Warkentin T E, Kelton J G
Department of Pathology, McMaster University Medical Centre, Hamilton, Ontario, Canada.
Hematol Oncol Clin North Am. 1990 Feb;4(1):243-64.
Heparin-induced thrombocytopenia is the most important immune drug-induced thrombocytopenia because of its relatively high frequency and association with arterial and venous thromboembolism. The reported incidence of thrombocytopenia (1 per cent for heparin of porcine mucosal, and 5 per cent for heparin of bovine lung origin) probably represents an underestimate of its true frequency because some patients have a heparin-induced fall in the platelet count that does not reach thrombocytopenic levels. The majority and possibly all cases of heparin-induced thrombocytopenia with or without thrombosis are caused by immune mechanisms. Recent evidence indicates that a heparin-antibody immune complex causes platelet activation by binding to platelet Fc receptors. The risk of heparin-induced thrombosis can be reduced by minimizing duration of heparin exposure, by using porcine instead of bovine heparin, possibly by monitoring the platelet count, and by early institution of alternate anticoagulation when the syndrome is recognized. It is hoped that a new heparin or heparinoid preparation will be developed that will not cause this syndrome.
肝素诱导的血小板减少症是最重要的免疫性药物诱导的血小板减少症，因为其发生率相对较高，且与动脉和静脉血栓栓塞有关。报道的血小板减少症发生率（猪黏膜肝素为1%，牛肺来源肝素为5%）可能低估了其实际发生率，因为一些患者的血小板计数因肝素诱导而下降，但未达到血小板减少水平。大多数甚至可能所有肝素诱导的血小板减少症病例，无论有无血栓形成，均由免疫机制引起。最近的证据表明，肝素-抗体免疫复合物通过与血小板Fc受体结合导致血小板活化。通过尽量缩短肝素暴露时间、使用猪肝素而非牛肝素、可能通过监测血小板计数以及在识别出该综合征时尽早采用替代抗凝治疗，可以降低肝素诱导血栓形成的风险。希望能研发出一种不会引起该综合征的新型肝素或类肝素制剂。
