Abstract
Heparin-induced thrombocytopenia (HIT) is a severe side effect of heparin treatment caused by platelet activating IgG antibodies generated against the platelet factor 4 (PF4)-heparin complex. Thrombocytopenia and thrombosis are the leading clinical symptoms of HIT. The clinical pretest probability of HIT was evaluated by the 4T score system. Laboratory testing of HIT was performed by immunological detection of antibodies against PF4-heparin complex (EIA) and two functional assays. Heparin-dependent activation of donor platelets by patient plasma was detected by flow cytometry. Increased binding of Annexin-V to platelets and elevated number of platelet-derived microparticles (PMP) were the indicators of platelet activation. EIA for IgG isotype HIT antibodies was performed in 405 suspected HIT patients. Based on negative EIA results, HIT was excluded in 365 (90%) of cases. In 40 patients with positive EIA test result functional tests were performed. Platelet activating antibodies were detected in 17 cases by Annexin V binding. PMP count analysis provided nearly identical results. The probability of a positive flow cytometric assay result was higher in patients with elevated antibody titer. 71% of patients with positive EIA and functional assay had thrombosis. EIA is an important first line laboratory test in the diagnosis of HIT; however, HIT must be confirmed by a functional test. Annexin V binding and PMP assays using flow cytometry are functional HIT tests convenient in a clinical diagnostic laboratory. The positive results of functional assays may predict the onset of thrombosis. © 2016 International Clinical Cytometry Society.
Highlights
Heparin-induced thrombocytopenia (HIT) is an immune response-mediated severe adverse effect of anticoagulant therapy by unfractionated (UFH) or low-molecular weight heparin (LMWH)
enzyme immunoassay (EIA) is an important first line laboratory test in the diagnosis of HIT, HIT must be confirmed by a functional test
The positive results of functional assays may predict the onset of thrombosis
Summary
Heparin-induced thrombocytopenia (HIT) is an immune response-mediated severe adverse effect of anticoagulant therapy by unfractionated (UFH) or low-molecular weight heparin (LMWH). Major clinical symptoms of HIT are thrombocytopenia and thrombosis due to the generation of IgG isotype HIT antibodies that recognize platelet factor 4 (PF4) bound to heparin. It causes heparin-dependent platelet activation through cross-linking FcγIIa receptors leading to the release of prothrombotic platelet-derived microparticles (PMPs) with platelet consumption and severe thrombocytopenia [1,2]. The laboratory evaluation for clinically suspected HIT should focus on the detection of heparin-dependent platelet activation induced by HIT antibodies [4]. Heparin-induced thrombocytopenia (HIT) is a severe side effect of heparin treatment caused by platelet activating IgG antibodies generated against the platelet factor 4 (PF4)-heparin complex. Thrombocytopenia and thrombosis are the leading clinical symptoms of HIT
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