Meloxicam, 15 mg/day, spares platelet function in healthy volunteers

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 μg/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 (ω). It was reduced by indomethacin to 7.3 ± 4.5 ω (P < .001), but not by meloxicam (19 ± 2.5 ω). Platelet aggregation in response to arachidonic acid at baseline was 12.2 ± 2.0 ω. It was reduced by indomethacin in all subjects to 0 ω, but not by meloxicam (11 ± 2.4 ω). 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. Clinical Pharmacology & Therapeutics (1999) 66, 425–430; doi: 10.1053/cp.1999.v66.a101063