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作 者:李达伟 田文艳[1] 梁程钰 陈兆基 Li Dawei;Tian Wenyan;Liang Chengyu;Chen Zhaoji(Department o f Neurology y Affiliated Hospital o f Hebei University,Baoding 071000,China)
出 处:《神经疾病与精神卫生》2020年第3期214-219,共6页Journal of Neuroscience and Mental Health
摘 要:在破裂的动脉粥样硬化斑块溃疡上,活化的血小板聚集导致血栓形成.阿司匹林是临床最常用的抗血小板聚集药物之一,但是部分患者服用阿司匹林后不能有效地抑制血小板聚集,产生阿司匹林抵抗现象,导致血栓事件再次发生.随着分子生物学技术的飞速发展及人类基因组计划的开展,越来越多的研究证实,遗传因素在血栓事件中发挥着重要的作用.基因变异会对血小板功能产生影响,导致血小板活性增加,影响阿司匹林治疗后的残存血小板聚集.现通过回顾国内外与单核苷酸多态性导致阿司匹林抵抗有关的研究,进一步认识了阿司匹林抵抗的遗传因素.Activated platelets accumulate on ruptured atherosclerotic plaque ulcers,leading to thrombosis.Aspirin is one of the most commonly used antiplatelet aggregation drugs in practice.However,some patients cannot effectively inhibit platelet aggregation after taking aspirin,resulting in aspirin resistance and leading to the recurrence of thrombus events.With the rapid development of molecular biology technology and the human genome project,increasing studies have confirmed that genetic factors play an essential role in thrombus events.Genetic variations can affect platelet function,lead to increased platelet activity,and affect residual platelet aggregation after aspirin treatment.This review provides a further understanding of the genetic factors of aspirin resistance by reviewing domestic and international studies on the role of single nucleotide polymorphisms in aspirin resistance.
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