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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Effects of vitamin therapy on plasma total homocysteine, endothelial injury markers, and fibrinolysis in stroke patients
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Effects of vitamin therapy on plasma total homocysteine, endothelial injury markers, and fibrinolysis in stroke patients

机译：维生素治疗对中风患者血浆总同型半胱氨酸，内皮损伤标志物和纤维蛋白溶解的影响

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Hyperhomocystinemia linked to B-vitamin deficiency is prevalent and associated with increased risk for stroke. While in vitro studies suggest homocysteine directly injures vascular endothelial thrombomodulin (TM), inhibits vonWillebrand factor (vWF) synthesis, and blocks tissue plasminogen activator (t-PA) receptor binding, these mechanisms and their reversibility by vitamin therapy are not established in humans. We investigated the effects of high-dose B-vitamin therapy on endogenous fibrinolysis and endothelial injury markers by randomizing 50 nonvitamin users with prior ischemic stroke to 3 months of treatment with multivitamins either containing folate (5 mg), B6 (100 mg), and B12 (1 mg), or lacking these components. Fasting before noon and post-methionine load plasma total homocysteine (tHcy), t-PA antigen levels, t-PA and plasminogen activator inhibitor (PAI) activities, total vWF antigen, and TM levels were measured before and after vitamin therapy. The primary analysis between treatment groups across time revealed no significant changes (P > .1) for any hematologic variables. However, within-groups analysis showed reductions of 23% in plasma TM (P < .005) and 27% in fasting tHcy levels (P < .0001) and a paradoxical 30% rise in vWF antigen levels (P < .05) after high-dose B-vitamin, treatment with no changes in controls. Pooled data revealed a significant and reproducible 20% to 28% decline in plasma t-PA activity after methionine load (n = 49, P < .02). Our findings demonstrate methionine load lowers plasma t-PA activity by a plasminogen activator inhibitor (PAI-1) independent mechanism that is not attenuated by 3 months of high-dose B-vitamin treatment. While not improving endogenous fibrinolysis profiles, these results provide initial evidence that B-vitamin treatment may selectively alter markers of vascular endothelial injury after stroke. Copyright < copyright > 2002 by National Stroke Association.
机译：与B族维生素缺乏症相关的高同型胱氨酸血症很普遍，并与中风风险增加相关。尽管体外研究表明高半胱氨酸会直接伤害血管内皮血栓调节蛋白（TM），抑制vonWillebrand因子（vWF）合成并阻止组织纤溶酶原激活剂（t-PA）受体结合，但是这些机制及其在维生素治疗中的可逆性尚未在人类中确立。我们通过将50名先前有缺血性卒中的非维生素使用者随机分为3种使用叶酸（5 mg，B 6）的复合维生素治疗3个月，研究了大剂量B维生素疗法对内源性纤溶和内皮损伤指标的影响。 inf>（100毫克）和B 12 （1毫克），或缺少这些成分。在维生素治疗前后测定空腹和蛋氨酸负荷后的空腹血浆总同型半胱氨酸（tHcy），t-PA抗原水平，t-PA和纤溶酶原激活物抑制剂（PAI）活性，总vWF抗原和TM水平。治疗组之间不同时间的初步分析显示，任何血液学变量均无显着变化（P> .1）。然而，组内分析显示，血浆TM降低23％（P <.005），空腹tHcy水平降低27％（P <.0001），而vWF抗原水平降低30％（P <.05），这是矛盾的。大剂量B-维生素，治疗无变化。汇总数据显示，蛋氨酸负荷后血浆t-PA活性显着且可重现降低20％至28％（n = 49，P <.02）。我们的发现表明蛋氨酸负荷通过纤溶酶原激活物抑制剂（PAI-1）独立的机制降低了血浆t-PA活性，这种机制在3个月的大剂量B-维生素治疗中不会减弱。这些结果虽然没有改善内源性纤溶作用，但提供了初步证据表明B-维生素治疗可能选择性改变卒中后血管内皮损伤的标志物。国家卒中协会版权所有2002。

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