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(Circulation. 2004;110:e454-e458.)
© 2004 American Heart Association, Inc.

Clinician Update

Heparin-Induced Thrombocytopenia

Diagnosis and Management

Theodore E. Warkentin, MD

From the Department of Pathology and Molecular Medicine and the Department of Medicine, McMaster University, Hamilton, Ontario, Canada.

Correspondence to Dr Ted Warkentin, Hamilton Regional Laboratory Medicine Program, Hamilton Health Sciences, General Site, 237 Barton St E, Hamilton, Ontario L8L 2X2, Canada. E-mail twarken@mcmaster.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction characterized by thrombocytopenia and a high risk for venous or arterial thrombosis.¹ It is caused by heparin-dependent, platelet-activating antibodies that recognize a "self" protein, platelet factor 4 (PF4), bound to heparin. The resulting platelet activation is associated with increased thrombin generation (Figure).² Typically, the platelet count fall begins 5 to 10 days after starting heparin, although a rapid platelet count fall can occur in a patient who has antibodies from recent heparin use.³ Remarkably, transience of HIT antibodies permits safe heparin reexposure in selected patients (for example, heart surgery patients) despite a history of HIT.^3,4

View larger version (66K): [in this window] [in a new window]   Pathogenesis of HIT. HIT antibodies of IgG class bind to multimolecular complexes of platelet factor 4 (PF4) and heparin on platelet surfaces, resulting in platelet activation when the IgG molecules interact with the platelet Fc receptors. Platelet-derived microparticles are generated, which enhance coagulation reactions. In addition, HIT antibodies can activate endothelium and monocytes, exacerbating the procoagulant response. Activation of platelets and increased production of thrombin could explain the high risk of arterial and venous thrombosis in HIT. Reprinted with permission from Greinacher and Warkentin.2

	Case Summary

 
A 61-year-old woman⁵ with Ray-naud’s phenomenon underwent mechanical aortic valve replacement for aortic insufficiency. She developed persistent vasospasm of fingers and toes after surgery that responded to warming measures. Unfractionated heparin (UFH) prophylaxis was given until postoperative day 4, and warfarin (5, 5, and 2.5 mg) was given from days 2 to 4. On day 8, the patient developed ischemic necrosis . . . [Full Text of this Article]

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