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首页> 外文期刊>Journal of cardiothoracic and vascular anesthesia >Heparin-induced thrombocytopenia during extracorporeal membrane oxygenation
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Heparin-induced thrombocytopenia during extracorporeal membrane oxygenation

机译:体外膜氧合期间肝素诱导的血小板减少

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摘要

HEPARIN-INDUCED THROMBOCYTOPENIA (HIT) is an immune-mediated adverse effect of heparin therapy. Two clinical entities of HIT can be distinguished: HIT I and HIT n. HIT I is a harmless pharmacologic phenomenon associated with decreased platelet count within 24-48 h after initiation of heparinization. Unlike HIT n, it is not associated with thrombosis and does not necessitate discontinuation of heparin. In contrast, HIT II can cause both bleeding and thrombotic complications. It is the most important and most frequent drug-induced immunologic thrombocytopenia.Besides orthopedic and vascular surgery patients, patients after cardiac surgery are at highest risk of developing HIT II (1-5%). Its clinical importance is based on its strong association with venous and arterial thrombosis and thromboembolism (heparin-induced thrombocytopenia with associated thrombosis, HITT). HIT is caused by the development of an IgG antibody that recognizes multimolecular complexes of platelet factor 4 (PF4) and heparin.
机译:肝素诱导的血小板减少症(HIT)是肝素治疗的免疫介导的不良反应。 HIT的两个临床实体可以区分:HIT I和HIT n。 HIT I是一种无害的药理学现象,与肝素化开始后24-48小时内血小板计数减少有关。与HIT n不同,它与血栓形成无关,也不需要中断肝素。相反,HIT II可能导致出血和血栓并发症。它是最重要,最频繁的药物诱导的免疫性血小板减少症。除了整形外科和血管外科手术患者,心脏手术后的患者发生HIT II的风险最高(1-5%)。其临床重要性是基于其与静脉和动脉血栓形成和血栓栓塞(肝素诱导的血小板减少症及相关血栓形成,HITT)的强烈关联。 HIT是由能够识别血小板因子4(PF4)和肝素的多分子复合物的IgG抗体引起的。

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