Biology, pathobiology and subclinical homocysteine in the human species
Biología, patobiología y bioclínica de la homocisteína eh la especie humana
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Homocystinuria was firstly described in 19aS en children with learning difficulties, and in 19a9 McCully reported autopsy evidence of extensive arterial thrombosis and atherosclerosis in children with elevated plasma homocysteine concentrations and homocystinuria. Homocysteine, a sulfur amino acid, is an intermediate metabolite of methionine, and in the both cases mentioned , on the basis of these finding biochemical, they proposed that elevated plasma homocysteine (hyperhomocysteinemia) can cause neural injury and atherosclerotic vascular disease. Hyperhomocysteinemia is now well established as an independent risk factor for atherosclerotic vascular disease. Mild hyperhomocysteinemia is quite prevalent in the general population. It can be caused by genetic defects in the enzymes involved in homocysteine metabolism or nutritional deficiencies in vitamin cofactors, certain medications, high methionie intake or renal disease. The homocysteine concentration can be lowered with folate, and it’ s so vitamin supplementation has thus been proposed in individuals with hyperhomocysteinemia in order to reduce their cardiovas- cular disease risk. In this article, we review the biology, pathobiology and bioclinic of the metabolism of homocysteine.
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