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Agonist‐inducible platelet activation in chronic idiopathic autoimmune thrombocytopenia
Author(s) -
Panzer Simon,
Höcker Lisa,
Rieger Miriam,
Vormittag Rainer,
Koren Daniela,
Dunkler Daniela,
Pabinger Ingrid
Publication year - 2007
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2007.00900.x
Subject(s) - platelet , agonist , platelet activation , in vivo , ristocetin , ex vivo , endocrinology , chemistry , medicine , immunology , receptor , in vitro , biology , biochemistry , von willebrand factor , microbiology and biotechnology
Abstract Objective: There are only few studies on agonist‐inducible platelet activation in chronic idiopathic autoimmune thrombocytopenia (cAITP). Materials and methods: We compared agonist (TRAP‐6, ADP, Arachidonic acid, Epinephrine, and Ristocetin) ‐inducible P‐selectin expression and PAC‐1 binding in 40 patients with cAITP (f/m ratio 23/17) with those in 20 healthy controls. Results were correlated with platelet counts, detectable platelet antibodies, and reticulated platelets. Results: The in vivo activation of platelets determined the in vitro inducible response to agonists. The stronger the in vivo activation the less the number of platelets responding to agonists, as illustrated by the inverse correlation of P‐selectin expression ex vivo and the relative increase after the exogenous addition of agonists. The agonist‐inducible platelet activation was not associated with the presence of detectable platelet antibodies to GPIb/IX or GPIIb/IIIa. Agonist‐inducible platelet activation was also not correlated with counts of reticulated platelets. Conclusion: Agonist‐inducible activation of platelets in cAITP is affected mainly by their in vivo activation.