Hyperhomocysteinemia: detection, risk assessment, and treatment.
Homocysteine is formed by the demethylation of methionine in the course of its normal metabolism. Hyperhomocysteinemia is an independent risk factor for vascular disease. It develops most commonly from folate deficiency, genetic abnormalities, and chronic renal failure. Current models favor direct angiotoxicity involving endothelial and vascular smooth muscle cells, and impaired thrombolysis. Folic acid reduces hyperhomocysteinemia and thus provides an opportunity for risk-factor modification.
Dennis
V W
VW
Department of Nephrology and Hypertension, Cleveland Clinic Foundation, OH 44195, USA. dennisv@cesmtp.ccf.org
Nurko
S
S
Robinson
K
K
D000818:Animals; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism; D008715:Methionine / Q000378:metabolism*; D012307:Risk Factors; D014652:Vascular Diseases / Q000097:blood / Q000209:etiology* / Q000517:prevention & control
D006710:Homocysteine; D008715:Methionine