Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sulfated proteoglycans have been shown to be involved in the binding of sporozoites of malaria parasites to hepatocytes. In this study, we have evaluated the effect of sulfated glycosaminoglycans on the invasion of erythrocytes by Plasmodium falciparum merozoites and cytoadherence of parasitized erythrocytes (PRBC) to endothelial cells. Invasion of erythrocytes by HB3EC-6 (an HB3 line selected for high binding to endothelial cells) was inhibited by dextran sulfate 500K, dextran sulfate 5K, sulfatides, fucoidan, and heparin but not by chondroitin sulfate A. With the exception of sulfatides, the invasion-inhibitory effect was not mediated by killing of parasites. Cytoadherence of HB3EC-6 to human microvascular endothelial cells (HMEC-1) and inhibited by these sulfated glycoconjugates. The highly sulfated dextran sulfate 500K had the highest inhibitory effect on both invasion and cytoadherence, whereas the positively charged protamine sulfate promoted cytoadherence. Because preincubation of PRBC with sulfated glycosaminoglycans and treatment of target cells with heparinase had no significant inhibition on cytoadherence, it is unlikely that sulfated glycoconjugates are used directly by endothelial cells as cytoadhesion receptors. In an vivo experiment, we found that the administration of dextran sulfate 500K to CBA/Ca mice infected with Plasmodium berghei ANKA reduced parasitemia and delayed the death associated with anemia. These observations suggest that sulfated polyanions inhibit the invasion of erythrocytes by merozoites and cytoadherence of PRBC to endothelial cells by increasing negative repulsive charge and sterically interfering with the ligand-receptor interaction after binding to target cells.
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PMID:Sulfated polyanions inhibit invasion of erythrocytes by plasmodial merozoites and cytoadherence of endothelial cells to parasitized erythrocytes. 860 3

The pathogenesis of poikilocytosis in calves was investigated. Nine calves 1 to 2 months old exhibiting poikilocytosis (poikilocytic calves), were examined. The proportion of poikilocytes in their blood was more than 70% in two calves (severely poikilocytic), while it averaged 30% in the remaining seven calves (moderately poikilocytic). All of the polikilocytic calves exhibited mild anemia. The concentration of plasma iron in 8 of them was 20-30% of that in normal calves, but it increased as the calves aged. The polikilocyte count in moderately poikilocytic calves decreased in proportion to the increase of the plasma iron concentration, though a high poikilocyte count was observed in a severely poikilocytic calf even after the plasma iron concentration reached the normal level. Column chromatography of a hemoglobin preparation from all the calves examined revealed 5 distinct peaks. Three peaks were embryonic, fetal and adult hemoglobins, respectively. The other peaks were tentatively designated Hb-2 and Hb-3, respectively. The amount of Hb-2 in the two severely poikilocytic calves was about three times that in the other calves including those moderately poikilocytic, and it decreased as the calves aged. The decrease of Hb-2 in one severely poikilocytic calf was related to a reduction of the proportion of poikilocytes in its peripheral blood. There was no significant difference in age-dependent changes of hemoglobin types between moderately poikilocytic calves and normal calves. Furthermore, SDS-PAGE analysis of red cell membrane revealed that protein 4.2 consisted of two polypeptides in the two severely poikilocytic, and three moderately poikilocytic calves, while it consisted of a single polypeptide in the remaining calves examined. These results indicated that the abnormalities of hemoglobin composition and protein 4.2 in the erythrocyte membrane observed in the severely poikilocytic calves might be responsible for the morphological changes in the erythrocytes, whereas iron deficiency was thought to be the predominant cause of poikilocytosis in the moderately poikilocytic calves.
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PMID:Hemoglobin types, erythrocyte membrane skeleton and plasma iron concentration in calves with poikilocytosis. 884 98

Allopurinol is a xanthine oxidase inhibitor used in management of chronic gout. It acts by reducing the amount of uric acid by inhibiting purine metabolism. A middle-aged hypertensive female who was on allopurinol for 7 months presented with generalized weakness and exertional dyspnea. Investigations revealed pancytopenia: normocytic normochromic anemia (Hb-3.2g/dL, TLC-3400/mm3) and severe thrombocytopenia (Platelets-1000/mm3) with mild hepatosplenomegaly and grade 2 medico renal disease with normal cardiac status. Nutritional, hemolytic and infective causes were ruled out. She was transfused with fresh whole blood, platelets, administered empirical antibiotics and started on steroids. Initially, she responded to treatment but later developed an episode of convulsions with anuria and succumbed to leukopenic sepsis secondary to hypo/aplastic anemia probably due to allopurinol. Allopurinol is used extensively in the management of chronic gout and is well tolerated due to its safety profile. But we here report a case of allopurinol induced aplastic anemia leading to the demise of a patient. Allopurinol though safe needs careful monitoring.
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PMID:Allopurinol: Sorrow to the marrow. 3275 32