Hyperhomocysteinemia: detection, risk assessment, and treatment
- 1 September 1997
- journal article
- review article
- Published by Wolters Kluwer Health in Current Opinion in Nephrology and Hypertension
- Vol. 6 (5) , 483-488
- https://doi.org/10.1097/00041552-199709000-00013
Abstract
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.Keywords
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