JAMA Surgery ( IF 15.7 ) Pub Date : 2018-10-01 , DOI: 10.1001/jamasurg.2018.1652 Areg Grigorian 1 , Sebastian Schubl 1 , Cristobal Barrios 1 , Victor Joe 1 , Matthew Dolich 1 , Michael Lekawa 1 , Jeffry Nahmias 1
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Heparin-induced thrombocytopenia (HIT) is a rare complication that has been reported to occur in 0.36% of trauma patients and is caused by antibody formation to complexes between heparin and platelet-factor 4 (PF4), leading to platelet activation and subsequent thrombosis.1,2 An earlier report demonstrated that PF4 can bind to bacteria, inducing an autoimmune response similar to the major antigen in HIT.3 We hypothesized that trauma patients with HIT have a higher incidence of bacterial infection during their hospitalization compared with patients without HIT. In addition, we provide a descriptive analysis of HIT in trauma patients.
中文翻译：
肝素诱导的血小板减少症与创伤患者细菌感染的关系
肝素诱导的血小板减少症（HIT）是一种罕见的并发症，据报道发生在0.36％的创伤患者中，由肝素和血小板因子4（PF4）之间复合物的抗体形成引起，导致血小板活化和随后的血栓形成。1 ，2先前的一份报告表明，PF4能结合细菌，诱导类似于在HIT的主要抗原的自身免疫应答。3我们假设与没有HIT的患者相比，具有HIT的创伤患者住院期间细菌感染的发生率更高。此外，我们提供了创伤患者中HIT的描述性分析。
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