Institut für Immunologie und Transfusionsmedizin, Sauerbruchstraße, 17487 Greifswald, Germany.
Expert Rev Hematol. 2008 Oct;1(1):75-85. doi: 10.1586/17474086.1.1.75.
Heparin-induced thrombocytopenia (HIT) is a clinicopathological syndrome associated with heparin therapy that is characterized by a decrease in platelet counts and/or the development of a new thrombosis. Two types of HIT exist, type I is nonimmune and self-resolves, whereas type II is immune-mediated and clinically important. The formation of antibodies against the platelet factor 4-heparin complexes results in platelet activation and thrombin formation, which lead to an increased risk of thrombosis. Unfractionated heparin is associated with a higher risk of HIT than low-molecular-weight heparins. Surgical patients, particularly those undergoing orthopedic or cardiac surgery, are at higher risk of HIT than medical patients. Treatment of HIT involves heparin cessation together with anticoagulation with direct thrombin inhibitors or indirect factor Xa inhibitors.
肝素诱导的血小板减少症（HIT）是一种与肝素治疗相关的临床病理综合征，其特征是血小板计数下降和/或新血栓形成。HIT 存在两种类型，I 型是非免疫性的，可自行缓解，而 II 型是免疫介导的，具有临床重要性。针对血小板因子 4-肝素复合物形成的抗体导致血小板激活和凝血酶形成，从而增加血栓形成的风险。未分级肝素与 HIT 的相关性高于低分子量肝素。外科患者，尤其是接受骨科或心脏手术的患者，比内科患者发生 HIT 的风险更高。HIT 的治疗包括停用肝素以及使用直接凝血酶抑制剂或间接因子 Xa 抑制剂进行抗凝治疗。
