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New molecules may overtake the COX 2 inhibitors debate
| The first 150 words of the full text of this article appear below. |
For many years, non-steroidal anti-inflammatory
drugs were regarded as a treatment for which there was no gain in
arthritis without the pain of gastroduodenal toxicity. This reflected
the understanding that non-steroidal anti-inflammatory drugs (NSAIDs) were cyclo-oxygenase inhibitors that reduced prostaglandin synthesis both in inflamed joints with benefit and in the stomach with detriment (figure). Recognition that a highly inducible enzyme,
cyclo-oxygenase-2, largely subserved the former and a constitutive
enzyme, cyclo-oxygenase-1, the latter provided an obvious selective
target. The consequent success of cyclo-oxygenase-2 (COX 2) inhibitors
arises, in part, from the conceptual simplicity of this idea. The
journey from concept to reality has, however, inevitably been more
complex, and one controversial issue is dealt with in an accompanying
editorial.1 The failure of the celecoxib long term
arthritis safety study (the CLASS study) may have more to do with the
design of the trial than with inadequacies of cyclo-oxygenase-2
inhibitors. Other limitations
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