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The Pathophysiology of Heparin-Induced Thrombocytopenia*: Biological Basis for Treatment

John G. Kelton, MD
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*From McMaster University, Hamilton, ON, Canada.

Correspondence to: John G. Kelton, MD, McMaster University, 1200 Main St West, Room 2E1, Hamilton, ON, L8N 3Z5, Canada; e-mail: keltonj@mcmaster.ca



Chest. 2005;127(2_suppl):9S-20S. doi:10.1378/chest.127.2_suppl.9S
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Heparin was discovered > 80 years ago,1 and within a short interval it was used as an anticoagulant.2 Heparin has advantages that led to its widespread use, including its immediate onset of action, its relatively short half-life (3 h), and its ability to be reversed using protamine.

In 1958, Weismann and Tobin3 described paradoxical thrombi during heparin therapy. Ten patients developed severe and sometimes catastrophic arterial occlusion while receiving heparin. Six of the 10 patients died as a result of the thrombosis.3 The clots were described as being a pale salmon color in appearance and platelet-rich when examined microscopically. An additional 11 patients were described 5 years later by another group.4 Once again, pale, platelet-rich arterial thrombi were described. And again, no mention of thrombocytopenia was made.4 We now recognize that although platelet-rich “white clots” can occur, they are uncommon, and the majority of thrombi complicating heparin-induced thrombocytopenia (HIT) are RBC-rich fibrin clots.

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