Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019045 (hemoglobinopathies)
 2,704 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genetic resistance to malaria is associated with various genetic factors, including erythrocytic variability and variability of the genes involved into the pathogenetic process. Some genetic anomalies resulted from selective malaria pressure, which brought into existence different forms of hemoglobinopathies, glucose-6-phosphate dehydrogenase deficiency, and no Duffy antigens, and ovalocytosis, etc., which ensured varying malaria resistance. Cell adhesion is a major factor in the pathogenesis of malaria. Adhesion molecules express on the cellular membranes of the endothelium, platelets, macrophages, red blood cells and serve as binding receptors for membrane proteins PFRMP-1 of P. falciparum. Polymorphism of the CD36, ICAM-1, and PECAM1 genes can lower binding to blood vessel endothelial cells, which reduces the number of clinical forms of malaria. The high serum TNF-alpha level that is caused by mutation in the promoter of the TNF-alpha gene is associated with cerebral malaria. TNF-alpha enhances the endothelial expression of adhesion molecules, by increasing the adhesion of infected erythrocytes, including that in cerebral capillaries, by inducing in patients local thrombosis and inflammation with release of the cytokines--TNF-alpha. The products of inflammatory infiltrates attack the endothelium, by leading to the imbibition of plasma and erythrocytes in brain tissue and causing a cerebral form of malaria.
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PMID:[Genetic resistance to malaria]. 1956 55