Immune Heparin-Induced Thrombocytopenia (HIT)

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  • Miyata,Shigeki
    Division of Transfusion Medicine, National Cerebral and Cardiovascular Center

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Other Title
  • ヘパリン起因性血小板減少症(<特集>血小板減少症とアフェレシス)

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Abstract

Immune heparin-induced thrombocytopenia (HIT) is a life-threatening side effect of heparin therapy. HIT has been better recognized even in Japan since argatroban, a direct thrombin inhibitor, was approved for the indication of HIT in July 2008. In addition, the indication of argatroban was expanded for HIT patients who undergo hemodialysis or percutaneous coronary intervention in May 2011. In heparin-treated patients, platelet activation often occurs, releasing platelet factor 4 (PF4). When heparin is injected, it rapidly forms complexes with PF4. Heparin binding causes a conformational change in PF4 that exposes neoantigens and induces antibodies against PF4/heparin complexes. A subset of these anti-PF4/heparin antibodies (HIT antibodies) can activate platelets and release procoagulant microparticles, resulting in increased thrombin generation. As a result, many HIT patients suffer from both arterial and venous thrombosis due to their thrombin-induced hypercoagulable state. Clotting of the hemodialysis circuit or occlusion of vascular access is also often observed in hemodialysis patients with HIT. HIT should be diagnosed using a combination of clinical probability and the detection of HIT antibodies as a clinicopathologic syndrome. For the treatment of HIT, it is important to administer a thrombin inhibitor such as argatroban not only for anticoagulation of the hemodialysis circuit but also for treatment of the hypercoagulable state, regardless of whether the HIT is complicated by thrombosis.

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