Semin Thromb Hemost 1997; 23(6): 569-574
DOI: 10.1055/s-2007-996138
Copyright © 1997 by Thieme Medical Publishers, Inc.

Recognition and Management of Heparin-Induced Thrombocytopenia (HIT) and Thrombosis

Barbara M. Alving* , Chitra Krishnamurti
  • From the *Department of Medicine, Washington Hospital Center, Washington, D.C., and the
  • †Department of Hematology and Vascular Biology, Walter Reed Army Institute of Research, Washington, D.C.
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Publikationsverlauf

Publikationsdatum:
08. Februar 2008 (online)

Abstract

An immune response to heparin, which is clinically manifested by the development of thrombocytopenia with or without thrombosis, is stimulated by a complex of heparin with platelet factor 4 (PF4). The primary thrombotic events in patients with heparin-induced thrombocytopenia (HIT) are more frequently venous than arterial. The development of antibodies, however, does not always result in thrombocytopenia or in catastrophic events. The antibodies, which are of the IgG, IgM, and IgA isotypes, can be easily measured by an ELISA that contains a complex of heparin-platelet factor 4 (PF4). Initial antibody formation can be greatly reduced by limiting the exposure to unfractionated heparin or by the use of low-molecular-weight heparin. For those patients who require anticoagulation and who have antibodies to heparin-PF4, danaparoid (OrgaranTM), a low-molecular weight heparinoid that does not react with the antibodies, is now commercially available; argatroban, a thrombin-specific inhibitor, can also be obtained for compassionate use. The use of these agents during anticoagulation with warfarin is preferable to the simple discontinuation of heparin and intitiation of warfarin, because the latter treatment can result in ongoing thrombosis.