Homocysteine and risk for atherothrombotic events

Homocysteine is formed during the metabolism of methionine. Plasma concentration of homocysteine depends on the activity of specific enzymes and/or serum concentration of folate, vitamin B6 and B12. Increased levels of plasma homocysteine are known to be an independent risk factor for atherothrombosis. Genetic and non-genetic causes are involved in the etiology of hyperhomocysteinemia. Several biochemical mechanisms underlie the vascular damage and the risk of thromboembolism associated with hyperhomocysteinemia. The overproduction of oxygen free radicals generated from the oxidation of homocysteine may be a major cause of endothelial injury and of the alterations in clotting and vascular function. New strategies have been suggested for the treatment of hyperhomocysteinemia, but more epidemiological data and clinical trials are needed.