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

Objective: To study the influence of meloxicam, a cyclooxygenase-2 (COX-2) preferential nonsteroidal antiinflammatory drug, on serum thromboxane and p latelet 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-i nflammatory drug-induced inhibition of platelet function. The following var iables were recorded: thromboxane B-2 serum concentrations by radioimmunoas say, platelet aggregation by whole blood aggregometry in response to collag en 1.1 mu g/L and to arachidonic acid 0.35 mmol/L, and closure time with us e of the PFA-100. Results: Serum thromboxane B-2 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 (Ome ga). It was reduced by indomethacin to 7.3 +/- 4.5 Omega (P < .001), but no t by meloxicam (19 +/- 2.5 Omega). Platelet aggregation in response to arac hidonic acid at baseline was 12.2 +/- 2.0 Omega. It was reduced by indometh acin in all subjects to 0 Omega, but not by meloxicam (11 +/- 2.4 Omega). C losure time at baseline was 128 +/- 24 seconds and was prolonged by indomet hacin to 286 +/- 38 seconds (P < .001), Meloxicam caused a minor prolongati on of the closure time (141 +/- 32 seconds; P < .05), Conclusion: Meloxicam, 15 mg/day caused a major reduction of maximum thromb oxane production but no reduction in collagen- or arachidonic acid-induced platelet aggregation and only minor increase of the closure time.