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dc.contributor.authorMaiden, Laurence
dc.contributor.authorThjodleifsson, Bjarni
dc.contributor.authorSeigal, Anna
dc.contributor.authorBjarnason, Ingvar Iain
dc.contributor.authorScott, David
dc.contributor.authorBirgisson, Sigurbjorn
dc.contributor.authorBjarnason, Ingvar
dc.date.accessioned2008-01-08T09:52:09Z
dc.date.available2008-01-08T09:52:09Z
dc.date.issued2007-09-01
dc.date.submitted2007-01-08
dc.identifier.citationClin. Gastroenterol. Hepatol. 2007, 5(9):1040-5en
dc.identifier.issn1542-7714
dc.identifier.pmid17625980
dc.identifier.doi10.1016/j.cgh.2007.04.031
dc.identifier.urihttp://hdl.handle.net/2336/15793
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractBACKGROUND & AIMS: Nonsteroidal anti-inflammatory drug (NSAID) gastropathy is sufficiently important as to warrant co-administration of misoprostol or proton pump inhibitors or a switch to selective cyclooxygenase (COX)-2 inhibitors. However, the serious ulcer outcome studies suggested that 40% of the clinically significant gastrointestinal bleeding originated more distally, presumably from NSAID enteropathy. We used capsule enteroscopy to study small-bowel damage in patients on long-term NSAIDs and COX-2-selective agents. METHODS: Sixty healthy volunteers acted as controls. One hundred twenty and 40 patients on long-term NSAIDs and COX-2 selective agents, respectively, underwent a capsule enteroscopy study. Small-bowel damage was categorized and quantitated. RESULTS: Sixty-two percent of patients on conventional NSAIDs were abnormal, which differed significantly (P < .001) from controls. The main pathology related to reddened folds (13%), denuded areas (39%), and mucosal breaks (29%). Two percent had diaphragm-like strictures and 3% had bleeding without an identifiable lesion. The damage, seen in 50% of patients on selective COX-2 inhibitors (reddened folds, 8%; denuded areas, 18%; and mucosal breaks, 22%), did not differ significantly (P > .5) from that seen with NSAIDs. CONCLUSIONS: Long-term NSAIDs and COX-2-selective agents cause comparable small-bowel damage. This suggests an important role for COX-2 in the maintenance of small-bowel integrity. The results have implications for strategies that aim to minimize the gastrointestinal damage in patients requiring anti-inflammatory analgesics.
dc.language.isoenen
dc.publisherW.B. Saunders for the American Gastroenterological Associationen
dc.relation.urlhttp://www.sciencedirect.com/science/article/B7GGW-4P59RY9-7/2/edc0bd21c1c7708840e08e604df2ae37en
dc.subject.meshAdministration, Oralen
dc.subject.meshAdolescenten
dc.subject.meshAdulten
dc.subject.meshAgeden
dc.subject.meshAged, 80 and overen
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidalen
dc.subject.meshCapsule Endoscopyen
dc.subject.meshConfidence Intervalsen
dc.subject.meshCross-Sectional Studiesen
dc.subject.meshCyclooxygenase 2 Inhibitorsen
dc.subject.meshEnglanden
dc.subject.meshFemaleen
dc.subject.meshFollow-Up Studiesen
dc.subject.meshHumansen
dc.subject.meshIcelanden
dc.subject.meshIntestinal Diseasesen
dc.subject.meshIntestinal Mucosaen
dc.subject.meshIntestine, Smallen
dc.subject.meshMaleen
dc.subject.meshMiddle Ageden
dc.subject.meshPrognosisen
dc.subject.meshRisk Factorsen
dc.subject.meshTime Factorsen
dc.titleLong-term effects of nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 selective agents on the small bowel: a cross-sectional capsule enteroscopy study.en
dc.typeArticleen
dc.contributor.departmentDepartment of Medicine, Landspitali University Hospital, Reykjavik, Icelanden
html.description.abstractBACKGROUND & AIMS: Nonsteroidal anti-inflammatory drug (NSAID) gastropathy is sufficiently important as to warrant co-administration of misoprostol or proton pump inhibitors or a switch to selective cyclooxygenase (COX)-2 inhibitors. However, the serious ulcer outcome studies suggested that 40% of the clinically significant gastrointestinal bleeding originated more distally, presumably from NSAID enteropathy. We used capsule enteroscopy to study small-bowel damage in patients on long-term NSAIDs and COX-2-selective agents. METHODS: Sixty healthy volunteers acted as controls. One hundred twenty and 40 patients on long-term NSAIDs and COX-2 selective agents, respectively, underwent a capsule enteroscopy study. Small-bowel damage was categorized and quantitated. RESULTS: Sixty-two percent of patients on conventional NSAIDs were abnormal, which differed significantly (P < .001) from controls. The main pathology related to reddened folds (13%), denuded areas (39%), and mucosal breaks (29%). Two percent had diaphragm-like strictures and 3% had bleeding without an identifiable lesion. The damage, seen in 50% of patients on selective COX-2 inhibitors (reddened folds, 8%; denuded areas, 18%; and mucosal breaks, 22%), did not differ significantly (P > .5) from that seen with NSAIDs. CONCLUSIONS: Long-term NSAIDs and COX-2-selective agents cause comparable small-bowel damage. This suggests an important role for COX-2 in the maintenance of small-bowel integrity. The results have implications for strategies that aim to minimize the gastrointestinal damage in patients requiring anti-inflammatory analgesics.


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