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Editorial |

Platelet Activation Testing for Heparin-Induced Thrombocytopenia Antibodies: A Problem That Needs Fixing?

Theodore E. Warkentin, MD
Author and Funding Information

FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST the following: T. E. W. reports receiving fees from Instrumentation Laboratory for serving on an advisory board; consulting fees from Aspen Global and W. L. Gore; lecture fees from Instrumentation Laboratory and Pfizer Canada; fees for providing expert testimony in cases regarding thrombocytopenia, coagulopathy, or ischemic limb losses; and royalties from Taylor & Francis Group (Informa) for editing a book on heparin-induced thrombocytopenia. T. E. W. also reports that his institution has received fees from Instrumentation Laboratory, Medtronic Diabetes, and W. L. Gore for research studies, as well as for performing the serotonin release assay.

Department of Pathology and Molecular Medicine, and the Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, ON, Canada

CORRESPONDENCE TO: Theodore E. Warkentin, MD, Room 1-180A, Hamilton Regional Laboratory Medicine Program, Hamilton Health Sciences (Hamilton General Site), 237 Barton St E, Hamilton, ON, Canada L8L2X2


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(3):478-480. doi:10.1016/j.chest.2016.04.001
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Extract

Heparin-induced thrombocytopenia (HIT) is an important drug reaction that causes life- and limb-threatening thrombosis. It is considered a “clinical-pathologic” disorder, as the diagnosis is generally made by evaluating various “clinical” criteria (Thrombocytopenia, its Timing of onset, Thrombosis, and absence of oTher explanations, ie, the 4Ts scoring system) and determining whether (“pathologic”) HIT antibodies can be detected in the laboratory. Pathogenic heparin-induced antibodies are of the IgG class and activate platelets via their FcγIIA receptors (platelet IgG receptors), at concentrations of heparin ranging from 0 to 0.5 International Units/mL; characteristically, platelet activation is inhibited at very high heparin concentrations (eg, 100 International Units/mL), as excess heparin disrupts the formation of HIT antigens. HIT antibodies recognize complexes composed of platelet factor 4 (PF4)—a positively charged chemokine found within platelet α-granules—and heparin or certain other polyanions. However, a key problem is that among the many patients who receive heparin and who form anti-PF4/heparin antibodies that are readily detected by enzyme-linked immunosorbent assay (ELISA), only a minority of those antibodies are of the requisite platelet-activating isotype class (IgG), recognize the appropriate antigen site(s), and found in sufficient quantities to trigger platelet activation.

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