Heparin-induced thrombocytopenia
Heparin-induced thrombocytopenia
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DOI：
10.1046/j.1538-7836.2003.00270.x
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发表时间：
2003-07-01
影响因子：
10.4
通讯作者：
Chong, BH
中科院分区：
文献类型：
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作者：
Chong, BH
肝素诱导的血小板减少症（HIT）不仅是一种常见的，而且是一种潜在的严重药物不良反应。与其他药物引起的血小板减少症不同，HIT通常不会引起出血，而是引起血栓形成。HIT中的血栓形成可导致肢体坏疽（需要截肢）甚至死亡。HIT由识别血小板因子4（PF 4）-肝素复合物上表位的抗体介导。抗体-PF 4-肝素复合物与血小板表面上的Fc γ RII受体结合并使受体交联。这诱导强烈的血小板活化和血小板聚集，并同时激活凝血途径。这些变化可能是HIT血栓形成的基础。HIT的诊断应主要根据临床标准进行，但应尽可能通过实验室检查进行确认，特别是在患有合并症的患者中，如果没有检查，则无法确定HIT的诊断。HIT抗体的测试是免疫测定（例如ELISA）或功能测试（例如C-14-血清素释放测定）。一旦临床诊断为HIT，应立即停用肝素，并开始使用替代抗凝剂（如达那肝素、r-水蛭素或阿加曲班）治疗。这应该持续至少5天，除非HIT的诊断随后被证明是不正确的。当患者临床稳定且血栓得到控制时，也应开始治疗。华法林和替代抗凝治疗之间应该有几天的重叠。
Heparin-induced thrombocytopenia (HIT) is not only a common but also a potentially serious drug adverse effect. Unlike other drug-induced thrombocytopenias, HIT does not usually cause bleeding, but instead causes thrombosis. Thrombosis in HIT can lead to limb gangrene (requiring leg amputation) or even death. HIT is mediated by an antibody that recognizes an epitope on the platelet factor 4 (PF4)-heparin complex. The antibody-PF4-heparin complex binds to FcgammaRII receptors on the platelet surface and cross-links the receptors. This induces intense platelet activation and platelet aggregation, and simultaneously activates blood-coagulation pathways. These changes are probably the basis of the thrombotic events in HIT. Diagnosis of HIT should be made mainly on clinical criteria but should be confirmed whenever possible by laboratory tests, particularly in patients with comorbid conditions, in whom the diagnosis of HIT cannot be made with certainty without testing. The tests for HIT antibodies are either immunoassays (e.g. ELISA), or functional tests, (e.g. C-14-serotonin release assay). Once a clinical diagnosis of HIT is made, heparin should be ceased immediately and treatment with an alternative anticoagulant (such as danaparoid, r-hirudin or argatroban) commenced. This should continue for at least 5 days unless the diagnosis of HIT is subsequently proven to be incorrect. Warfarin should also be commenced when the patient is clinically stable and thrombosis is under control. There should be an overlap of a few days between warfarin and the alternative anticoagulant therapy.