Tran Michael, Sheth Chirag, Bhandari Rohan, Cameron Scott J, Hornacek Deborah
Heart Vascular and Thoracic Institute, Department of Cardiovascular Medicine, Section of Vascular Medicine, Cleveland Clinic Foundation, Desk J-35, Cleveland Clinic Foundation, Cleveland, OH 44195 USA.
Department of Cardiovascular and Metabolic Sciences. Cleveland Clinic Lerner College of Medicine, Cleveland, OH 44195 USA.
Thromb J. 2020 Sep 3;18:16. doi: 10.1186/s12959-020-00229-8. eCollection 2020.
Patients infected with SARS-CoV-2 often develop venous and arterial thrombosis. The high patient mortality is partly attributed to thrombotic events. An emerging trend is the presence of immunological phenomena including antiphospholipid antibodies which may promote thrombosis. The mechanism for these observations is not clear though many patients with SARS-CoV-2 develop thrombocytopenia.
We describe a patient with SARS-CoV-2 pneumonitis who presented with intermediate risk pulmonary embolism (PE). Careful attention to his daily platelet count suggested the possibility of immune mediated heparin-induced thrombocytopenia (HIT) which was confirmed by laboratory testing and resolved when anticoagulation was switched to a direct thrombin inhibitor.
Since excessive platelet activation and in situ thrombosis occur in HIT, this case underscores the need to consider that thrombocytopenia in patients with SARS-CoV-2-most of whom receive heparinoids-may be unrecognized HIT. A central role for the platelet in the etiology of thrombosis during the COVID-19 pandemic should be explored.
感染严重急性呼吸综合征冠状病毒2（SARS-CoV-2）的患者常出现静脉和动脉血栓形成。患者的高死亡率部分归因于血栓形成事件。一个新出现的趋势是存在包括抗磷脂抗体在内的免疫现象，这些现象可能促进血栓形成。尽管许多感染SARS-CoV-2的患者会出现血小板减少症，但这些观察结果的机制尚不清楚。
我们描述了一名患有SARS-CoV-2肺炎的患者，该患者出现中度风险的肺栓塞（PE）。仔细关注他的每日血小板计数提示可能存在免疫介导的肝素诱导的血小板减少症（HIT），实验室检测证实了这一点，当抗凝治疗改为直接凝血酶抑制剂时，该症状得到缓解。
由于HIT中会出现血小板过度活化和原位血栓形成，该病例强调了需要考虑到，感染SARS-CoV-2的患者（其中大多数接受类肝素治疗）出现的血小板减少症可能是未被识别的HIT。应探讨血小板在2019冠状病毒病大流行期间血栓形成病因中的核心作用。
