Biswas Arijit, Ranjan Ravi, Meena Arvind, Akhter Mohammad Suhail, Yadav Birendra Kumar, Munisamy Murali, Subbiah Vivekanandhan, Behari Madhuri, Saxena Renu
Department of Hematology, All India Institute of Medical Sciences, New Delhi, India.
J Stroke Cerebrovasc Dis. 2009 Mar-Apr;18(2):103-10. doi: 10.1016/j.jstrokecerebrovasdis.2008.09.014.
Homocysteine has been for a fairly long time been debated to be a risk factor for stroke. Opinions are divided as to whether raised levels of homocysteine seen in stroke patients are the cause or consequence of stroke. A large number of studies have been conducted in the Caucasian as well as on the Oriental population, which tend to suggest contradictory findings at many times. However, there have been no reports forthcoming from the Asian Indian population, which is a genetically different population than the previously studied populations.
In our present study, we looked at homocysteine levels and four commonly seen polymorphisms of homocysteine metabolizing enzymes and their respective prevalence in 120 acute onset ischemic stroke patients compared with an equal number of age and gender matched healthy population. We also tested the influence of folic acid dosage (5 mg OD) on the levels of homocysteine and the allied vitamin supplements, vitamin B12 and folate in smaller groups selected from the larger group.
We found homocysteine levels to be significantly raised in the stroke population compared with healthy controls [patients: 12 micromol/L (range: 5.3-39.1 micromol/L), controls: 11.2 micromol/L (range: 6.2-14.2 micromol/L); P =0.001]. There was an almost total response to folic acid dosage as all hyperhomocysteinemic patients showed lowering of homocysteine levels in response to the dosage. The MTHFR 677 C > T polymorphisms showed association with both homocysteine levels as well as stroke (P < 0.001). Nutritional deficiency plays a dominant role in hyperhomocysteinemic conditions in our stroke population, however. Genetic determinants of homocysteine level may also have some part in determining hyperhomocysteinemic conditions in the Asian Indian populations.
很长一段时间以来，同型半胱氨酸一直被认为是中风的一个风险因素。对于中风患者中同型半胱氨酸水平升高是中风的原因还是结果，存在不同观点。已经在白种人和东方人群中进行了大量研究，这些研究往往多次得出相互矛盾的结果。然而，亚洲印度人群尚未有相关报道，该人群在基因上与之前研究的人群不同。
在我们目前的研究中，我们观察了120例急性缺血性中风患者与同等数量年龄和性别匹配的健康人群的同型半胱氨酸水平以及同型半胱氨酸代谢酶的四种常见多态性及其各自的患病率。我们还在从较大组中选出的较小组中测试了叶酸剂量（5毫克每日一次）对同型半胱氨酸水平以及相关维生素补充剂（维生素B12和叶酸）的影响。
我们发现中风人群的同型半胱氨酸水平与健康对照组相比显著升高[患者：12微摩尔/升（范围：5.3 - 39.1微摩尔/升），对照组：11.2微摩尔/升（范围：6.2 - 14.2微摩尔/升）；P = 0.001]。几乎所有高同型半胱氨酸血症患者对叶酸剂量都有反应，即同型半胱氨酸水平因剂量而降低。MTHFR 677 C>T多态性与同型半胱氨酸水平以及中风均有关联（P < 0.001）。然而，在我们的中风人群中，营养缺乏在高同型半胱氨酸血症情况中起主导作用。同型半胱氨酸水平的遗传决定因素在亚洲印度人群高同型半胱氨酸血症情况的决定中可能也起一定作用。
