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出 处:《医学综述》2009年第17期2664-2666,共3页Medical Recapitulate
摘 要:阿司匹林具有抗血小板聚集的作用。阿司匹林抵抗是指患者规律服用常规剂量的阿司匹林仍不能减少临床动脉血栓栓塞性缺血事件的发生,其可能机制包括依从性差、药物剂量不足、肠道吸收减少、药物间的相互作用;相关基因多态性、血小板更新加快、血栓素生成旁路途径等。明确抵抗机制并在临床上采取措施减少阿司匹林抵抗,将使广大患者获益,本文就近年来有关阿司匹林抵抗机制的新进展和新认识予以综述。Aspirin is an effective anti-platelet agent. Aspirin resistance (AR) is defined as the failure of Aspirin to prevent clinical atherothromboembolic ischaemic event in patients prescribed aspirin, the possible mechanisms of AR include poor compliance, aspirin underdose, decrease in intestinal absorption, drug inter- action, genetic ploymorphisms of cyclooxygenase-1, platelet glycoprotein Ⅱ b/Ⅲa and platelet ADP receptor P2Y1 ,increase turnover of platelet, and upregulation of alternate (non-platelet) pathways of thromboxane A2 production, and etc. Therefore,defining the mechanisms of AR and the clinical counter-measure to reduce AR will be of great benefit to patients with coronary artery disease. This article provides a brief review of new recognition and the research progress for mechanisms of aspirin resistance.
分 类 号:R543[医药卫生—心血管疾病] R973[医药卫生—内科学]
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