title: Clinical implications of prostaglandin inhibition in the small bowel.
abstract: NSAID-induced intestinal toxicity is more common than previously recognized and may have clinically significant sequelae, especially in elderly arthritic patients. Increased awareness of the potential intestinal complications associated with prostaglandin inhibition is required for early recognition and appropriate management. An increase in the level of suspicion by physicians may lead to earlier diagnosis and subsequent discontinuation of the offending NSAID; this is important in that discontinuation of the offending agent may be preferable to multiple endoscopic radiologic and surgical procedures in the patient with obscure blood loss and anemia. Appropriate diagnosis in selected patients may prevent the increased morbidity and mortality associated with small intestinal surgery. The emergence of selective COX-2 inhibitors likely will bring this issue to the forefront because it will become increasingly important to determine the effects of these agents on the small intestine and colon, in addition to their effects on the gastroduodenal mucosa. The new generation of selective COX-2 inhibitors may offer a potential therapeutic advantage over the nonselective NSAIDs with respect to their intestinal toxicity. Well-designed safety trials that have intestinal injury as a predefined end point will provide important information as to the overall gastrointestinal safety of these compounds. These agents must be evaluated with respect to their overall safety profile and not just by their gastrointestinal safety. Nevertheless, these agents are continuing to provide new directions for exciting basic and clinical scientific investigation.
authors.affiliation: Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA. chouchen@im.wash.edu
authors.forename: C W
authors.initials: CW
authors.lastname: Houchen
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000627:therapeutic use; D003251:Constriction, Pathologic; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000009:adverse effects*; D006471:Gastrointestinal Hemorrhage / Q000139:chemically induced*; D006801:Humans; D007249:Inflammation / Q000139:chemically induced; D007413:Intestinal Mucosa / Q000473:pathology; D007416:Intestinal Perforation / Q000139:chemically induced; D007421:Intestine, Small / Q000187:drug effects* / Q000473:pathology; D007527:Isoenzymes / Q000037:antagonists & inhibitors; D008565:Membrane Proteins; D011448:Prostaglandin Antagonists / Q000009:adverse effects*; D011451:Prostaglandin-Endoperoxide Synthases; D051381:Rats
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D011448:Prostaglandin Antagonists; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases