title: Evaluation of platelet function and pharmacological platelet inhibition in patients with myeloproliferative disorders using multiple electrode aggregometry.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Central Laboratory, Department of Internal Medicine, Hospital Barmherzige Brueder Graz-Eggenberg, Austria. christoph.robier@bbegg.at
authors.forename: Christoph
authors.initials: C
authors.lastname: Robier
authors.forename: Manfred
authors.initials: M
authors.lastname: Neubauer
authors.forename: Heinz
authors.initials: H
authors.lastname: Sternad
authors.forename: Franz
authors.initials: F
authors.lastname: Quehenberger
authors.forename: Franz
authors.initials: F
authors.lastname: Rainer
authors.forename: Peter
authors.initials: P
authors.lastname: Neumeister
mesh_terms: D000244:Adenosine Diphosphate; D000328:Adult; D000368:Aged; D016718:Arachidonic Acid; D001241:Aspirin / Q000627:therapeutic use*; D001317:Austria; D016022:Case-Control Studies; D000077144:Clopidogrel; D004566:Electrodes; D005260:Female; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D010455:Peptides; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010979:Platelet Function Tests / Q000295:instrumentation; D011087:Polycythemia Vera / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D011237:Predictive Value of Tests; D015203:Reproducibility of Results; D013920:Thrombocythemia, Essential / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D013927:Thrombosis / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D016718:Arachidonic Acid; D000244:Adenosine Diphosphate; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin