title: Impact of the patient population on the risk for heparin-induced thrombocytopenia.
abstract: 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. (Blood. 2000;96:1703-1708)
authors.affiliation: Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada. twarken@fhs.mcmaster.ca
authors.forename: T E
authors.initials: TE
authors.lastname: Warkentin
authors.forename: J A
authors.initials: JA
authors.lastname: Sheppard
authors.forename: P
authors.initials: P
authors.lastname: Horsewood
authors.forename: P J
authors.initials: PJ
authors.lastname: Simpson
authors.forename: J C
authors.initials: JC
authors.lastname: Moore
authors.forename: J G
authors.initials: JG
authors.lastname: Kelton
mesh_terms: D000925:Anticoagulants / Q000009:adverse effects* / Q000276:immunology; D001792:Blood Platelets / Q000378:metabolism; D006348:Cardiac Surgical Procedures; D015331:Cohort Studies; D006493:Heparin / Q000009:adverse effects* / Q000276:immunology; D006495:Heparin, Low-Molecular-Weight / Q000009:adverse effects / Q000276:immunology; D006801:Humans; D007124:Immunoenzyme Techniques; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D019637:Orthopedic Procedures; D010976:Platelet Count / Q000187:drug effects; D010978:Platelet Factor 4 / Q000276:immunology; D011183:Postoperative Complications / Q000139:chemically induced / Q000276:immunology; D012307:Risk Factors; D012701:Serotonin / Q000378:metabolism; D013921:Thrombocytopenia / Q000139:chemically induced / Q000175:diagnosis*
chemical_list: D000925:Anticoagulants; D006495:Heparin, Low-Molecular-Weight; D007074:Immunoglobulin G; D012701:Serotonin; D010978:Platelet Factor 4; D006493:Heparin