Inhibition by nonsteroidal anti-inflammatory drugs (NSAIDs) on pathways of cyclo-oxygenase (COX) and prostaglandin synthesis [33]. The recent demonstration of the existence of functionally distinct isoforms of the cox enzyme has major clinical significance, as it now appears that one form of cox is operative in the gastric mucosa and kidney for prostaglandin generation (COX-1) whereas an inducible and functionally distinct form of cox is operative in the production of prostaglandins in the sites of inflammation and pain (COX-2) [33]. The clinical therapeutic consequence is that an NSAID with inhibitory effects dominantly or exclusively upon the cox isoenzyme induced at a site of inflammation may produce the desired therapeutic effects without the hazards of deleterious effects on the kidneys or gastrointestinal tract. PG—prostaglandin; TxA2—thromboxane A2.

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