Heparin-induced thrombocytopenia: Impact of bovine versus porcine heparin in HIT pathogenesis

Abstract

Heparin-induced thrombocytopenia (HIT) is a complication of heparin therapy in cardiovascular/hematologic indications. Heparin is a mixture of sulfated mucopolysaccharide with heterogeneity and is capable of forming multiple complexes with platelet factor 4 (PF4), released from activated platelets. HPF4 antibodies may cause platelet/endothelial cell activation to promote HIT pathogenesis. HIT is a clinico-pathologic syndrome and its diagnosis primarily remains a clinical one; however, the serologic confirmation of the presence of HPF4 antibodies is also necessary part of the evaluation. Assays are based on the immunodetection of HPF4 antibodies and/or their functional ability to activate cells. Currently, there are several assays in use and a few newer/rapid immunoassays are becoming available. Recent studies have confirmed that HPF4 antibody generation (seroconversion) is common after cardiac surgery and suggest that patients receiving bovine heparin are more likely to generate functional (pathogenic) HPF4 antibodies of the IgG subclass. Thus, the use of bovine heparin in cardiovascular surgery should be avoided. A brief account of the currently available options for the management of HIT patients with non-heparin anticoagulants is provided.