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Nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with small-intestinal damage ranging from increased permeability to frank ulceration. The pathogenesis of this damage is unclear and may involve intestinal bacteria.
To determine whether intestinal bacteria play a pathogenic role in NSAID enteropathy, investigators in Europe randomized 60 healthy volunteers with ≤1 mucosal break on video capsule endoscopy (VCE) to receive diclofenac (75 mg twice daily), omeprazole (20 mg daily), and either the antibiotic rifaximin-EIR (400 mg twice daily) or placebo for 14 days. Patients then underwent another VCE to determine the number of small-bowel mucosal breaks.
Fewer patients in the rifaximin group versus the placebo group developed at least …