title: Meloxicam, 15 mg/day, spares platelet function in healthy volunteers.
abstract: OBJECTIVE
  To study the influence of meloxicam, a cyclooxygenase-2 (COX-2) preferential nonsteroidal anti-inflammatory drug, on serum thromboxane and platelet function in healthy volunteers with use of the maximum recommended daily dosage of 15 mg/day.
  
  
  METHODS
  This study used an open, randomized crossover design. Indomethacin (INN, indometacin) was given as a positive control for nonsteroidal anti-inflammatory drug-induced inhibition of platelet function. The following variables were recorded: thromboxane B2 serum concentrations by radioimmunoassay, platelet aggregation by whole blood aggregometry in response to collagen 1.1 microg/L and to arachidonic acid 0.35 mmol/L, and closure time with use of the PFA-100.
  
  
  RESULTS
  Serum thromboxane B2 at baseline was 535+/-233 nmol/L (mean +/- SD) and was reduced for 95% by indomethacin to 26+/-19 nmol/L (P < .001) and for 66% by meloxicam to 183+/-62 nmol/L (P < .001). Maximal platelet aggregation in response to collagen at baseline was 18.7+/-1.6 ohms (ohms). It was reduced by indomethacin to 7.3+/-4.5 ohms (P < .001), but not by meloxicam (19+/-2.5 ohms). Platelet aggregation in response to arachidonic acid at baseline was 12.2+/-2.0 ohms. It was reduced by indomethacin in all subjects to 0 ohms, but not by meloxicam (11+/-2.4 ohms). Closure time at baseline was 128+/-24 seconds and was prolonged by indomethacin to 286+/-38 seconds (P < .001). Meloxicam caused a minor prolongation of the closure time (141+/-32 seconds; P < .05).
  
  
  CONCLUSIONS
  Meloxicam, 15 mg/day caused a major reduction of maximum thromboxane production but no reduction in collagen- or arachidonic acid-induced platelet aggregation and only minor increase of the closure time.
authors.affiliation: Department of Clinical Pharmacy and Clinical Chemistry, Canisius Wilhelmina Hospital, Nijmegen, The Netherlands.
authors.forename: A
authors.initials: A
authors.lastname: de Meijer
authors.forename: H
authors.initials: H
authors.lastname: Vollaard
authors.forename: M
authors.initials: M
authors.lastname: de Metz
authors.forename: B
authors.initials: B
authors.lastname: Verbruggen
authors.forename: C
authors.initials: C
authors.lastname: Thomas
authors.forename: I
authors.initials: I
authors.lastname: Novakova
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage* / Q000494:pharmacology*; D016718:Arachidonic Acid / Q000008:administration & dosage / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects*; D018592:Cross-Over Studies; D016861:Cyclooxygenase Inhibitors / Q000008:administration & dosage* / Q000494:pharmacology*; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D000077239:Meloxicam; D010974:Platelet Aggregation / Q000187:drug effects; D011863:Radioimmunoassay; D012016:Reference Values; D013843:Thiazines / Q000008:administration & dosage* / Q000494:pharmacology*; D013844:Thiazoles / Q000008:administration & dosage* / Q000494:pharmacology*; D013929:Thromboxane B2 / Q000097:blood*; D013997:Time Factors
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D013843:Thiazines; D013844:Thiazoles; D016718:Arachidonic Acid; D013929:Thromboxane B2; D000077239:Meloxicam; D007213:Indomethacin