Comparison of the effects of ketoprofen on platelet function in the presence and absence of aspirin

PURPOSE: Although aspirin and other nonsteroidal anti-inflammatory drugs (N SAIDs) exert inhibitory effects on platelets in vitro and in vivo, there ar e insufficient data to substantiate the use of NSAIDs alone as antiplatelet drugs in patients already taking aspirin. We therefore sought to determine whether aspirin, added to NSAID therapy, further suppresses platelet funct ion. SUBJECTS AND METHODS: We enrolled 25 healthy adult volunteers who were admi nistered ketoprofen (extended-release capsules, 200 mg daily) for I week, f ollowed by ketoprofen (200 mg daily) and aspirin (325 mg daily) or ketoprof en (200 mg daily) alone during the second week. Platelet aggregation, stimu lated by epinephrine and arachidonic acid, and cyclooxygenase activity, mea sured by thromboxane B-2, were measured at baseline, on day 8, and on day 1 5. RESULTS: On day 8, all subjects demonstrated abnormal platelet aggregation (> 50% inhibition), which persisted at day 15 in both the aspirin and no as pirin groups. One week of ketoprofen treatment reduced thromboxane B-2 leve ls by 84% in the aspirin group and by 85% in the no aspirin group (P = 0.8) , without any further inhibition measured on day 15. CONCLUSION: Extended-release ketoprofen significantly inhibited platelet ag gregation and thromboxane B, production in healthy volunteers. Addition of aspirin had no additional effect. Trials are warranted to determine whether these in vitro effects result in clinical antiplatelet activity in patient s who require chronic treatment with NSAIDs, thereby avoiding the toxicity of NSAID/aspirin combination therapy. (C) 2001 by Excerpta Medica, Inc.