Homocysteine and vitamins in cardiovascular disease.
Homocysteine and vitamins in cardiovascular disease.
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DOI：
10.1093/clinchem/44.8.1833
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发表时间：
1998-08
影响因子：
9.3
通讯作者：
D. Jacobsen
中科院分区：
文献类型：
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作者：
D. Jacobsen
基于最近的回顾性和前瞻性研究，现在广泛接受血浆总同型半胱氨酸升高是心血管疾病的危险因素。由于基因突变或缺乏必需的B族维生素叶酸、B12和B6而导致酶功能受损可导致高同型半胱氨酸血症。氧化型同型半胱氨酸占血浆同型半胱氨酸总量的98-99%。尽管尚不确定同型半胱氨酸升高是否是心血管疾病的原因或仅仅是心血管疾病的代表，但一些证据表明它可能在动脉粥样硬化性血栓形成疾病中发挥作用。同型半胱氨酸似乎改变了内皮细胞的抗凝特性，使其成为促凝血表型。轻度升高的同型半胱氨酸会导致血管内皮功能障碍。叶酸能有效降低血浆中的同型半胱氨酸浓度。因此，迫切需要进行干预研究，以确定降低同型半胱氨酸是否能有效降低心血管疾病的发病率和死亡率。
On the basis of recent retrospective and prospective studies, it is now widely accepted that increased total plasma homocysteine is a risk factor for cardiovascular disease. Impaired enzyme function as a result of genetic mutation or deficiency of the essential B vitamins folic acid, B12, and B6 can lead to hyperhomocysteinemia. Oxidized forms of homocysteine account for 98-99% of total plasma homocysteine. Although there is uncertainty as to whether increased homocysteine is causal or merely a proxy for cardiovascular disease, several lines of evidence suggest that it may play a role in atherothrombotic disease. Homocysteine appears to alter the anticoagulant properties of endothelial cells to a procoagulant phenotype. Mildly increased homocysteine causes dysfunction of the vascular endothelium. Folic acid effectively lowers homocysteine concentration in the plasma. Intervention studies are urgently needed to determine if lowering homocysteine is effective in decreasing the morbidity and mortality of cardiovascular disease.