Pharmacodynamics and Drug Action
Clinical Pharmacology & Therapeutics (1999) 66, 425–430; doi: 10.1053/cp.1999.v66.a101063
Meloxicam, 15 mg/day, spares platelet function in healthy volunteers*
Arthur de Meijer MD1, Hans Vollaard PhD1, Menno de Metz PhD1, Bert Verbruggen1, Chris Thomas PhD1 and Irena Novakova MD, PhD1
1Department of Clinical Pharmacy and Clinical Chemistry, Canisius Wilhelmina Hospital, and the Department of Hematology, the Central Hematological Laboratory, and the Department of Obstetrics, Gynaecology and Chemical Endocrinology, University Hospital St Radboud, Nijmegen The Netherlands
Correspondence: Arthur de Meijer, MD, Marga Klompelaan 26, NL-6532 SC Nijmegen, The Netherlands
*Supported by the Department of Clinical Pharmacy, Canisius Wilhelmina Hospital, Nijmegen, The Netherlands.
Received 4 February 1999; Accepted 23 June 1999.
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 
g/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 (
). It was reduced by indomethacin to 7.3 4.5 (P < .001), but not by meloxicam (19 2.5 ). Platelet aggregation in response to arachidonic acid at baseline was 12.2 2.0 . It was reduced by indomethacin in all subjects to 0 , but not by meloxicam (11 2.4 ). 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).
Conclusion: 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.
