Journal
THROMBOSIS RESEARCH
Volume 128, Issue 3, Pages 256-260Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.thromres.2011.05.003
Keywords
Heparin-induced thrombocytopenia; HIT; laboratory testing; heparin; PF4
Categories
Funding
- Deutsche Forschungsgemeinschaft Graduiertenkolleg [GRK-840]
- German Federal Ministry for Education and Research [CAN04/006]
- Zentrum fur Innovations-kompetenz Humorale Immunreaktionen bei Herz-Kreislauf Erkrankungen ZIK-HIKE [03Z2CK1, ZIK-HIKE 03Z2CI1]
- Forschungsverbund Molekulare Medizin of the Ernst-Moritz-Arndt-University Greifswald [FOMM 2009-04]
- Department of Cardiovascular Medicine of the Medical School of the Ernst-Moritz-Arndt University, Greifswald
- Heart and Stroke Foundation, Ontario, Canada [T6950]
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Background: IgG-specific anti-PF4/heparin enzyme-immunoassays (EIAs) are sensitive but not specific for platelet-activating antibodies, the cause of heparin-induced thrombocytopenia (HIT). Two features of EIA reactivity predict for presence of HIT antibodies - the magnitude of a positive result (in optical density [OD] units) and the inhibition of reactivity at high heparin concentrations - but their combined utility remains uncertain. Objective: To determine for an IgG-specific EIA how the OD values of a positive reaction and its inhibition by high heparin can be optimally combined. Methods: We screened 1,000 consecutive patients with suspected HIT using an IgG-specific PF4/heparin in-house EIA with and without high heparin (100 IU/mL); and by the heparin-induced platelet activation test. Results: Platelet-activating antibodies were rarely detected (<0.2%) when the IgG-specific EIA was negative at the conventional cut-off (OD, 0.5). However, an OD cut-off of 1.0 resulted in an unacceptable loss of sensitivity (14/83 = 17%) for detecting platelet-activating antibodies. The high heparin step increased specificity for platelet-activating antibodies from 72% to 89% without loss of sensitivity when applied to weak-positive sera (OD <= 1.0). However, decreased sensitivity was observed with strong-positive sera (OD > 1.0): 11/69 such sera (16%) that did not show >40% inhibition by high heparin nevertheless contained platelet-activating antibodies. Conclusion: Specificity of an IgG-specific EIA for detecting platelet-activating antibodies can be optimized by applying the high heparin inhibition step to weak-positive reactions (0.5- <= 1.0 OD). However, applying the high heparin inhibition step to strong-positive reactions (>1.0 OD) in our in-house assay risks falsely classifying a serum as negative for platelet-activating antibodies. (C) 2011 Elsevier Ltd. All rights reserved.
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