Mattioli Maria, Paoli Giorgia, Cambò Benedetta, Bonura Rosario
Unità di Terapia Intensiva Coronarica (UTIC), Cardiology Unit, Parma University Hospital, Parma, Italy.
Ematologia e CTMO, Parma University Hospital, Parma, Italy.
Eur Heart J Case Rep. 2023 Jan 7;7(1):ytad005. doi: 10.1093/ehjcr/ytad005. eCollection 2023 Jan.
Glycoprotein (GP) IIb-IIIa inhibitors are antithrombotic drugs used in selected patients during and after percutaneous coronary interventions (PCIs), usually as a bail-out in the setting of no-reflow or thrombotic complications. A notorious life-threatening adverse effect of this drug class is immune-mediated drug-induced thrombocytopenia (DITP). Thrombotic microangiopathy (TMA) induced by GP IIb-IIIa inhibitors has never been reported.
A 72-year-old woman admitted for anterior myocardial infarction treated with primary PCI and stent implantation underwent a first tirofiban infusion as a bail-out strategy. After a new procedure for stent thrombosis, she received a second tirofiban infusion and developed sudden severe thrombocytopenia (platelet count <20 000/µL). Tirofiban was stopped but no observed increase in platelet count. Acute kidney injury due to renal ischaemia and left ventricular thrombosis followed. Unexpectedly, evidence for haemolysis and schistocytosis at peripheral blood smear prompted a diagnosis of TMA. Plasma exchange was immediately started with evidence for initial increase in platelet count, but the patient died due to sudden haemodynamic and respiratory deterioration.
Tirofiban is known to rarely cause immune-dependent DITP. However, it has never been associated with TMA. This case report not only describes the first case of probable tirofiban-induced TMA, but also highlights the importance of a systematic approach to severe thrombocytopenia, even in the setting of low platelet count from a known DITP-related drug. Treatment of TMA in the difficult context of recent myocardial infarction and stent thrombosis requires a complex interplay between cardiologist, haematologist, transfusionist, and nephrologist, carefully balancing thrombotic and haemorrhagic risk.
糖蛋白（GP）IIb-IIIa抑制剂是用于经皮冠状动脉介入治疗（PCI）期间及术后特定患者的抗血栓药物，通常在出现无复流或血栓形成并发症时作为补救措施使用。这类药物一个众所周知的危及生命的不良反应是免疫介导的药物性血小板减少症（DITP）。从未有过关于GP IIb-IIIa抑制剂诱发血栓性微血管病（TMA）的报道。
一名72岁女性因前壁心肌梗死入院，接受了直接PCI和支架植入治疗，作为补救策略首次输注替罗非班。在因支架血栓形成进行了新的手术后，她接受了第二次替罗非班输注，并突然出现严重血小板减少（血小板计数<20 000/µL）。停用替罗非班，但血小板计数未观察到增加。随后出现了因肾缺血导致的急性肾损伤和左心室血栓形成。出乎意料的是，外周血涂片显示有溶血和裂红细胞增多的证据，提示诊断为TMA。立即开始血浆置换，血小板计数初步增加，但患者因突然的血流动力学和呼吸恶化而死亡。
已知替罗非班很少引起免疫依赖性DITP。然而，它从未与TMA相关联。本病例报告不仅描述了首例可能由替罗非班诱发的TMA，还强调了即使在已知与DITP相关药物导致血小板计数较低的情况下，对严重血小板减少采取系统方法的重要性。在近期心肌梗死和支架血栓形成的困难背景下治疗TMA需要心脏病专家、血液科医生、输血科医生和肾内科医生之间复杂的相互协作，仔细平衡血栓形成和出血风险。
