Activation of platelets by heparin-induced thrombocytopenia antibodies in the serotonin release assay is not dependent on the presence of heparin

The serotonin release assay (SRA) tests for antibodies responsible for heparin-induced thrombocytopenia (HIT). By definition, SRA-positive antibodies cause platelet serotonin release in vitro, in the presence of low concentrations of heparin, but not with excess heparin. Many SRA-positive sera activ...

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Bibliographic Details
Published in:Journal of thrombosis and haemostasis 2005-10, Vol.3 (10), p.2168
Main Authors: Prechel, M M, McDonald, M K, Jeske, W P, Messmore, H L, Walenga, J M
Format: Article
Language:English
Subjects:
Antibodies - isolation & purification
Antibodies - physiology
Carbon Radioisotopes
Heparin - adverse effects
Heparin - immunology
Heparin Lyase - metabolism
Humans
Immunoglobulin G - isolation & purification
Platelet Activation - drug effects
Platelet Activation - immunology
Serotonin - metabolism
Thrombocytopenia - chemically induced
Thrombocytopenia - immunology
Time Factors
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Summary:The serotonin release assay (SRA) tests for antibodies responsible for heparin-induced thrombocytopenia (HIT). By definition, SRA-positive antibodies cause platelet serotonin release in vitro, in the presence of low concentrations of heparin, but not with excess heparin. Many SRA-positive sera activate platelets in the presence of saline without drug, either as a result of residual heparin in the specimen, or because of intrinsic features of the HIT antibodies. The present experiments show that neither exhaustive heparinase treatment, nor chromatographic removal of heparin abrogates the spontaneous platelet activation caused by these HIT antibodies. This is the first study to systematically demonstrate that in vitro activity of HIT antibodies can be independent of heparin. In addition, T-gel chromatography demonstrated differences among fractions of enzyme-linked-immunosorbent assay (ELISA)-positive HIT antibodies within individual specimens. Certain ELISA-positive fractions had SRA activity while others did not, and the SRA activity was not proportional to HIT antibody ELISA titer. These data suggest that antibodies formed as a result of heparin treatment are heterogeneous, and that some can contribute to the pathogenesis of HIT even when heparin is no longer present.
ISSN:1538-7933
DOI:10.1111/j.1538-7836.2005.01560.x