Division of Hematology, Duke University Medical Center, Durham, NC (G.M.A.).
Divisions of Hematopathology, Transfusion Medicine, and Experimental Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN (A.P.).
Arterioscler Thromb Vasc Biol. 2021 Jan;41(1):141-152. doi: 10.1161/ATVBAHA.120.315445. Epub 2020 Dec 3.
Heparin-induced thrombocytopenia is an immune-mediated disorder caused by antibodies that recognize complexes of platelet factor 4 and heparin. Thrombosis is a central and unpredictable feature of this syndrome. Despite optimal management, disease morbidity and mortality from thrombosis remain high. The hypercoagulable state in heparin-induced thrombocytopenia is biologically distinct from other thrombophilic disorders in that clinical complications are directly attributable to circulating ultra-large immune complexes. In some individuals, ultra-large immune complexes elicit unchecked cellular procoagulant responses that culminate in thrombosis. To date, the clinical and biologic risk factors associated with thrombotic risk in heparin-induced thrombocytopenia remain elusive. This review will summarize our current understanding of thrombosis in heparin-induced thrombocytopenia with attention to its clinical features, cellular mechanisms, and its management.
肝素诱导的血小板减少症是一种由抗体识别血小板因子 4 和肝素复合物引起的免疫介导的疾病。血栓形成是该综合征的中心和不可预测的特征。尽管进行了最佳治疗，但是血栓形成导致的疾病发病率和死亡率仍然很高。肝素诱导的血小板减少症中的高凝状态在生物学上与其他血栓形成性疾病不同，因为临床并发症直接归因于循环中的超大免疫复合物。在某些个体中，超大免疫复合物引发不受控制的细胞促凝反应，最终导致血栓形成。迄今为止，与肝素诱导的血小板减少症中的血栓形成风险相关的临床和生物学危险因素仍难以捉摸。本综述将总结我们目前对肝素诱导的血小板减少症中血栓形成的理解，重点关注其临床特征、细胞机制及其治疗。
