Abstract
Nonsteroidal anti-inflammatory drugs (NSAIDs) are capable of damaging the whole gastrointestinal tract. Small and large intestinal injuries manifest as acute changes in permeability with endoscopic erosions, chronic erosions and ulcers, diaphragms in the small bowel, and an increase in small and large bowel complications including perforation and diverticular bleeding. It is quite likely, though not proven, that such lesions contribute to anemia in patients taking them. A growing body of data shows that selective inhibitors of the cyclooxygenase-2 enzyme have much reduced toxicity in this respect. In addition, NSAID use has also been associated with development or relapse of ulcerative colitis. Whether the same is true of Crohn's disease, particularly of the small bowel, is less clear. An important point is that there are data that suggest that paracetamol may also not be devoid of toxicity. This makes use of selective cyclooxygenase-2 inhibitors attractive. There have been a number of reports of their use in inflammatory bowel disease. However, many of these have principally involved Crohn's disease and there have not been enough to be clear whether they affect the influence of relapse of ulcerative colitis.
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