Homocysteine: Role and implications in atherosclerosis

被引：166

作者：

Guthikonda S. ^{[1
]}

Haynes W.G. ^{[1
]}

机构：

[1] Department of Cardiology, Baylor College of Medicine, Houston, TX 77584

来源：

Current Atherosclerosis Reports | 2006年 / 8卷 / 2期

关键词：

Folic Acid; Homocysteine; Homocysteine Level; Hyperhomocysteinemia; Plasma Homocysteine;

D O I：

10.1007/s11883-006-0046-4

中图分类号：

学科分类号：

摘要：

Hyperhomocysteinemia promotes atherosclerosis and is most commonly caused by B-vitamin deficiencies, especially folic acid, B6, and B12; genetic disorders; certain drugs; and renal impairment. Elevated homocysteine promotes atherosclerosis through increased oxidant stress, impaired endothelial function, and induction of thrombosis. Prospective studies have shown that elevated plasma homocysteine concentrations increase risk of cardiovascular disease by twofold and risk of cerebrovascular disease to a lesser degree. Hyperhomocysteinemia should be identified in patients with progressive or unexplained atherosclerosis and treated appropriately. Treatment of hyperhomocysteinemia is primarily through vitamin supplementation; folic acid and vitamins B6 and B12 are the mainstay of therapy. Betaine and 5-methyl tetrahydrofolate are also effective in lowering homocysteine levels. Treatment of moderately elevated plasma homocysteine in patients without atherosclerosis should be deferred until the completion of randomized outcome trials. Copyright © 2006 by Current Science Inc.

引用

页码：100 / 106

页数：6

共 50 条

[1]

McCully K.S., Vascular pathology of homocysteinemia: Implications for the pathogenesis of arteriosclerosis, Am J Pathol, 56, pp. 111-128, (1969)

[2]

Stampfer M.J., Malinow M.R., Willett M.C., Et al., A prospective study of plasma homocysteine and risk of myocardial infarction in US physicians, JAMA, 268, pp. 877-881, (1992)

[3]

Kang S.S., Passen E.L., Ruggie N., Et al., Thermolabile defect of methylenetetrahydrofolate reductase in coronary artery disease, Circulation, 88, pp. 1463-1469, (1993)

[4]

Jacques P.F., Rosenberg I.H., Rogers G., Et al., Serum total homocysteine concentrations in adolescent and adult Americans: Results from the third national health and nutrition examination survey, Am J Clin Nutr, 69, pp. 482-489, (1999)

[5]

Selhub J., Jacques P.F., Wilson P.W., Et al., Vitamin status and intake as primary determinants of homocysteinemia in an elderly population, JAMA, 270, pp. 2693-2698, (1993)

[6]

Nygard O., Refsum H., Ueland P.M., Vollset S.E., Major lifestyle determinants of plasma total homocysteine distribution: The Hordaland homocysteine study, Am J Clin Nutr, 67, pp. 263-270, (1998)

[7]

Guttormsen A.B., Schneede J., Fiskerstrand T., Et al., Plasma concentrations of homocysteine and other aminothiol compounds are related to food intake in healthy human subjects, J Nutr, 124, pp. 1934-1941, (1994)

[8]

Graeber J.E., Slott J.H., Ulane R.E., Et al., Effect of homocysteine and homocystine on platelet and vascular arachidonic acid metabolism, Pediatr Res, 16, pp. 490-493, (1982)

[9]

Fryer R.H., Wilson B.D., Gubler D.B., Et al., Homocysteine, a risk factor for premature vascular disease and thrombosis, induces tissue factor activity in endothelial cells, Arterioscler Thromb, 13, pp. 1327-1333, (1993)

[10]

Lentz S.R., Sadler J.E., Inhibition of thrombomodulin surface expression and protein C activation by the thrombogenic agent homocysteine, J Clin Invest, 88, pp. 1906-1914, (1991)

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