Vw. Dennis et al., HYPERHOMOCYSTEINEMIA - DETECTION, RISK ASSESSMENT, AND TREATMENT, Current opinion in nephrology and hypertension, 6(5), 1997, pp. 483-488
Homocysteine is formed by the demethylation of methionine in the cours
e of its normal metabolism. Hyperhomocysteinemia is an independent ris
k factor for vascular disease. It develops most commonly from folate d
eficiency, genetic abnormalities, and chronic renal failure. Current m
odels favor direct angiotoxicity involving endothelial and vascular sm
ooth muscle cells, and impaired thrombolysis. Folic acid reduces hyper
homocysteinemia and thus provides an opportunity for risk-factor modif
ication.