Deitcher S R, Carman T L
Section of Clinical Thrombosis, Department of Vascular Medicine, The Cleveland Clinic Foundation, OH 44195, USA.
Vasc Med. 2001;6(2):113-9.
Heparin-induced thrombocytopenia (HIT) is an under-recognized, limb- and life-threatening complication of pharmacologic heparin administration. Antibody formation against heparin complexed to platelet factor 4 (PF4) is central to the pathogenesis of HIT. Heparin:PF4 antibodies promote platelet activation and aggregation as well as excess thrombin generation which may lead to clinical thrombosis. HIT should be suspected in patients who develop thrombocytopenia with or without associated arterial or venous thrombosis while on heparin. HIT is a clinical diagnosis. Specialized HIT assays should be interpreted with care. The cornerstone of HIT management is the discontinuation of all forms of heparin exposure and the institution of anticoagulation with an alternative agent. The direct thrombin inhibitors lepirudin and argatroban are currently available and approved for use in patients with HIT.
肝素诱导的血小板减少症（HIT）是药物性肝素治疗中一种未被充分认识的、可危及肢体和生命的并发症。针对与血小板因子4（PF4）结合的肝素形成抗体是HIT发病机制的核心。肝素：PF4抗体促进血小板活化和聚集以及过量凝血酶生成，这可能导致临床血栓形成。在使用肝素期间出现血小板减少症且伴有或不伴有相关动脉或静脉血栓形成的患者应怀疑HIT。HIT是一种临床诊断。应谨慎解读专门的HIT检测结果。HIT管理的基石是停止所有形式的肝素暴露，并使用替代药物进行抗凝治疗。目前已有直接凝血酶抑制剂来匹卢定和阿加曲班可供使用并被批准用于HIT患者。
