Abstract

The major adverse effects of aspirin are due to its gastric irritant effects. The use of aspirin in children under the age of 12 is extremely limited. Some of the effects of aspirin on the gastrointestinal tract are enhanced by alcohol. Concurrent administration of aspirin and dipyridamole may result in raised peak plasma salicylate levels and an increased area under the time-concentration curve (AUC) for the salicylate. Administration of aspirin together with carbonic anhydrase inhibitors or the j8-blocker, metoprolol, may elevate salicylate plasma concentrations to toxic levels. Salicylate concentrations in patients with rheumatoid arthritis may be reduced by concurrent corticosteroids, but may be raised to toxic levels if corticosteroids are withdrawn. Antacids and adsorbents may increase the excretion of aspirin in alkaline urine. Nonsteroidal anti-inflammatory drugs (NSAIDs) are thought to act through inhibition of cyclooxygenase-1 and -2 (Cox-1 and Cox-2), which are involved in the synthesis of prostaglandins. Cox-1 is associated with adverse gastrointestinal effects, while Cox-2 is associated with anti-inflammatory activity. Hence, the interest is in highly selective inhibitors of Cox-2. Meloxicam and nimesulide are two such drugs.

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