Homocyst(e)ine, atherosclerosis, and thrombosis.
Ample clinical and epidemiologic evidence exists to implicate homocyst(e)ine as a risk factor for atherosclerotic vascular disease and thrombosis. The precise mechanisms by which this occurs are uncertain but probably involve injury to endothelium, impairment of endothelial function, lipid peroxidation, oxidation of low-density lipoprotein, and creation of a prothrombotic environment in areas of endothelial injury. Plasma homocyst(e)ine concentration (PHC) can be effectively reduced with oral administration of folic acid. Whether vitamins B6 and B12 are also required in the absence of vitamin deficiency remains uncertain. Studies currently in progress may help to determine whether reduction of PHC will translate into a decrease in clinical vascular events.
Alpert
M A
MA
Division of Cardiology, University of South Alabama College of Medicine, Mobile, USA.
D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000503:physiopathology / Q000517:prevention & control*; D005260:Female; D005492:Folic Acid / Q000627:therapeutic use; D006710:Homocysteine / Q000378:metabolism*; D006711:Homocystine / Q000378:metabolism*; D006712:Homocystinuria / Q000235:genetics; D006801:Humans; D020138:Hyperhomocysteinemia / Q000209:etiology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D013927:Thrombosis / Q000503:physiopathology / Q000517:prevention & control*
D006710:Homocysteine; D006711:Homocystine; D005492:Folic Acid