Agonist-inducible platelet activation in chronic idiopathic autoimmune thrombocytopenia

  1. Simon Panzer1,
  2. Lisa Höcker1,
  3. Miriam Rieger2,
  4. Rainer Vormittag2,
  5. Daniela Koren1,
  6. Daniela Dunkler3,
  7. Ingrid Pabinger2

Article first published online: 20 JUN 2007

DOI: 10.1111/j.1600-0609.2007.00900.x

Issue

European Journal of Haematology

European Journal of Haematology

Volume 79, Issue 3, pages 198–204, September 2007

Additional Information

How to Cite

Panzer, S., Höcker, L., Rieger, M., Vormittag, R., Koren, D., Dunkler, D. and Pabinger, I. (2007), Agonist-inducible platelet activation in chronic idiopathic autoimmune thrombocytopenia. European Journal of Haematology, 79: 198–204. doi: 10.1111/j.1600-0609.2007.00900.x

Author Information

  1. 1

    Clinic for Blood Group Serology

  2. 2

    Department of Internal Medicine I, Division of Haematology and Haemostaseology

  3. 3

    Core Unit for Medical Statistics and Informatics, Section of Clinical Biometrics, Medical University of Vienna, Vienna, Austria

*Simon Panzer, MD, Clinic for Blood Group Serology, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria. Tel: +43 1 40400 5320; Fax: +43 1 40400 5321; e-mail: simon.panzer@meduniwien.ac.at

Publication History

  1. Issue published online: 20 JUN 2007
  2. Article first published online: 20 JUN 2007
  3. Accepted for publication 20 May 2007

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Keywords:

  • chronic autoimmune thrombocytopenia;
  • platelet activation;
  • platelet agonists;
  • platelet antibodies;
  • reticulated platelets

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.

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