The Treatment of Hyperhomocysteinemia

被引:214
作者
Maron, Bradley A. [1 ]
Loscalzo, Joseph [1 ]
机构
[1] Harvard Univ, Brigham & Womens Hosp, Dept Med, Sch Med,Cardiovasc Div, Boston, MA 02115 USA
来源
ANNUAL REVIEW OF MEDICINE | 2009年 / 60卷
关键词
B vitamins; folic acid; cardiovascular risk factor; cognitive impairment; clinical trials; osteoporosis; FOLIC-ACID SUPPLEMENTATION; HUMAN ENDOTHELIAL-CELLS; CHRONIC KIDNEY-DISEASE; SMOOTH-MUSCLE-CELLS; STAGE RENAL-DISEASE; PLASMA HOMOCYSTEINE; CARDIOVASCULAR EVENTS; VASCULAR-DISEASE; B-VITAMINS; LOWERING HOMOCYSTEINE;
D O I
10.1146/annurev.med.60.041807.123308
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The unique biochemical profile of homocysteine is characterized by chemical reactivity supporting a wide range of molecular effects and by a tendency to promote oxidant stress-induced cellular toxicity. Numerous epidemiological reports have established hyperhomocysteinemia as an independent risk factor for cardiovascular disease, cerebrovascular disease, dementia-type disorders,and osteoporosis-associated fractures. Although combined folic acid and B-vitamin therapy substantially reduces homocysteine levels, results from randomized placebo-controlled clinical trials testing the effect of vitamin therapy on outcome in these diseases have generally fallen short of expectations. These results have led some to abandon homocysteine monitoring in the management of patients with cardiovascular or cognitive disorders. These trials, however, have generally included patients with only mildly elevated homocysteine levels and have not addressed several clinical scenarios in which homocysteine reduction may be effective, including the primary prevention of atherothrombotic disease in individuals at low or intermediate risk, or those with severe hyperhomocysteinemia.
引用
收藏
页码:39 / 54
页数:16
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