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We may receive compensation for some links and banners.Evaluation of toxicity to the gut by non-steroidal anti-inflammatory drugs.
All non-steroidal anti-inflammatory drugs (NSAIDs) have the potential to cause severe damage to the gut mucosa. Acute toxicity is manifested in the clinical picture of NSAID enteropathy, whereas chronic use may lead to the development of colorectal adenomatous polyps. The mechanism of gut toxicity is thought to involve increased cellular proliferation, altered cell turnover and cellular replication in the colon and antral regions of the small bowel. The proliferative response in the gut appears to be dose related. Reduced chloride absorption (leading to fluid retention) may be responsible for the development of adverse gastrointestinal (GI) effects. NSAIDs such as salicylates, aminophenols, indomethacin and sulindac affect the gastric mucosa by a number of mechanisms such as inhibition of prostaglandin synthesis, inhibition of cyclo-oxygenase, stimulation of parietal cell proliferation, release of mucus and inhibition of gastric acid secretion. They are also involved in the inhibition of reabsorption of sodium and chloride. The agent that is primarily responsible for NSAID-related damage to the small bowel appears to be hydroxylated metabolites of the NSAID and duodenal ulcers are reported in up to 25% of patients. The toxicity of NSAIDs is largely dependent on dose, site of action and patient characteristics such as age, nutritional status and genetic susceptibility. Inhibitors of cyclo-oxygenase are found in commercial preparations such as naproxen and related compounds such as piroxicam. The other NSAIDs, however, are currently manufactured to contain only very low levels of cyclo-oxygenase inhibiting metabolites. This review evaluates the evidence supporting the view that specific NSAIDs may be more or less toxic to the GI tract. We conclude that there is an absence of good evidence of

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