Journal
GASTROENTEROLOGY CLINICS OF NORTH AMERICA
Volume 38, Issue 2, Pages 333-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.gtc.2009.03.007
Keywords
Nonsteroidal anti-inflammatory drugs; Gastrointestinal bleeding; Gastrointestinal ulcers; Lower gastrointestinal tract; Bacteria; Gut inflammation
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Nonsteroidal anti-inflammatory drug (NSAID)-associated intestinal damage to the small and/or large bowel is frequent and may be present in up to 60% to 70% of patients taking these drugs long term. Intestinal damage is subclinical in most cases (eg, increased mucosal permeability, inflammation, erosions, ulceration), but more serious clinical outcomes, such as anemia and overall bleeding, perforation, obstruction, diverticulitis, and deaths, have also been described. Recent data suggest that serious lower gastrointestinal (GI) clinical events linked to NSAID use may be as frequent and severe as upper GI complications. Treatment and prevention strategies of NSAID-induced damage to the lower GI tract have not been defined so far. Misoprostol, antibiotics, and sulphasalazine have been proven to be effective in animal models, but they have not been properly tested in humans. Preliminary studies with COX-2 selective inhibitors in healthy volunteers have shown that these drugs are associated with less small bowel damage than traditional NSAIDs plus proton pump initiator, although their longterm effects in patients need to be tested. Post hoc analysis of previous outcome studies with these agents have shown contradictory results in the lower GI tract so far.
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