Aster Richard H
Blood Research Institute, The Blood Center of Southeastern Wisconsin, PO Box 2178, Milwaukee, WI 53201-2178, USA.
Chest. 2005 Feb;127(2 Suppl):53S-59S. doi: 10.1378/chest.127.2_suppl.53S.
Agents that react with the platelet glycoprotein (GP) IIb/IIIa complex (alphaIIb/beta3 integrin) to block fibrinogen binding and platelet-platelet aggregation have been proved to be effective in reducing the incidence of complications following coronary angioplasty and are now widely used for this purpose. Acute thrombocytopenia, which is sometimes severe and life-threatening, is a recognized side effect of this class of drugs. In contrast to other types of drug-induced thrombocytopenia, this complication can occur within a few hours of a patient's first exposure to the medication. Accumulating evidence has indicated that drug-dependent antibodies, which can be naturally occurring, are the cause of platelet destruction in such individuals. In this review, we will consider the clinical aspects of thrombocytopenia resulting from sensitivity to GPIIb/IIIa inhibitors and will review evidence that the platelet destruction is antibody-mediated.
已证实,与血小板糖蛋白(GP)IIb/IIIa复合物(αIIb/β3整合素)发生反应以阻断纤维蛋白原结合及血小板-血小板聚集的药物,在降低冠状动脉血管成形术后并发症发生率方面是有效的,目前已广泛用于此目的。急性血小板减少症,有时严重且危及生命,是这类药物公认的副作用。与其他类型的药物性血小板减少症不同,这种并发症可在患者首次接触该药物后的数小时内发生。越来越多的证据表明,药物依赖性抗体(可为天然存在)是此类个体血小板破坏的原因。在本综述中,我们将探讨对GPIIb/IIIa抑制剂敏感所致血小板减少症的临床情况,并回顾血小板破坏是由抗体介导的证据。