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肝素诱导的血小板减少症——发病机制与治疗

Heparin-induced thrombocytopenia--pathogenesis and treatment.

作者信息

Greinacher A

机构信息

Institute for Immunology and Transfusion Medicine, Ernst-Moritz-Arndt-University, Greifswald, Germany.

出版信息

Thromb Haemost. 1999 Sep;82 Suppl 1:148-56.

PMID:10695507
Abstract

Heparin-induced thrombocytopenia (HIT) is now recognized as the most frequent immune-mediated adverse drug reaction. During the last decade, fundamental aspects of the pathogenesis of HIT have been resolved. The understanding of some the mechanisms underlying the development of new, paradox thromboembolic complications in HIT led to the concept that thrombin generation plays a key-role in clinically manifest HIT. Consequently new therapeutic concepts imply the use of drugs with either indirect or direct anti-thrombin activity such as donaparoid-sodium and the recombinant hirudin lepirudin. During the last years results of first prospective studies assessing various treatment regimens in HIT became available. Although data of randomized trials are still missing some treatment recommendations can already be drawn from these studies. This review summarizes key aspects of the pathogenesis of HIT and provides an overview of current treatment strategies.

摘要

肝素诱导的血小板减少症(HIT)目前被认为是最常见的免疫介导的药物不良反应。在过去十年中,HIT发病机制的基本方面已得到解决。对HIT中新出现的矛盾性血栓栓塞并发症发生发展的一些潜在机制的理解,引出了凝血酶生成在临床显性HIT中起关键作用的概念。因此,新的治疗概念意味着使用具有间接或直接抗凝血酶活性的药物,如达那肝素钠和重组水蛭素比伐卢定。在过去几年中,评估HIT各种治疗方案的首批前瞻性研究结果已经问世。尽管随机试验的数据仍然缺失,但已经可以从这些研究中得出一些治疗建议。本综述总结了HIT发病机制的关键方面,并概述了当前的治疗策略。

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