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Ann Thorac Surg 2007;83:21-23
© 2007 The Society of Thoracic Surgeons


Editorial

When is HIT Really HIT?

Theodore E. Warkentin, MDa,b,*, Mark A. Crowther, MDb

a Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada
b Department of Medicine, McMaster University, Hamilton, Ontario, Canada

* Address correspondence to Dr Warkentin, Hamilton Regional Laboratory Medicine Program, Hamilton Health Sciences (General Site), Room 1-180A, 237 Barton St E, Hamilton, Ontario, L8L 2X2 Canada (Email: twarken@mcmaster.ca).

The first 300 words of the full text of this article appear below.

Immune heparin-induced thrombocytopenia (HIT) is caused by platelet-activating antibodies of immunoglobulin G class that recognize multi-molecular complexes of platelet factor 4 (a member of the C-X-C subfamily of chemokines) bound to heparin or certain other polyanions. Clinically, HIT is characterized by thrombocytopenia or thrombosis, or both, that bear a temporal relationship to heparin exposure and resulting immunization. Typically there is a minimum interval of 5 days from the immunizing exposure to heparin, and the subsequent clinical sequela(e) of HIT, whether this is a platelet count fall or thrombosis, or both.

Heparin-induced thrombocytopenia is relatively common in patients receiving postoperative antithrombotic prophylaxis with unfractionated heparin. Indeed, HIT was found in approximately 5% of patients receiving unfractionated heparin thromboprophylaxis in two orthopedic surgery studies [1, 2]. Typically, in HIT the platelet count begins to fall 5 to 10 days after starting heparin (ie, a time when the platelet count is expected to be rising after the initial period of early postoperative thrombocytopenia) [3, 4]. By defining thrombocytopenia as a relative (proportional) fall in platelet count of 50% or more that begins on or after day 5 of heparin therapy, and by testing for the pathogenic heparin-dependent platelet-activating antibodies, it is relatively easy to distinguish HIT from mimicking thrombocytopenic disorders [3, 4]. This is because postoperative complications causing thrombocytopenia are uncommon this long after surgery [3]. However the situation is more complex when evaluating disorders in which there is a high frequency of major and persisting thrombocytopenia. One of these situations is the patient who is critically ill.

Recently two European studies of patients receiving unfractionated heparin for anticoagulation associated with use of a ventricular assist device (VAD) have reported particularly high frequencies of HIT. Schenk and coworkers [5] observed HIT in 12 . . . [Full Text of this Article]


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Andreas Koster, Sabine Huebler, Evgenij Potapov, Oliver Meyer, Michael Jurmann, Yuguo Weng, Miralem Pasic, Thorsten Drews, Hermann Kuppe, Matthias Loebe, and Roland Hetzer
Ann. Thorac. Surg. 2007 83: 72-76. [Abstract] [Full Text] [PDF]



This article has been cited by other articles:


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N. Barzaghi, A. Locatelli, and M. Ranucci
Ventricular Assist Device Implantation and the Risk for Heparin-Induced Thrombocytopenia
Ann. Thorac. Surg., January 1, 2008; 85(1): 360 - 361.
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Ann. Thorac. Surg., January 1, 2008; 85(1): 361 - 361.
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Ann. Thorac. Surg., October 1, 2007; 84(4): 1423 - 1424.
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