| Theme | Antiplatelet and Anticoagulation Therapy in Patients with Chronic Kidney Disease -- up to date of evidence | |
|---|---|---|
| Title | Pathogenesis and treatment of heparin-induced thrombocytopenia (HIT) | |
| Publish Date | 2012/07 | |
| Author | Shigeki Miyata | Division of Transfusion Medicine, National Cerebral and Cardiovascular Center |
| [ Summary ] | Heparin-induced thrombocytopenia (HIT) treatment has improved since argatroban was approved for HIT therapy in 2008 and indications for its use were expanded to include HIT patients undergoing hemodialysis in 2011. Heparin administration causes a conformational change in platelet factor 4 (PF4) which exposes neoantigens, leading to the production of IgG antibodies which recognize multimolecular complexes of PF4 and heparin (anti-PF4/heparin antibodies). In HIT patients, a subset of these antibodies (HIT antibodies) activates platelets and releases 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 in the hemodialysis circuit or occlusion of vascular access is also often observed in hemodialysis patients with HIT. HIT should be carefully diagnosed based on the determination of a compatible clinical situation and the detection of HIT antibodies. For HIT treatment, it is important to administer a thrombin inhibitor such as argatroban not only for anticoagulation in the hemodialysis circuit but also for treatment of hypercoagulable states, regardless of whether the HIT is complicated by thorombosis. |
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