COMPARISON OF THE EFFECT OF INTRAVENOUS KETOPROFEN, KETOROLAC AND DICLOFENAC ON PLATELET-FUNCTION IN VOLUNTEERS

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit pros taglandin synthesis which may result in impaired platelet function. Be cause NSAIDs have different abilities to inhibit cyclo-oxygenases we c ompared the effect of intravenous ketoprofen, ketorolac and diclofenac on platelet function in volunteers. Methods: Ten healthy male volunte ers were given ketoprofen 1.4 mg.kg(-1) ketorolac 0.4 mg.kg(-1) and di clofenac 1.1 mg.kg(-1) in saline i.v. on three different occasions, at more than one-week intervals, in a randomized double-blind crossover study. Platelet function was evaluated before (sample 0), 2 (sample 2) and 24 h (sample 3) after the beginning of the infusion. Results: Two of the volunteers had no secondary platelet aggregation in their aggr egation curves before the experiment (sample 0, studied three times) a nd their results were excluded from the final analysis. Diclofenac inh ibited adrenaline (0.9 mu g.ml(-1)) induced platelet aggregation less (median maximal aggregation 22.5%) than ketoprofen (18.3%) and ketorol ac (15.7%) (P<0.05) in sample 2. In the ketorolac group in sample 3 an impairment of adrenaline (0.9 mu g.ml(-1)) induced platelet aggregati on was still seen (26.7%) (P<0.05) but not in the other groups. Diclof enac did not affect adenosine diphosphate (ADP) induced platelet aggre gation. However, ketorolac caused an impairment in ADP (3 mu M and 6 m u M) induced platelet aggregation and ketoprofen in ABP (6 mu M) induc ed platelet aggregation in sample 2. Bleeding time was prolonged (P<0. 05) after ketoprofen and ketorolac (sample 2) but not after diclofenac . Platelet retention on glass beads was unaffected by the tested drugs . Conclusion Ketoprofen, ketorolac and diclofenac caused a reversible platelet dysfunction. Diclofenac had the mildest effect, while platele t dysfunction was still seen 24 h after the beginning of ketorolac.