Heparin-induced thrombocytopenia. Pathogenesis, frequency, avoidance and management

Heparin-induced thrombocytopenia (HIT) is an immunoglobulin-mediated adverse drug reaction associated with a high risk of thrombotic complications. The pathogenic antibody, usually immunoglobulin (Ig) G (HIT-IgG), recognises a multimolecular complex of heparin and platelet factor 4, resulting in platelet activation via platelet Fc receptors. In addition to in vivo platelet activation, it is now recognised that there is a concomitant activation of coagulation, as shown by marked elevations in thrombin-antithrombin complex levels. It is possible that this increased thrombin generation predisposes HIT patients to a newly recognised complication: warfarin-induced venous limb gangrene. This syndrome is characterised clinically by necrosis complicating deep venous thrombosis in the absence of large-vessel arterial occlusion, and appears to result from acquired protein C deficiency during warfarin therapy for deep vein thrombosis and HIT. The recommended treatment for HIT is an agent that reduces thrombin generation, either indirectly via factor Xa inhibition [e.g. danaparoid sodium (a mixture of anticoagulant glycosaminoglycans)] or directly using a specific thrombin inhibitor (e.g. recombinant hirudin; argatroban). HIT is potentially preventable: there is a lower frequency of HIT, associated thrombosis and HIT-IgG seroconversion in patients treated with low-molecular-weight heparins, compared with unfractionated heparin.

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This review of heparin-induced thrombocytopenia describes its pathogenesis via heparin-platelet factor 4 antibodies, complications such as warfarin-induced venous limb gangrene, and recommended treatments including recombinant hirudin and argatroban to reduce thrombin generation.

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