Arepally Gowthami M
Division of Hematology, Duke University Medical Center, Durham, NC.
Blood. 2017 May 25;129(21):2864-2872. doi: 10.1182/blood-2016-11-709873. Epub 2017 Apr 17.
Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. Pathogenic antibodies to PF4/heparin bind and activate cellular FcγRIIA on platelets and monocytes to propagate a hypercoagulable state culminating in life-threatening thrombosis. It is now recognized that anti-PF4/heparin antibodies develop commonly after heparin exposure, but only a subset of sensitized patients progress to life-threatening complications of thrombocytopenia and thrombosis. Recent scientific developments have clarified mechanisms underlying PF4/heparin immunogenicity, disease susceptibility, and clinical manifestations of disease. Insights from clinical and laboratory findings have also been recently harnessed for disease prevention. This review will summarize our current understanding of HIT by reviewing pathogenesis, essential clinical and laboratory features, and management.
肝素诱导的血小板减少症(HIT)是肝素治疗的一种免疫并发症,由针对血小板因子4(PF4)与肝素复合物的抗体引起。PF4/肝素的致病性抗体结合并激活血小板和单核细胞上的细胞FcγRIIA,以引发高凝状态,最终导致危及生命的血栓形成。现在已经认识到,抗PF4/肝素抗体在肝素暴露后通常会产生,但只有一部分致敏患者会发展为血小板减少症和血栓形成等危及生命的并发症。最近的科学进展阐明了PF4/肝素免疫原性、疾病易感性以及疾病临床表现的潜在机制。临床和实验室研究结果的见解最近也被用于疾病预防。本综述将通过回顾发病机制、基本临床和实验室特征以及治疗方法,总结我们目前对HIT的认识。