Evaluation of platelet function and pharmacological platelet inhibition in patients with myeloproliferative disorders using multiple electrode aggregometry

Robier, Christoph; Neubauer, Manfred; Sternad, Heinz; Quehenberger, Franz; Rainer, Franz; Neumeister, Peter

doi:10.1016/j.thromres.2010.06.014

« Previous Next »Thrombosis Research
Volume 126, Issue 3 , Pages 232-237, September 2010

Evaluation of platelet function and pharmacological platelet inhibition in patients with myeloproliferative disorders using multiple electrode aggregometry

Christoph Robier
- Central Laboratory, Department of Internal Medicine, Hospital Barmherzige Brueder Graz-Eggenberg, Austria
- Corresponding author. Central Laboratory, Hospital Barmherzige Brueder, Graz-Eggenberg, Bergstrasse 27, A-8020 Graz, Austria. Tel.: +43 316 5989 6671; fax: +43 316 5989 1505.
Manfred Neubauer
- Central Laboratory, Department of Internal Medicine, Hospital Barmherzige Brueder Graz-Eggenberg, Austria
Heinz Sternad
- Central Laboratory, Department of Internal Medicine, Hospital Barmherzige Brueder Graz-Eggenberg, Austria
Franz Quehenberger
- Institute of Medical Informatics, Statistics and Documentation, Medical University of Graz, Austria
Franz Rainer
- Central Laboratory, Department of Internal Medicine, Hospital Barmherzige Brueder Graz-Eggenberg, Austria
Peter Neumeister
- Department of Hematology, Medical University of Graz, Austria

Received 2 February 2010; received in revised form 7 June 2010; accepted 17 June 2010. published online 15 July 2010.

Abstract

Background

The aim of this study was to describe platelet aggregation characteristics by multiple electrode aggregometry (MEA) and to evaluate MEA for its potential to detect platelet dysfunction and response to anti-aggregatory drugs in patients with myeloproliferative disorders (MPD).

Methods

We compared the platelet response to arachidonic acid (ASPI test), adenosine diphosphate (ADP test) and thrombin receptor activating peptide (TRAP test) in hirudin-anticoagulated blood of 55 patients with polycythaemia vera and essential thrombocythaemia and 75 controls.

Results

Comparing MPD patients and controls no statistically significant difference indicative of platelet dysfunction was found in MPD patients. Analysis of covariance revealed platelet- and leukocyte count as a significant influencing factor on MEA function. Furthermore we could demonstrate that ASA and clopidogrel treatment results in a statistically significant lower ASPI (Controls: p<0.0001, MPD: p<0.0001) and ADPtest value (MPD: p=0.00125) compared to untreated patients thereby validating the method for monitoring of anti-aggregatory therapy.

Conclusion

In this study MEA was confirmed as a valid method for monitoring of ASA and clopidogrel treatment in patients with MPD and normal control subjects. The platelet and leukocyte count were identified as major influencing factors on MEA aggregation tests both in MPD patients and controls. No functional platelet abnormalities were detected in MPD patients.

Abbreviations: MEA, multiple electrode aggregometry, MPD, myeloproliferative disorders, ET, essential thrombocythaemia, PV, polycythaemia vera, ASPI test, arachidonic acid, ADP test, adenosine diphosphate, TRAP test, thrombin receptor activating peptide, PLT, platelet count, RT, reactive thrombocytosis, ASA, acetylsalicylic acid, ANCOVA, analysis of covariance, COX-2, cyclooxygenase 2