An Overview of the Heparin-Induced Thrombocytopenia Syndrome

摘要: Heparin-induced thrombocytopenia (HIT) is caused by heparin-dependent, platelet-activating IgG antibodies that increase thrombin generation in vivo, producing a prothrombotic phenotype. In addition to platelet activation, there vitro evidence activation of endothelium and monocytes occurs, perhaps directly HIT antibodies, but more likely through activated (or microparticle)-endothelial-leukocyte interactions. Patients with cardiac disease receiving heparin present important diagnostic therapeutic issues when unexpected arises. Concomitant vascular burden intravascular catheter use further risk HIT-associated arterial thrombosis this patient population. Whether simply reflects the "hypercoagulability state" interacting diseased or injured arteries, whether "white clots" reflect additional effects via endothelial monocyte remains uncertain. can also develop deep-vein thrombosis, which progress limb loss if coumarin (warfarin) leads severe protein C depletion (coumarin-induced venous gangrene). Therapy for patients strongly suspected have should focus on inhibiting its generation) pharmacologically. Two direct inhibitors (lepirudin, argatroban) are approved treating HIT. When using these agents, anticoagulation be delayed pending substantial resolution thrombocytopenia, before cautiously introducing overlapping therapy.