Should Selective COX-2 Inhibitors be Used More? Should Selective COX-2 Inhibitors be Used More? Should Selective COX-2 Inhibitors be Used More? Should Selective COX-2 Inhibitors be Used More? Should Selective COX-2 Inhibitors be Used More?

Cyclooxygenase (COX) catalyses the conversion of arachidonic acid (AA) to prostaglandins (PGs), prostacyclins, and thromboxanes. It is well reported that the traditional nonselective nonaspirin nonsteroidal antiinflammatory drugs (NSAIDs) provide their effects through the inhibition of these COX enzymes 1 . Subsequent studies in the same direction demonstrated that COX enzymes have two isoforms, viz., COX-1 and COX-2. The COX-1 is constitutive in nature and expressed in tissues, such as gastrointestinal (GI) mucosa to produce mucoprotective prostaglandins. The COX-1 enzyme plays housekeeping roles in stomach protection, platelet activation, and kidney function; while COX-2, an inducible enzyme expressed in response to tissue inflammation, is responsible for the associated pathology of diseases 2,3 . The recognition of two isoforms of COX enzymes led to the concept that COX-1 enzyme is responsible for production of ‘good’ PGs for physiological functions, including stomach protection, platelets and kidney functions; while COX-2 enzyme is responsible for production of ‘bad’ PGs for pathological functions, including arthritis, hyperalgesia, neurodegenerative disorders and colorectal cancer. In addition, this hypothesis also suggested that inhibition of COX-1-mediated production of ‘good’ PGs by traditional nonaspirin NSAIDs is mainly responsible for their unwanted side effects such as GI bleeding 4 . Therefore,