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Query: UMLS:C0002878 (hemolytic anemia)
 7,530 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute hemolytic anemia was experimentally induced in chickens with the oxidant chemical phenylhydrazine. From results of the graded doses trial, subcutaneously injected 6 mg/100 g body weight single dose was designated as standardised. The anemic response, characterized by marked reductions in hemoglobin, packed cell volume and total erythrocyte count, was perceptible on day 1 post-injection. Peak anemia was observed on day 3. Compensatory erythropoiesis was discernible on day 5. The hematological profile indicated near complete recovery on day 11 post-injection. This avian model is proposed for study of the basic mechanisms of hemolytic anemia in chickens.
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PMID:An avian model for the study of acute hemolytic anemia in the domestic fowl (Gallus domesticus). 228 66

The bone marrow blood flow in the femur of the rabbit with acute hemolytic anemia was measured by the radioactive microsphere method. Acute hemolytic anemia was induced by a single intraperitoneal injection of phenylhydrazine. An increase in the bone marrow blood flow was detected three days after the induction of anemia and continued for about one week. The bone marrow blood flow of the anemic rabbit (66 ml/min/100 g marrow) was about three times that of the control (20 ml/min/100 g marrow). The increased blood flow to the bone marrow appeared to be correlated to the increased erythropoietic activity.
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PMID:Increased bone marrow blood flow in rabbits with acute hemolytic anemia. 395 65

A panel of 11 IgG monoclonal antierythrocyte antibodies was generated by fusing spleen and bone marrow cells from unimmunized New Zealand black mice with the nonsecreting murine plasmacytoma cell line P3.X63.NS1. The monoclonal antibodies were detected by indirect hemagglutination of unaltered erythrocytes from several strains of mice. Seven of the antibodies cross-reacted with rat erythrocytes, but none of the antibodies agglutinated erythrocytes from any other species tested. Seven of the monoclonal antibodies were also capable of fixing rabbit complement. In vivo studies utilizing these 11 IgG-secreting hybridomas were performed in syngeneic BALB/c mice. Mice injected with nine of the hybridomas showed positive direct antiglobulin test results but did not become anemic. In contrast, hybridoma 114, secreting an IgG3 antibody, and hybridoma 245, secreting an IgG1 antibody, were both capable of mediating an acute, rapidly fatal hemolytic anemia. Intraperitoneal injection of hybridomas 114 and 245 resulted in positive direct and indirect antiglobulin test results, decreased hematocrit level, and reticulocytosis 3 to 6 days after cell injection. The mice survived a mean of 8 days, and death was associated with severe anemia and spontaneous erythrocyte agglutination. Autopsy studies revealed hepatosplenomegaly, small mesenteric tumor (hybridoma) mass, and no ascites. The liver and spleens were characterized histologically by erythrophagocytosis, extramedullary hematopoiesis, and hemosiderin deposition. Acute hemolytic anemia in BALB/c mice mediated by hybridomas 114 and 245 represents a new animal model that can be used to further define the mechanisms of immune hemolytic disease.
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PMID:Monoclonal antibody-induced murine hemolytic anemia. 648 Dec 19

Tacrolimus (formerly known as FK506) is a macrolide immunosuppressant that has been used to prevent rejection of solid organ allografts. Acute hemolytic anemia is one of the side effects associated with tacrolimus therapy, and two mechanisms have been described to account for acute hemolytic anemia in patients receiving tacrolimus: drug-induced hemolysis and alloimmune hemolysis resulting from donor lymphocytes derived from the allograft (passenger lymphocyte syndrome). We report a case of a liver transplant recipient who developed fatal autoimmune hemolytic anemia while under treatment with tacrolimus for allograft rejection, and in whom postmortem examination revealed a clinically unsuspected posttransplant lymphoproliferative disorder. This case implicates autoimmune hemolytic anemia as a novel mechanism of acute hemolysis in patients treated with tacrolimus and further suggests that acute hemolytic anemia in this group of patients may herald an occult lymphoproliferative disorder.
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PMID:Tacrolimus-related posttransplant lymphoproliferative disorder presenting as autoimmune hemolytic anemia. 862 6

Acute hemolytic anemia is one of the side effects associated with cyclosporin and tacrolimus therapy, and three mechanisms have been described to account for hemolytic anemia in patients receiving these drugs: drug induced hemolysis, autoimmune hemolysis and alloimmune hemolysis resulting from donor lymphocytes derived from the allograft (passenger lymphocyte syndrome). We report four cases of renal transplant recipients who developed alloimmune hemolytic anemia due to minor ABO incompatibility while under treatment with cyclosporin (two) and tacrolimus (two). The anti-erythrocyte antibodies responsible for hemolysis were of the IgG isotype and showed anti-A or anti-B specificity. These findings suggest that the hemolysis could be related to alloantibodies derived from the clonal development of donor B lymphocytes in the recipients (microchimerism). In summary, hemolytic anemia due to ABO-minor incompatibility occurs infrequently after renal transplantation. Risks are higher for patients A, B or AB blood group receiving an O blood group graft under treatment with cyclosporin or tacrolimus. Follow-up of these patients is warranted for the early detection and optimal management may be achieved by reduction of immunosuppression and change to mycophenolate mofetil.
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PMID:[Hemolytic anemia caused by graft-versus-host reaction in ABO-nonidentical renal transplants from blood group O donors]. 1181 17

Acute hemolytic anemia associated with red blood cell (RBC) glucose-6-phosphate dehydrogenase (G6PD) deficiency is commonly encountered in the Mediterranean basin. Nevertheless, concomitant clinical evidence of white blood cell G6PD deficiency is extremely rare in Israel. This study sought to assess simultaneously levels of G6PD activity in polymorphonuclear leukocytes (PMN) and in red blood cells (RBC) of patients with G6PD deficiency, including full-term newborn infants. In PMN, the correlation between G6PD activity, hexose monophosphate shunt activity, and superoxide anion release was evaluated. In G6PD-deficient patients, a parallel and significantly decreased G6PD activity was found in neutrophils (range of activity 0-4.5 IU/10(6) PMN) and erythrocytes (range of activity 0-1.8 IU/g Hb), compared with healthy controls (5-23 IU/10(6) PMN and 2.4-6.4 IU/g Hb, respectively). A positive correlation was found in PMN between the levels of G6PD activity, hexose monophosphate (HMP) shunt activity, and superoxide anion release (p < 0.01). Nevertheless, all patients' bactericidal activity of neutrophils remained in the range of healthy controls. Although many episodes of acute hemolytic anemia were recorded, no increased incidence of pyogenic infections was observed in any group of patients investigated. Neutrophil and erythrocyte G6PD levels were re-assessed in some of these patients several times a day. A significant diurnal fluctuation of the enzyme activity was found. It is speculated that the patients produce fluctuating daily quantities of NADPH, sufficient to initiate the neutrophil respiratory burst and to achieve normal bactericidal activity, necessary to prevent the development of microbial infections.
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PMID:Diurnal fluctuation of leukocyte G6PD activity. A possible explanation for the normal neutrophil bactericidal activity and the low incidence of pyogenic infections in patients with severe G6PD deficiency in Israel. 1497 80

Acute hemolytic anemia (AHA) due to glucose 6-phosphate dehydrogenase (G6PD) deficiency has rarely been recognized as a contributor to the development of frostbite. We discuss a case of frostbite in a 32-year-old male Marine with G6PD deficiency during military training on Mount McKinley in Alaska, which eventually led to a permanent disability. In this report, the pathophysiology of G6PD deficiency, the effects of hemolytic anemia, and factors that contribute to frostbite will be discussed, as well as the clinical findings, treatment course, and the outcome of this case. The patient was evacuated and admitted to Alaska Regional Hospital. He was treated for fourth-degree frostbite, ultimately resulting in the complete or partial amputation of all toes. Although it cannot be proved that AHA occurred in this patient, this case potentially adds frostbite to the list of rare but possible clinical presentations of G6PD deficiency.
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PMID:Frostbite: A Novel Presentation of Glucose-6-Phosphate Dehydrogenase Deficiency? 2636 Mar 47

Glucose 6-phosphate dehydrogenase (G6PD) deficiency is 1 of the commonest human enzymopathies, caused by inherited mutations of the X-linked gene G6PD. G6PD deficiency makes red cells highly vulnerable to oxidative damage, and therefore susceptible to hemolysis. Over 200 G6PD mutations are known: approximately one-half are polymorphic and therefore common in various populations. Some 500 million persons with any of these mutations are mostly asymptomatic throughout their lifetime; however, any of them may develop acute and sometimes very severe hemolytic anemia when triggered by ingestion of fava beans, by any of a number of drugs (for example, primaquine, rasburicase), or, more rarely, by infection. Approximately one-half of the G6PD mutations are instead sporadic: rare patients with these mutations present with chronic nonspherocytic hemolytic anemia. Almost all G6PD mutations are missense mutations, causing amino acid replacements that entail deficiency of G6PD enzyme activity: they compromise the stability of the protein, the catalytic activity is decreased, or a combination of both mechanisms occurs. Thus, genotype-phenotype correlations have been reasonably well clarified in many cases. G6PD deficiency correlates remarkably, in its geographic distribution, with past/present malaria endemicity: indeed, it is a unique example of an X-linked human polymorphism balanced through protection of heterozygotes from malaria mortality. Acute hemolytic anemia can be managed effectively provided it is promptly diagnosed. Reliable diagnostic procedures are available, with point-of-care tests becoming increasingly important where primaquine and its recently introduced analog tafenoquine are required for the elimination of malaria.
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PMID:Glucose-6-phosphate dehydrogenase deficiency. 3270 56