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Comparison between different laboratory tests for the detection and prevention of heparin‐induced thrombocytopenia
Author(s) -
Vitale Marco,
Tazzari Pierluigi,
Ricci Francesca,
Mazza Maria Anna,
Zauli Giorgio,
Martini Giuliana,
Caimi Luigi,
Manzoli Francesco A.,
Conte Roberto
Publication year - 2001
Publication title -
cytometry
Language(s) - English
Resource type - Journals
eISSN - 1097-0320
pISSN - 0196-4763
DOI - 10.1002/cyto.1170
Subject(s) - flow cytometry , heparin induced thrombocytopenia , platelet , platelet activation , heparin , annexin , cytometry , annexin a5 , immunoassay , medicine , antibody , cd63 , immunology , platelet factor 4 , chemistry , biochemistry , microrna , microvesicles , gene
Abstract Background: Heparin‐induced thrombocytopenia (HIT) is a possible complication of heparin therapy that can evolve with life‐threatening thromboembolism, for which early diagnosis is essential. However, the specific laboratory approach to the diagnosis of HIT is still controversial. Methods: Sera from 13 patients with HIT, from 15 patients with non‐HIT thrombocytopenia, and from 10 normal subjects were used to compare nonfunctional and functional methods to detect anti‐heparin:PF‐4 antibodies and platelet activation. We used three enzyme‐linked immunosorbent assays (ELISAs) and the particle gel immunoassay as nonfunctional tests, and platelet aggregometry, CD62p (p‐selectin) phenotypical expression, and Annexin V binding as functional assays. Results: CD62p expression was positive in 85% of the cases and Annexin V was positive in 40% of the HIT cases examined. Aggregometry gave variable results that depend strongly on the donor. Conclusion: Functional tests for platelet activation are more reliable for HIT diagnosis than the nonfunctional tests. We conclude that the phenotypical expression of p‐selectin detected by flow cytometry on activated platelets appears to be a good functional marker for the diagnosis of HIT and its possible thromboembolic complications. Cytometry (Comm. Clin. Cytometry) 46:290–295, 2001. © 2001 Wiley‐Liss, Inc.

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