Hemostasis and Thrombosis Center, Duke University Medical Center, Durham, NC 27710, USA.
Hematology Am Soc Hematol Educ Program. 2009:225-32. doi: 10.1182/asheducation-2009.1.225.
Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of approximately 50 to 60 x 10(9) platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.
肝素诱导的血小板减少症（HIT）是一种由血小板因子 4（PF4）和肝素抗体引起的免疫介导性疾病。血小板减少症通常为中度，血小板计数的中位数最低点约为 50 至 60×10(9)血小板/L。在 HIT 患者中已描述了严重的血小板减少症，并且在这些患者中抗体水平较高，已报道了严重的临床结局（例如弥漫性血管内凝血伴微血管血栓形成）。血小板减少症与肝素治疗开始之间的时间关系至关重要，血小板计数在开始使用肝素后 5 至 10 天内开始下降。在最近接触肝素（在过去 3 个月内）的患者中，由于存在预先形成的抗肝素/PF4 抗体，血小板计数可能会更快下降。也已描述了一种延迟型 HIT，其在肝素停用后数天或数周内发展。与其他药物诱导的血小板减少症不同，HIT 的特征是血栓栓塞并发症的风险增加，主要是静脉血栓栓塞。应停用肝素和所有含肝素的产品，并启动替代的非肝素抗凝剂。在 HIT 患者中有效使用的替代药物包括 lepirudin、argatroban、bivalirudin 和 danaparoid，尽管最后一种药物在北美不可用。在少数 HIT 患者中使用了fondaparinux，并且通常似乎是安全的。在血小板计数恢复且患者全身抗凝后，才应开始华法林治疗，并且在诊断 HIT 时应向接受华法林的患者给予维生素 K。
