Abstract

The authors challenge the traditional view that the analgesic effect of NSAIDs can be universally attributed to their inhibitory effects on the synthesis of peripherally formed prostaglandins. Recent clinical evidence is reviewed which supports the concept that peripheral events alone cannot adequately account for the phenomena of hyperalgesia and allodynia following injury to joints and muscle. A corollary of these findings is that in the management of acute pain, pharmacological intervention may be less effective when aimed solely at peripheral events, such as prostaglandin synthesis. In our survey we critically review the results of 26 different studies which were conducted under double-blind conditions and included a placebo control group. Of these, 14 studies demonstrated a significant difference between NSAID and placebo for nine NSAIDs - azapropazone, clonixin, ketoprofen, naproxen, diclofenac, fenbufen, ibuprofen, indomethacin, and piroxicam. In those studies where concomitant physical therapy was administered, we identified four NSAIDs which were demonstrated unequivocably to provide additional benefit - azapropazone, clonixin, ketoprofen, and naproxen. In the light of these findings we discuss the emerging view that, at least for some NSAIDs, effects on nociceptive pathways independent of prostaglandin synthesis may explain their analgesic character. Verf.-Referat (gekuerzt)