Abstract
Data from animal studies suggest thatNSAIDs-induced gastric damage may be due to increasedgastric motility. Such a mechanism, however, has neverbeen tested or demonstrated in man. We evaluated theeffects of two frequently prescribed NSAIDs,indomethacin and diclofenac sodium, on postprandialgastric motor activity (a physiologically reproduciblestimulus) in healthy volunteers to see whether thesecompounds increase gastric motility. Twenty-four healthyvolunteers of both sexes, 21-35 years of age, underwenta basal gastric motility recording. Thereafter, theywere randomized in three groups to receive either placebo, indomethacin (50 mg three times a day)or diclofenac sodium (50 mg three times a day) for aweek. At the end of the week, they underwent anidentical manometric study. Analysis of the motility tracings showed no difference in gastric antralmotility index and in amplitude of gastric antralcontractions after NSAIDs with respect to the basalstudy and to the placebo group. About 50% of subjects (two in the placebo group) complained of sideeffects. These were transient and mild, except in twosubjects taking indomethacin, in whom endoscopy wasnecessary; one of these had a small prepyloric ulcer. It is concluded that in man NSAID-relatedgastric damage is unlikely to be due to increasedgastric motility.
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Bassotti, G., Bucaneve, G., Furno, P. et al. Double-Blind, Placebo-Controlled Study on Effects of Diclofenac Sodium and Indomethacin on Postprandial Gastric Motility in Man. Dig Dis Sci 43, 1172–1176 (1998). https://doi.org/10.1023/A:1018883102636
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DOI: https://doi.org/10.1023/A:1018883102636