Dorsch Michael P, Montague Debbie, Rodgers Jo E, Patterson Cam
Department of Pharmacy Services, University of Michigan Hospitals and Health Clinics, Ann Arbor, Michigan 48109, USA.
Pharmacotherapy. 2006 Mar;26(3):423-7. doi: 10.1592/phco.26.3.423.
A 62-year-old man with a history of coronary artery disease and coronary artery bypass graft, chronic heart failure, and peripheral vascular disease required percutaneous coronary intervention (PCI) after progression of shortness of breath and fatigue over 2 years. Four hours after the procedure, the patient developed hematemesis and was found to be thrombocytopenic. The thrombocytopenia was presumed to be due to the abciximab infusion the patient received during and shortly after the PCI. Further review of the patient's medical history revealed that a similar episode had occurred 11 years earlier. At that time, he was enrolled in a clinical trial comparing tirofiban and heparin in patients with unstable angina; he developed profound thrombocytopenia within 24 hours of randomization. After the study unblinding, investigators discovered that the patient received tirofiban, which was thought to be the cause of his thrombocytopenia. Both abciximab and tirofiban are glycoprotein IIb-IIIa inhibitors, and thrombocytopenia induced by this class of drugs is a serious and potentially life-threatening adverse reaction. The mechanism is not well understood but has been described as immune mediated with both ligand-mimetic agents (tirofiban and eptifibatide) and abciximab. Our patient's situation was unusual in that he developed thrombocytopenia from a ligand-mimetic agent and subsequently had a similar reaction to abciximab. To our knowledge, this case report is the first documentation of thrombocytopenia associated with both tirofiban and abciximab in a single patient, and suggests that care should be given in administering glycoprotein IIb-IIIa inhibitors of either type to patients with a history of thrombocytopenia due to one of these agents.
一名62岁男性,有冠状动脉疾病、冠状动脉旁路移植术、慢性心力衰竭和外周血管疾病史,在2年中出现气短和疲劳加重后需要进行经皮冠状动脉介入治疗(PCI)。术后4小时,患者出现呕血,且发现血小板减少。血小板减少被推测是由于患者在PCI期间及术后不久接受了阿昔单抗输注。进一步查阅患者病史发现,11年前曾发生过类似情况。当时,他参加了一项比较替罗非班和肝素治疗不稳定型心绞痛患者的临床试验;随机分组后24小时内他出现了严重的血小板减少。研究揭盲后,研究人员发现该患者接受了替罗非班,认为这是其血小板减少的原因。阿昔单抗和替罗非班都是糖蛋白IIb-IIIa抑制剂,这类药物引起的血小板减少是一种严重且可能危及生命的不良反应。其机制尚不完全清楚,但已被描述为与配体模拟剂(替罗非班和依替巴肽)及阿昔单抗均有关的免疫介导。我们患者的情况不同寻常,他先因一种配体模拟剂出现血小板减少,随后对阿昔单抗产生了类似反应。据我们所知,本病例报告是首例记录单一患者同时发生与替罗非班和阿昔单抗相关的血小板减少的情况,提示对于有因其中一种药物导致血小板减少病史的患者,给予任何一种糖蛋白IIb-IIIa抑制剂时都应谨慎。