Suárez García I, Gómez Cerezo J F, Ríos Blanco J J, Barbado Hernández F J, Vázquez Rodríguez J J
Servicio de Medicina Interna, Hospital Universitario La Paz, Paseo de la Castellana, 261, 28046 Madrid.
An Med Interna. 2001 Apr;18(4):211-7.
Several epidemiologic studies have demonstrated that hyperhomocysteinemia is a risk factor for arteriosclerosis in coronary, cerebral, peripheral and aortic arteries. This risk is independent of other cardiovascular risk factors, and it is dose related. However, prospective studies show contradictory findings. Hyperhomocysteinemia is also associated with a higher risk of venous thrombosis to which other coagulation disorders, such as factor V Leiden, could contribute. Hyperhomocysteinemia can be due to genetic defects in the enzymes that control homocysteine metabolism, and also to other factors, mainly nutritional (deficiencies in vitamin B6, vitamin B12, or folic acid). Dietary supplements of these vitamins reduce plasma homocysteine levels. Randomized clinical trials are still needed to demonstrate that reducing plasma homocysteine levels will reduce the risk for cardiovascular disease.
多项流行病学研究表明,高同型半胱氨酸血症是冠状动脉、脑动脉、外周动脉和主动脉发生动脉硬化的一个危险因素。这种风险独立于其他心血管危险因素,且与剂量相关。然而,前瞻性研究显示出相互矛盾的结果。高同型半胱氨酸血症还与静脉血栓形成风险较高有关,其他凝血障碍(如因子V莱顿突变)可能也会导致这种情况。高同型半胱氨酸血症可能是由于控制同型半胱氨酸代谢的酶存在基因缺陷,也可能是由于其他因素,主要是营养方面的因素(维生素B6、维生素B12或叶酸缺乏)。补充这些维生素的膳食补充剂可降低血浆同型半胱氨酸水平。仍需要进行随机临床试验来证明降低血浆同型半胱氨酸水平是否会降低心血管疾病的风险。