Russell Kimberly N, Schnabel Joseph G, Rochetto Richard P, Tanner Matthew C
College of Pharmacy, Oregon State University, Corvallis, Oregon, USA.
Pharmacotherapy. 2009 Jul;29(7):867-74. doi: 10.1592/phco.29.7.867.
The glycoprotein IIb-IIIa inhibitor eptifibatide has been shown to be beneficial in the treatment of acute coronary syndromes and during percutaneous coronary intervention (PCI). Case reports of acute profound thrombocytopenia have been reported with eptifibatide, yet the true incidence of this reaction is unknown. We describe a 50-year-old woman with severe coronary artery disease who developed acute profound thrombocytopenia after readministration of eptifibatide. Eptifibatide was administered through hospital day 3, when it was discontinued in preparation for coronary angiography and PCI; the drug was restarted on day 5. On hospital day 6, she was noted to have a platelet count below 5 x 10(3)/mm,(3) indicating a profound decrease from a baseline of 456 x 10(3)/mm(3) on admission. Eptifibatide, heparin, vancomycin, and clopidogrel were potential causative agents. Anticoagulation and vancomycin were stopped, and her platelet count increased to 30 x 10(3)/mm(3) on day 7. Subsequent reexposure to heparin and vancomycin yielded no adverse effects. The patient's platelet count increased over the remainder of her hospitalization, and she was discharged home on day 19. Based on clinical presentation and negative heparin platelet factor 4 antibody test, eptifibatide was the most likely cause of thrombocytopenia. Use of the Naranjo adverse drug reaction probability scale indicated that eptifibatide was the probable cause of thrombocytopenia (score of 5); scores of 1 (possible) or 0 (doubtful) were derived with heparin, vancomycin, and clopidogrel. We conducted a literature search and compiled information from published case reports to describe the pattern of onset and recovery of eptifibatide-induced thrombocytopenia. In all patients receiving eptifibatide, routine platelet counts should be monitored at baseline and within 2-6 hours after starting the drug.
糖蛋白IIb-IIIa抑制剂依替巴肽已被证明在治疗急性冠状动脉综合征及经皮冠状动脉介入治疗(PCI)期间有益。有依替巴肽导致急性严重血小板减少的病例报告,但这种反应的真实发生率尚不清楚。我们描述了一名50岁患有严重冠状动脉疾病的女性,在再次使用依替巴肽后发生了急性严重血小板减少。依替巴肽持续使用至住院第3天,为准备冠状动脉造影和PCI而停药;第5天重新开始用药。在住院第6天,发现她的血小板计数低于5×10³/mm³,表明与入院时456×10³/mm³的基线相比大幅下降。依替巴肽、肝素、万古霉素和氯吡格雷均可能是致病因素。停用抗凝药和万古霉素后,她的血小板计数在第7天升至30×10³/mm³。随后再次接触肝素和万古霉素未产生不良反应。患者的血小板计数在住院剩余时间内升高,她于第19天出院。根据临床表现及肝素血小板因子4抗体检测阴性,依替巴肽最有可能是血小板减少的原因。使用Naranjo药物不良反应概率量表表明依替巴肽是血小板减少的可能原因(评分为5分);肝素、万古霉素和氯吡格雷的评分为1分(可能)或0分(可疑)。我们进行了文献检索,并从已发表的病例报告中收集信息,以描述依替巴肽所致血小板减少的起病和恢复模式。在所有接受依替巴肽治疗的患者中,应在基线时及开始用药后2 - 6小时内监测常规血小板计数。