Hyperhomocysteinemia and Thrombosis: An Overview (Report)
Homocysteine is a sulfur-containing amino acid absent in naturally occurring dietary sources. It is closely related to the essential amino acid methionine and to cysteine. Butz and Du Vigneaud (1) described the formation of homocystine from treating methionine with concentrated acid. Homocysteine is a metabolic intermediary in transmethylation and transsulfuration reactions. S-Adenosylmethionine (SAM), an intermediary in the methionine-homocysteine cycle, is an essential methyl donor in more than 100 known reactions including methylation of nucleic acids, proteins, phospholipids, myelin, polysaccharides, choline, and catecholamines. Impaired methylation is associated with abnormal cellular growth, differentiation, and function. The synthesis of glutathione, an important endogenous antioxidant, is dependent on the transsulfuration of homocysteine. Aberrant homocysteine metabolism is associated with many disorders. In 1969, McCully (2) first described the association between homocystinemia and premature atherosclerotic vascular disease in homocystinuria. Presently, hundreds of publications discuss abnormal plasma homocysteine levels and various diseases. Hyperhomocysteinemia increases the likelihood of developing atherosclerosis. Hyperhomocysteinemia, alone or with other thrombophilic risk factors, may be associated with vascular occlusive pathology underlying varied clinical presentations.