Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty two patients who were seen and satisfied the French-American-British (FAB) diagnostic criteria for myelodysplastic syndromes (MDS) over a 6-year period at the University of Zimbabwe's Department of Haematology, Harare, are presented. Their overall ages ranged from 29 to 75 years with a mean +/- SD of 57.8 +/- 11.2 years. Males outnumbered females with a male to female ratio of 1.2:1. Refractory anaemia (RA) occurred in 33.3%; refractory anaemia with ringed sideroblasts (RARS) in 16.7%; refractory anaemia with excess blasts (RAEB) in 21.4%; refractory anaemia with excess blasts in transformation (RAEB-T) in 16.7% and chronic myelomonocytic leukaemia (CMML) in 11.9% of the patients. In 90.5% the disease was primary and in 9.5% prior exposure to myelotoxic agents resulted in secondary MDS. The study reveals that MDS as a cause of anaemia in the African population is usually hidden in the big number of well known anaemias due to rampant malaria, malnutrition and a host of nutritional deficiencies. There is therefore the need to increase diagnostic awareness among our clinicians about the existence of these disorders.
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PMID:Myelodysplastic syndromes (MDS) in Central Africans. 816 30

Death from malaria occurs from the complications of the infection: cerebral manifestations leading to coma and a severe and refractory anemia leading to hypoxia and cardiac decompensation. Several mechanisms have been identified to play a role in the pathogenesis of malarial anemia, such as erythrocyte lysis and phagocytosis, and sequestration of parasitized red blood cells, but recent data indicate that these mechanisms (singly or in combination) do not adequately explain the severity of this anemia. By contrast, hematologic studies have shown that bone marrow suppression and ineffective erythropoiesis contribute importantly to the severe anemia of malaria infection. The host mechanisms responsible for suppression of erythropoiesis may involve an excessive or sustained innate immune response or a pathologic skewing of the T-cell differentiation response with the attendant production of certain proinflammatory cytokines. Experimental data also indicate that severe malarial anemia is associated with the immunologic expression of a circulating inhibitor of erythropoiesis that functionally antagonizes the action of erythropoietin. We review the clinical and experimental basis for these concepts and discuss ongoing experimental and genetic studies aimed at unraveling the molecular basis of this malaria-induced bone marrow suppression.
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PMID:The anemia of malaria infection: role of inflammatory cytokines. 1496 85

To elucidate the relationship between falciparum malaria-associated anemia and serum erythropoietin (Epo) levels and reticulocyte response during acute malaria infection, 87 adults aged 18-65 years presenting with acute, uncomplicated malaria were examined on enrollment and for 28 days of follow-up. The 87 patients were divided into 2 groups: those with anemia (n = 45) and those without (n = 42). Serum samples were taken on admission (Day 0), then on Days 7, 21, and 28, to measure the reticulocyte count, absolute reticulocyte count, reticulocyte hemoglobin content, and erythropoietin level (Epo). The absolute reticulocyte counts for the anemic patients were significantly higher than for those without anemia on Days 0, 7, 21, and 28. The serum Epo levels for the anemic patients were significantly higher than the non-anemic group only on Day 0 (44.39 +/- 4.06 vs 25.91 +/- 4.86 mlU/ml, p < 0.001). Inadequate Epo production was found in 31.03% (27/87) of patients on Day 0, 37.93% (33/87) on Day 7, 43.67% (38/87) on Day 21, and 39.08% (34/87) on Day 28. These results indicate defective Epo production and reticulocyte response in adult patients suffering from acute P. falciparum malaria, which differs from pediatric patients. Our findings may provide the basis for further study into the choice of therapeutic strategies to treat acute P. falciparum malaria-associated anemia with recombinant human Epo to correct refractory anemia due to malaria.
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PMID:Defective erythropoietin production and reticulocyte response in acute Plasmodium falciparum malaria-associated anemia. 1905 93