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Blood, 1 September 2000, Vol. 96, No. 5, pp. 1703-1708

CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS

Impact of the patient population on the risk for heparin-induced thrombocytopenia

Theodore E. Warkentin, Jo-Ann I. Sheppard, Peter Horsewood, Patricia J. Simpson, Jane C. Moore, and John G. Kelton

From the Department of Pathology and Molecular Medicine and the Department of Medicine, McMaster University; and from the Hamilton Regional Laboratory Medicine Program, Hamilton Health Sciences Corporation, Hamilton, Ontario, Canada.

The frequency of immune heparin-induced thrombocytopenia (HIT) varies among prospective studies. It is unknown whether this is caused by differences in the heparin preparations, the patient populations, or the types of serologic assay used to confirm the diagnosis. Seven hundred forty-four patients were studied from 3 different clinical treatment settings, as follows: unfractionated heparin (UFH) during or after cardiac surgery (n = 100), UFH after orthopedic surgery (n = 205), and low-molecular-weight heparin (LMWH) after orthopedic surgery (n = 439). Both an activation assay and an antigen assay were used to detect heparin-dependent IgG (HIT-IgG) antibodies. By activation assay, the frequency of HIT-IgG formation ranged from a low of 3.2% in orthopedic patients receiving LMWH to a high of 20% in cardiac patients receiving UFH; by antigen assay, the corresponding frequencies ranged from 7.5% to 50%. Both UFH use (P = .002) and cardiac surgery (P = .01) were more likely to be associated with HIT-IgG formation. However, among patients in whom HIT-IgG formed and who were administered UFH, the probability for HIT was higher among orthopedic patients than among cardiac patients (by activation assay: 52.6% compared with 5%; odds ratio, 21.1 [95% CI, 2.2-962.8]; P = .001; by antigen assay: 34.5% compared with 2.0%; odds ratio, 25.8 [95% CI, 3.2-1141]; P < .001). It is concluded that there is an unexpected dissociation between the frequency of HIT-IgG formation and the risk for HIT that is dependent on the patient population. HIT-IgG antibodies are more likely to form in patients who undergo cardiac surgery than in orthopedic patients, but among patients in whom antibodies do form, orthopedic patients are more likely to develop HIT.

© 2000 by The American Society of Hematology.
 

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BloodHome page
B. M. Alving
How I treat heparin-induced thrombocytopenia and thrombosis
Blood, January 1, 2003; 101(1): 31 - 37.
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CLIN APPL THROMB HEMOSTHome page
E. Lindhoff-Last, B. Wenning, M. Stein, F. Gerdsen, R. Bauersachs, and R. Wagnert
Risk Factors and Long-term Follow-up of Patients with the Immune Type of Heparin-Induced Thrombocytopenia
Clinical and Applied Thrombosis/Hemostasis, October 1, 2002; 8(4): 347 - 352.
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NEJMHome page
W. C. Aird and E. J. Mark
Case 15-2002 - A 53-Year-Old Man with a Myocardial Infarct and Thromboses after Coronary-Artery Bypass Grafting
N. Engl. J. Med., May 16, 2002; 346(20): 1562 - 1570.
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BloodHome page
Z. Q. Li, W. Liu, K. S. Park, B. S. Sachais, G. M. Arepally, D. B. Cines, and M. Poncz
Defining a second epitope for heparin-induced thrombocytopenia/thrombosis antibodies using KKO, a murine HIT-like monoclonal antibody
Blood, February 15, 2002; 99(4): 1230 - 1236.
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ANN INTERN MEDHome page
T. E. Warkentin and J. G. Kelton
Delayed-Onset Heparin-Induced Thrombocytopenia and Thrombosis
Ann Intern Med, October 2, 2001; 135(7): 502 - 506.
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CLIN APPL THROMB HEMOSTHome page
E. Lindhoff-Last, C. Betz, and R. Bauersachs
Use of a Low-Molecular-Weight Heparinoid (Danaparoid Sodium) for Continuous Renal Replacement Therapy in Intensive Care Patients
Clinical and Applied Thrombosis/Hemostasis, October 1, 2001; 7(4): 300 - 304.
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BloodHome page
G. M. Arepally and I. M. Mayer
Antibodies from patients with heparin-induced thrombocytopenia stimulate monocytic cells to express tissue factor and secrete interleukin-8
Blood, August 15, 2001; 98(4): 1252 - 1254.
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Arterioscler. Thromb. Vasc. Bio.Home page
J. Hirsh, S. S. Anand, J. L. Halperin, and V. Fuster
Guide to Anticoagulant Therapy: Heparin : A Statement for Healthcare Professionals From the American Heart Association
Arterioscler Thromb Vasc Biol, July 1, 2001; 21 (7): e9 - e9.
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CirculationHome page
J. Hirsh, S. S. Anand, J. L. Halperin, and V. Fuster
Guide to Anticoagulant Therapy: Heparin : A Statement for Healthcare Professionals From the American Heart Association
Circulation, June 19, 2001; 103(24): 2994 - 3018.
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NEJMHome page
T. E. Warkentin and J. G. Kelton
Temporal Aspects of Heparin-Induced Thrombocytopenia
N. Engl. J. Med., April 26, 2001; 344(17): 1286 - 1292.
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ASH Education BookHome page
K. R. McCrae, J. B. Bussel, P. M. Mannucci, G. Remuzzi, and D. B. Cines
Platelets: An Update on Diagnosis and Management of Thrombocytopenic Disorders
Hematology, January 1, 2001; 2001(1): 282 - 305.
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ASH Education BookHome page
J. A. Ginsberg, M. A. Crowther, R. H. White, and T. L. Ortel
Anticoagulation Therapy
Hematology, January 1, 2001; 2001(1): 339 - 357.
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ChestHome page
J. Hirsh, T. E. Warkentin, S. G. Shaughnessy, S. S. Anand, J. L. Halperin, R. Raschke, C. Granger, E. M. Ohman, and J. E. Dalen
Heparin and Low-Molecular-Weight Heparin Mechanisms of Action, Pharmacokinetics, Dosing, Monitoring, Efficacy, and Safety
Chest, January 1, 2001; 119 (2009): 64S - 94S.
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