Semin Thromb Hemost 2011; 37(6): 653-663
DOI: 10.1055/s-0031-1291375
© Thieme Medical Publishers

Heparin-Induced Thrombocytopenia: Real-World Issues

Lori-Ann Linkins1 , Theodore E. Warkentin1 , 2
  • 1Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada
  • 2Pathology and Molecular Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada
Further Information

Publication History

Publication Date:
18 November 2011 (online)

ABSTRACT

Heparin-induced thrombocytopenia (HIT) is a prothrombotic drug reaction caused by platelet-activating antibodies. HIT sera often activate platelets without needing heparin—such heparin-“independent” platelet activation can be associated with HIT beginning or worsening despite stopping heparin (“delayed-onset HIT”). We address important issues in HIT diagnosis and therapy, using a recent cohort of HIT patients to illustrate influences of heparin type; triggers for HIT investigation; serological features of heparin-independent platelet activation; and treatment. In our cohort of recent HIT cases (n = 13), low-molecular-weight heparin (dalteparin) was a common causative agent (n = 8, 62%); most patients were diagnosed after HIT-thrombosis had occurred; and danaparoid was the most frequently selected treatment. Heparin-independent platelet activation was common (7/13 [54%]) and predicted slower platelet count recovery (>1 week) among evaluable patients (5/5 vs 1/6; p = 0.015). In our experience with argatroban-treated patients, HIT-associated consumptive coagulopathy confounds anticoagulant monitoring. Our observations provide guidance on practical aspects of HIT diagnosis and management.

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Theodore E WarkentinM.D. 

Hamilton Regional Laboratory Medicine Program, Room 1-270B, Hamilton Health Sciences, Hamilton General Site

237 Barton Street East, Hamilton, ON L8L 2X2, Canada

Email: twarken@mcmaster.ca

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