Heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia (HIT) is a clinicopathologic syndrome, characterised clinically by thrombocytopenia and a high risk for thrombosis, and pathologically by the formation of heparin-dependent immunoglobulin G that activates platelets via their Fc receptor. The pathogenic antibody causes platelets to generate procoagulant, platelet-derived microparticles in vitro and in vivo; this result in increased thrombin generation and leads to a high risk for venous and arterial thrombosis in these patients. Recently, the syndrome of warfarin-induced venous limb gangrene complicating HIT has been linked to a profound disturbance in procoagulant anticoagulant balance: the interaction of marked thrombin generation triggered by platelet activation in HIT, together with a severe reduction in protein C levels caused by warfarin used to treat the HIT. Increased appreciation of the role of thrombin generation in HIT patients has led to new treatment approaches that emphasise inhibition of factor Xa (e.g., danaparoid) or thrombin (e.g., birudin, argatroban).