Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) are used by millions of patients for many painful pathological disorders. Studies demonstrate their clinical efficacy in both acute and chronic pain. When compared with placebo, NSAIDs show superior analgesic efficacy across a wide spectrum of conditions including postoperative pain, cancer pain, and musculoskeletal conditions. However, NSAIDs have failed to show any benefit in neuropathic pain. Conventional NSAIDs reversibly inhibit the enzyme cyclooxygenase (COX), thereby preventing the production of both prostaglandins and thromboxanes from membrane phospholipids. There are two isoforms of the COX enzyme, COX-1 and COX-2. These isoforms vary in their distribution and expression but are similar in size, substrate specificity, and kinetics. Conventional NSAIDs inhibit the two isoforms to varying degrees, which can cause adverse effects in the gastrointestinal (GI) tract, kidney, respiratory system, and platelets. These sideeffects led to the development of cyclooxygenase-2 inhibitors (coxibs). Coxibs are selective inhibitors of the COX-2 isoenzyme. As the anti-inflammatory effects of conventional NSAIDs were predominantly believed to be mediated by inhibition of COX-2, and their GI side-effects by inhibition of COX-1, it was hypothesized that selective coxibs would provide a safer alternative to conventional NSAIDs.
Published Version
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