components. The hemolytic activity of the serum was restored by the addition of partially purified C3 component. The isolated C3 deficiency could be attributed to the presence of a C3-cleaving activity in the serum of the propositus. This activity was identified as C3 nephritic factor (C3NeF) since it was heat-stable, was absorbed by Cowan I strain of Staphylococcus aureus and was-eluted in the IgG fraction after DEAE-chromatography of the serum. The levels of H and I factors of the alternative pathway in the serum of the propositus and of C3 in the serum samples of her parents and two siblings were found to be within the normal range. The previous clinical history of the girl and the follow-up for a period of approximately 5 years showed that she was apparently healthy and did not reveal clinical and/or laboratory evidence of glomerulonephritis, lipodystrophy or repeated bacterial infections usually associated with the presence of C3NeF in the serum. PMID:3834579

Tedesco, F; Tovo, P A; Tamaro, G; Basaglia, M; Perticarari, S; Villa, M A

1985-01-01

436

Anemia and risk of dementia in older adults  

PubMed Central

Objective: To determine whether anemia is associated with incident dementia in older adults. Methods: We studied 2,552 older adults (mean age 76.1 years; 38.9% black; 51.8% female) participating in the Health, Aging, and Body Composition study and free of dementia at baseline. We defined anemia using WHO criteria (hemoglobin concentration <13 g/dL for men and <12 g/dL for women). Dementia diagnosis was determined by dementia medication use, hospital records, or a change in Modified Mini-Mental State (3MS) score of more than 1.5 SD from mean. Discrete time Cox proportional hazard regression models were used to examine the hazard for developing dementia associated with anemia. Results: Of 2,552 participants, 392 (15.4%) older adults had anemia at baseline. Over 11 years of follow-up, 455 (17.8%) participants developed dementia. In the unadjusted model, those with baseline anemia had an increased risk of dementia (23% vs 17%, hazard ratio = 1.64; 95% confidence interval 1.30, 2.07) compared to those without anemia. The association remained significant after adjusting for demographics, APOE ?4, baseline 3MS score, comorbidities, and renal function. Additional adjustment for other anemia measures (mean corpuscular volume, red cell distribution width), erythropoietin, and C-reactive protein did not appreciably change the results. There was no interaction by sex and race on risk of developing dementia. Conclusion: Among older adults, anemia is associated with an increased risk of developing dementia. Findings suggest that further study of anemia as a risk factor for dementia and a target for intervention for cognitive health is warranted. PMID:23902706

Hong, Chang Hyung; Falvey, Cherie; Harris, Tamara B.; Simonsick, Eleanor M.; Satterfield, Suzanne; Ferrucci, Luigi; Metti, Andrea L.; Patel, Kushang V.

2013-01-01

437

Iron and anemia in human biology: a review of mechanisms.  

PubMed

The biology of iron in relation to anemia is best understood by a review of the iron cycle, since the majority of iron for erythropoiesis is provided by iron recovered from senescent erythrocytes. In iron-deficiency anemia, storage iron declines until iron delivery to the bone marrow is insufficient for erythropoiesis. This can be monitored with clinical indicators, beginning with low plasma ferritin, followed by decreased plasma iron and transferrin saturation, and culminating in red blood cells with low-Hb content. When adequate dietary iron is provided, these markers show return to normal, indicating a response to the dietary supplement. Anemia of inflammation (also known as anemia of chronic disease, or ACD) follows a different course, because in this form of anemia storage iron is often abundant but not available for erythropoiesis. The diagnosis of ACD is more difficult than the diagnosis of iron-deficiency anemia, and often the first identified symptom is the failure to show a response to a dietary iron supplement. Confirmation of ACD is best obtained from elevated markers of inflammation. The treatment of ACD, which typically employs erythropoietin (EPO) supplements and intravenous iron (i.v.-iron), is empirical and often falls shorts of therapeutic goals. Dialysis patients show a complex pattern of anemia, which results from inadequate EPO production by the kidney, inflammation, changes in nutrition, and blood losses during treatment. EPO and i.v.-iron are the mainstays of treatment. Patients with heart failure can be anemic, with incidence as high as 50%. The causes are multifactorial; inflammation now appears to be the primary cause of this form of anemia, with contributions from increased plasma volume, effects of drug therapy, and other complications of heart disease. Discerning the mechanisms of anemia for the heart failure patient may aid rational therapy in each case. PMID:18363095

Handelman, Garry J; Levin, Nathan W

2008-12-01

438

Preoperative anemia increases mortality and postoperative morbidity after cardiac surgery  

PubMed Central

Background Anemia is an established adverse risk factor in cardiovascular disease. However, the effect of preoperative anemia is not well defined in heart surgery. This study evaluates the effect of preoperative anemia on early clinical outcomes in patients undergoing cardiac surgery. Methods A retrospective, observational, cohort study of prospectively collected data was undertaken on 7,738 consecutive patients undergoing heart surgery between April 2003 and February 2009. Of these, 1,856 patients with preoperative anemia were compared to 5,882 patients without anemia (control group). According to the World Health Organization, anemia was defined as hemoglobin level?anemia was associated with tripling in the risk of death (4.6% vs 1.5%, p??7days (54% vs 36.7%, p?anemia was an independent predictor of mortality (odds ratio [OR] 1.44, 95% confidence interval [CI] 1.02 to 2.03), postoperative renal dysfunction (OR 1.73, 95% CI 1.43 to 2.1) and length of hospital stay?>?7days (OR 1.3, 95% CI 1.15 to 1.47). Conclusion In patients undergoing heart surgery, preoperative anemia is associated with an increased risk of mortality and postoperative morbidity. PMID:25096231

2014-01-01

439

Anemia management: development of a rapidaccess anemia and intravenous iron service  

PubMed Central

This article describes the initiation and evolution of the Rapid-Access Anemia Clinic (RAAC) at Guys and St Thomas Hospitals, London, UK. This clinic was set up to provide diagnosis and treatment, and to coordinate investigative procedures, where necessary, into the underlying causes of anemia. Initially piloted with anemic preoperative orthopedic patients, the clinic now treats a wide range of conditions, deriving from both internal and external referrals. Treatment includes dietary advice, supplementation with iron, vitamin B12 and folate, and blood transfusion. Most patients at the RAAC need iron replacement, the majority of which require intravenous (IV) iron. Therefore the first-line IV iron-administration protocol is carefully considered to ensure viability of the service and patient satisfaction. Four IV irons available in the UK are discussed, with explanation of the benefits and drawbacks of each product and the reasoning behind the IV iron choice at different stages of the RAACs development. Costs to the service, affected by IV iron price and administration regimen, are considered, as well as the products contraindications. Finally, the authors reflect on the success of the RAAC and how it has improved patients quality-of-treatment experience, in addition to benefiting the hospital and National Health Service in achieving specific health-care mandates and directives. Drawing from the authors experiences, recommendations are given to assist others in setting up and providing a successful rapid-access anemia service or similar facility. PMID:23950666

Radia, Deepti;