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Inflammation is a complex response to cell injury that primarily occurs in vascularized connective tissue and often involves the immune response. The mediators of inflammation function to eliminate the cause of cell injury and clear away debris, in preparation for tissue repair. Unfortunately, inflammation also causes pain and, in instances in which the cause of cell injury is not eliminated, can result in a chronic condition of pain and tissue damage such as that seen in rheumatoid arthritis. The nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen are often effective in controlling inflammatory pain. Other treatment strategies applied to the reduction of inflammation are targeted at immune processes. These include glucocorticoids and disease-modifying antirheumatic drugs (DMARDs). Gout is an inflammatory joint disease caused by precipitation of uric acid crystals. Treatment of acute episodes targets inflammation, whereas treatment of chronic gout targets both inflammatory processes and the production and elimination of uric acid.
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Classification and Prototypes
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Aspirin (acetylsalicylic acid) is the prototype of the salicylates and other NSAIDs (Table 36–1). The other older nonselective NSAIDs (ibuprofen, indomethacin, many others) vary primarily in their potency, analgesic and anti-inflammatory effectiveness, and duration of action. Ibuprofen and naproxen have moderate effectiveness; indomethacin has greater anti-inflammatory effectiveness; and ketorolac has greater analgesic effectiveness. Celecoxib was the first member of a newer NSAID subgroup, the cyclooxygenase-2 (COX-2)-selective inhibitors, which were developed in an attempt to lessen the gastrointestinal toxicity associated with COX inhibition while preserving efficacy. Unfortunately, clinical trials involving some of the highly selective COX-2 inhibitors have shown a higher incidence of cardiovascular thrombotic events than the nonselective drugs.
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