缺血性卒中和真性红细胞增多症患者的血栓形成性

M. Tanashyan, A. Shabalina, E. Roitman, T. Vavilova, P. Kuznetsova
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引用次数: 3

摘要

缺血性卒中(IS)和真性红细胞增多症(PV)患者的血栓形成及其原因是一个重要的临床问题。本研究的目的是确定与IS和既往PV患者血栓形成性增加相关的因素范围。我们对127例处于超急性脑卒中期及其后16-18个月的患者进行了体格检查和实验室检查。其中有PV 68例(主要组),无PV 59例(对照组)。通过实验室检查评估血液流变学、止血、内皮功能、血管生成、促炎细胞因子水平;我们还测试了患者JAK2基因中V617F突变的存在,并分析了所有研究参数对血栓和出血性并发症发展的贡献。我们发现两组之间的神经学图像没有差异:NIHSS平均得分分别为12分和13分。比较IS患者和既往PV患者与对照组的红细胞和血小板形态学和功能特征、止血和细胞因子谱。JAK2 V617F等位基因负担是增加IS和PV患者血栓性并发症的关键因素之一。所获得的数据表明,已确定的促进卒中后PV患者血栓形成的因素的累积效应超过了抗血小板治疗的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Thrombogenicity in patients with ischemic stroke and pre-existing polycythemia vera
Thrombogenicity and its causes in patients with ischemic stroke (IS) and pre-existing polycythemia vera (PV) is a significant clinical concern. The aim of this study was to identify the range of factors associated with increased thrombogenicity in patients with IS and pre-existing PV. We performed a physical examination and laboratory tests on 127 patients in the hyperacute stroke stage and 16-18 months after. Of them, 68 patients had PV (the main group) and 59 did not have this condition (the comparison group). Laboratory tests were conducted to evaluate blood rheology, hemostasis, endothelial function, angiogenesis, proinflammatory cytokine levels; we also tested patients for the presence of the V617F mutation in the JAK2 gene and analyzed the contribution of all studied parameters to the development of thrombotic and hemorrhagic complications. We found that the neurological picture did not differ between the groups: mean NIHSS scores were 12 and 13 points, respectively. Morphological and functional characteristics of red blood cells and platelets, hemostasis and cytokine profiles were compared between patients with IS and pre-existing PV and the comparison group. One of the key elements in potentiating thrombotic complications in patients with IS and PV was JAK2 V617F allele burden. The obtained data suggest the cumulative effect of the identified factors promoting thrombus formation in post-stroke patients with PV and overpowering the effect of antiplatelet therapy.
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