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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An increased frequency of high titers of antibodies against A, B, ORh+ trypsinized, and ORh+ neuraminidase-treated human red blood cells was observed in the sera of Africans living in a malaria endemic area, and Europeans with primary malaria attacks. In the latter group, titers of agglutinins against neuraminidase treated RBC were increased in 84% of individuals and were of the IgM class. Inhibition experiments with beta-D-galactose and lactose showed that this agglutinin was directed to the T antigen of human RBC. Its possible implication in malaria related anemia is discussed.
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PMID:[Demonstration of an abnormal increase of anti-T hemagglutinin titers in malaria infected patients]. 640 66

A shortened life of erythrocytes in uremia has been suggested as one of the causes of anemia in this condition. Since partially desialylated erythrocytes are promptly removed from the circulation, we examined whether sera from renal failure patients would exhibit increased neuraminidase activity which could be held responsible for this phenomenon. Sera of 22 patients with end stage renal failure were examined for neuraminidase activity by assessing their effect on desialylation upon incubation at 37 degrees C for 2 and 1 h, respectively, of erythrocytes of healthy donors matched for blood group and of fetuin as substrate. As deduced from the residual content of sialic acid of erythrocytes and of the amount of sialic acid released from fetuin, the results showed a statistically higher neuraminidase-like activity of patients' sera as compared to sera of healthy individuals. It is suggested that increase in neuraminidase activity could be one of the factors involved in the mechanism of generation of anemia in uremia by acting on erythrocytes, rendering them more prone to sequestration by the liver and spleen.
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PMID:Neuraminidase-like activity in sera of uremic anemic patients. 671 3

1. The surface membrane proteins of red blood cells from normal, hyperbled or acetylphenylhydrazine-treated BALB/c mice and NZB mice of different ages were labelled by lactoperoxidase-catalyzed radioiodination. Sialoglyoproteins were labelled by periodate/NaB3H4 or galactose oxidase +/- neuraminidase/Na3H4 treatments. 2. Anaemia produced several changes in radioiodinated proteins. 3. Sialoglycoprotein radiolabelling was unchanged, even with over 90% reticulocytosis. 4. Decreased periodate/NaB3H4-dependent labelling of red blood cells from Plasmodium berghei-infected BALB/c mice (Howard et al., 1980; Howard & Day, 1981) cannot therefore be due to anaemia per se, but must be related more specifically with infection.
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PMID:Surface membrane proteins and glycoproteins of red blood cells from normal and anaemic mice. 708 22

Erythrocyte surface and free serum sialic acid concentrations were determined during experimental Trypanosoma vivax infection in cattle. All infected calves developed mild trypanosomiasis, with significant decreases in mean packed cell volume occurring 15, 16, 20, 22 and 24 days after infection. The anaemia was preceded by significant decreases in mean erythrocyte surface sialic acid concentrations on days 7, 13 and 14, with yet another significant decrease on day 31 after infection. These decreases in erythrocyte surface sialic acid concentrations coincided with the parasitaemic waves. Free serum sialic acid concentration, however, showed an increase, though non-significantly, on day 8, which coincided with both a decrease in erythrocyte surface sialic acid and the initial parasitaemic wave. It is postulated that the early anaemia observed in infected animals may be attributable to the activities of the circulating trypanosomes which produce neuraminidase which, in turn, cleaves off surface sialic acid, thus rendering the erythrocyte more prone to phagocytosis by the recticuloendothelial system.
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PMID:Variation in erythrocyte surface and free serum sialic acid concentrations during experimental Trypanosoma vivax infection in cattle. 708 71

After an upper respiratory tract infection an eight months old infant developed a severe hemolytic uremic syndrome with anemia, thrombocytopenia and anuria. Remarkable was a lesion of the erythrocytes by neuraminidase producing microorganisms. By early hemodialysis, blood transfusions and accurate fluid therapy the acute stage could be managed. The proceeding course was complicated by hypertension, seizures, coma, abdominal pain attacks and a fibrinous hemorrhagic pericarditis, which made an incomplete pericardectomy necessary. Although it came again to diuresis a severe chronic renal failure with its concluding effects as anemia, acidosis, hypertension and inanition resulted. After a four months period the patient died of biventricular congestive heart failure.
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PMID:[Severe course of a hemolytic-uremic syndrome]. 715 51

The prevalence of antibodies against (i) human red blood cells (RBC) of A and B groups, (ii) trypsinized O Rh+ RBC and (iii) neuraminidase treated O Rh+ RBC were investigated both in sera of Africans from a malaria endemic area of Upper Volta and in sera of Europeans with acute malaria from a Paris hospital. An increased frequency of high titres of haemagglutinins was observed against A and B as well as O Rh+ trypsinized human RBC, thus confirming previously published results. In addition, agglutination of neuraminidase treated RBC showed that the titres were increased in about 40% of Africans studied and in about 80% of patients with acute malaria. Using agglutination with a specific anti-T lectin and inhibition with two ligands, it was found that sera of malarious patients contain high titres of antibodies directed against the T antigen of neuraminidase treated RBC. The mechanisms of appearance of high titres of autohaemagglutinins in malaria and their possible interference in the anaemia associated with this disease are discussed.
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PMID:High titres of anti-T antibodies and other haemagglutinins in human malaria. 717 12

Lactoperoxidase-catalysed radio-iodination was used to compare the surface proteins on red cells from Plasmodium yoelii-infected with normal BALB/c mice. The profile of radio-iodinated proteins separated by SDS-polyacrylamide gel electrophoresis was different for infected blood of similar parasitaemia from mice inoculated with different doses of the parasite. Inoculation with different doses of the parasite. Inoculation with the lower dose resulted in the appearance of a major radio-iodinated protein of apparent molecular weight (Mr) 76 000 which was labelled to a similar extent on uninfected red cells from infected blood and purified multinucleate infected cells. Several minor radio-iodinated bands, with identical mobilities to the minor bands on normal BALB/c erythrocytes, were also present on red cells from this infected blood. In contrast, the higher inoculation dose produced changes in the minor labelled bands, and the band with Mr of 76 000 was absent. In this case, the minor radio-iodinated proteins of the normal BALB/c erythrocyte (with Mr of 65 000, 57 000, 48 000, 38 000 and 32 000) were replaced by a series of bands with Mr of 60 000, 50 000, 43 000 and 28 000 on both uninfected and infected red cells. These differences with inoculation dose may be related to the different duration of these infections, the development of anaemia and the extent of pathological changes at the erythrocyte surface. P. yoelii infection caused a marked loss in periodate-dependent labelling of sialoglycoproteins on most, if not all, red cells in infected blood. There was also a large decrease in galactose oxidase-dependent glycoprotein labelling with or without neuraminidase treatment. These changes in the carbohydrate groups on red cell membrane glycoproteins may be linked to the excessive loss of both uninfected and infected red cells during some malaria infections.
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PMID:Characterization of surface proteins and glycoproteins on red blood cells from mice infected with haemosporidia: Plasmodium yoelii infections of BALB/c mice. 744 94

A factor capable of deforming erythrocyte membranes, found in the culture supernatants of Bartonella bacilliformis, was purified 1840-fold using hydrophobic, ion exchange and gel exclusion chromatography. The final fractions contained a single detectable polypeptide species, referred to as deformin, having a molecular weight of 67000 by SDS-PAGE and a native molecular weight of 130,000 by gel exclusion chromatography or velocity sedimentation in a glycerol gradient. Erythrocytes treated with deformin acquire trenches, indentations, and invaginations which could be reversed by vanadate, dilauroylphosphatidylcholine (DLPC), or by raising the internal Ca2+ concentrations with the inophore A23187. Internal vacuoles also form. Erythrocytes treated with trypsin or neuraminidase are much more sensitive to deformin than untreated erythrocytes; erythrocytes treated with phospholipase D are less sensitive to deformin. This protein may play a role in causing the severe anemia which can result as a consequence of infection by B. bacilliformis.
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PMID:Purification of deformin, an extracellular protein synthesized by Bartonella bacilliformis which causes deformation of erythrocyte membranes. 769 92

Reactivity of anti-erythrocyte membrane (RBCm) antibody in sera of B. gibosni-infected dogs on native RBCm and erythrocyte surface (RBCs) was examined using an enzyme linked immunosorbent assay. Anti-RBCm antibody attached to native RBCm and the surface of erythrocytes (RBC) treated with phenylhydrazine or neuraminidase, but not to the surface of non-treated RBC. Based on these results, anti-cytoskeletal protein antibody in sera of B. gibsoni-infected dogs is considered to attach to native RBCm, and furthermore free radical-induced oxidative stress imposed on RBC and sialic acid removal from glycoproteins of RBC are considered necessary for anti-transmembrane protein antibody in sera of B. gibsoni-infected dogs to be bound to RBCs. These are important to elucidating the mechanism of the marked increase in RBCs-bound IgG value and anemia in B. gibsoni infection.
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PMID:Reactivity of serum anti-erythrocyte membrane antibody in Babesia gibsoni-infected dogs. 786 10

Hemolytic uremic syndrome (HUS) in associated with infections of neuraminidase-producing streptococcus pneumoniae was rarely reported in the literature. We report two infants with proven pneumococcal meningitis associated with anemia, thrombocytopenia, renal failure, and T-antigen activation characteristic of neuraminidase activity. This supports a common pathogenesis in HUS following infection of neuraminidase-producing strains of S. pneumoniae. One infant complicated with status epilepticus died, and the other infant survived without sequelae. We recommend that neuraminidase production should be considered in case of pneumococcal meningitis associated with anemia and thrombocytopenia without diffuse bleeding tendency. Early recognition of HUS associated S. pneumoniae neuraminidase production is vital. The use of compatible washed red blood cells, meticulous supportive care and appropriate use of dialysis will improve survival.
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PMID:Pneumococcal meningitis complicated with hemolytic uremic syndrome: report of two cases. 955 96


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