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Original Research: ANTITHROMBOTIC THERAPY |

Prevalence and Risk of Preexisting Heparin-Induced Thrombocytopenia Antibodies in Patients With Acute VTERisk of Heparin-Induced Thrombocytopenia

Theodore E. Warkentin, MD; Bruce L. Davidson, MD, MPH, FCCP; Harry R. Büller, MD, PhD; Alexander Gallus, MD; Michael Gent, DSc; Anthonie W. A. Lensing, MD, PhD; Franco Piovella, MD; Martin H. Prins, MD, PhD; Annelise E. M. Segers, MD; John G. Kelton, MD
Author and Funding Information

From the Faculty of Health Sciences (Drs Warkentin, Gent, and Kelton), McMaster University, Hamilton, ON, Canada; University of Washington School of Medicine (Dr Davidson), Seattle, WA; Academic Medical Center (Drs Büller, Lensing, and Segers), Amsterdam, The Netherlands; Flinders Medical Center (Dr Gallus), Adelaide, SA, Australia; Fondazione IRCCS (Dr Piovella), Policlinico San Matteo, Pavia, Italy; and University Hospital of Maastricht (Dr Prins), Maastricht, The Netherlands.

Correspondence to: Bruce L. Davidson, MD, MPH, FCCP, 12209 Shorewood Dr SW, Burien, WA 98146; e-mail: brucedavidson@pobox.com


Drs Warkentin and Davidson contributed equally to this work.

Funding/Support: The Matisse-PE and Matisse-DVT clinical trials, with the serologic studies, were originally sponsored by Sanofi-Synthélabo and Organon International. We also acknowledge the support of the Heart and Stroke Foundation of Ontario [(to Dr Warkentin) T6157; to (Dr Kelton) T5542]. Work on this study by the other coauthors was unfunded.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(2):366-373. doi:10.1378/chest.10-1599
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Background:  Some patients with acute VTE who may previously have been exposed to heparin products have unrecognized antibodies implicated in heparin-induced thrombocytopenia (HIT). Antibody prevalence and patient consequences upon exposure to heparin, low-molecular-weight heparin, and fondaparinux are uncertain.

Methods:  In this secondary analysis, we tested patients in the Matisse VTE studies at study entry for heparin-dependent antibodies and further tested patients with enzyme-linked immunosorbent assay (ELISA)-positive results for platelet-activating antibodies. We compared the risk of HIT (> 50% fall in platelet count, heparin-dependent antibodies, no contradicting features) between patients treated with heparin (either unfractionated or low molecular weight [enoxaparin]) vs those who received fondaparinux. Comparison groups for thrombocytopenia occurrence comprised patients with ELISA-positive, platelet-activating, antibody-positive results; ELISA-positive, but platelet-activating antibody-negative results; and randomly selected antibody-negative results.

Results:  A total of 127 of 3,994 patients (3.2%) had ELISA-positive results at baseline, but only 14 (0.4%; 95% CI, 0.2%-0.6%) had platelet-activating antibodies. Among these 14, four treated with unfractionated or low-molecular-weight heparin developed HIT compared with zero of 10 fondaparinux-treated patients (OR, 95; 95% CI, 8-1,123; P < .001). This frequency (four of four, 100%) significantly differed from that of both heparin-treated patients whose results were ELISA positive but platelet-activating antibody negative and from heparin-treated antibody-negative control subjects (zero of 15 and zero of 27, respectively; P < .001 for both).

Conclusions:  Of patients with VTE, 0.4% had pathologic platelet-activating heparin-dependent antibodies rather than the 3.2% detected by the recommended cutoff of the commercial ELISA. Among study patients with acute VTE who had platelet-activating antibodies, treatment with fondaparinux reduced the risk of precipitating rapid-onset HIT.

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