Can antibiotics help prevent NSAID-associated mucosal injury?

Last Updated: 2017-01-03

By Reuters Staff

NEW YORK (Reuters Health) - New research suggests the possibility that rifaximin-EIR may help prevent mucosal lesions associated with daily non-steroidal anti-inflammatory drug (NSAID) use, but the result did not reach statistical significance.

"Although short-term studies, such as this one, and mucosal breaks may not have straightforward clinical implications, the results of this proof-of-concept study strongly suggest the role of enteric bacteria in the pathogenesis of NSAID-enteropathy, and call for a prospective trial in patients on long-term therapy," Dr. Carmelo Scarpignato of the University of Parma and Maggiore University Hospital in Parma, Italy, and colleagues conclude.

Roughly 75% of NSAID users have mucosal injury in the small intestine, Dr. Scarpignato and his team note in their report, published online December 19 in Gastroenterology. The mechanism behind this injury is not fully understood, they add, although experimental research suggests that commensal enterobacteria may play a role.

To investigate whether rifaximin-EIR (Alfa Wasserman, Bologna, Italy), an antibiotic, might help prevent NSAID-associated injury, the researchers randomly assigned 60 healthy individuals to receive diclofenac SR 75 mg BID and omeprazole 20 mg OD plus either rifaximin-EIR 400 mg or a placebo BID for two weeks.

Video capsule endoscopy at two weeks found at least one mucosal lesion in six patients in the rifaximin group and 13 in the placebo group.

Based on modified full analysis, the odds ratio for mucosal lesion associated with rifaximin was 0.33 (95% confidence interval, 0.10-1.03), while it was 0.35 in the per protocol analysis (95% CI, 0.11-1.12).

The difference between the two groups reached statistical significance on post-hoc sensitivity analysis with age as a covariate.

Average mucosal score was 0.87 with rifaximin and 1.83 with placebo (p=0.021). Patients in the placebo group averaged 1.2 mucosal lesions, versus 0.3 for the rifaximin group.

While no patients in the rifaximin group developed large lesions, nine in the placebo group did.

"After almost 40 years, with the advancement of knowledge on the pathogenic role of gut microbiota in NSAID-enteropathy, the time seems now ripe to study in well-designed, large, randomized, clinical trials microbiota-directed interventions to protect the small bowel from NSAID injury and to allow safer anti-inflammatory therapy," the authors conclude.

Alfa Wasserman supported the study. Dr. Scarpignato and two coauthors are advisors to the company, while two others are employees.

Dr. Scarpignato was not available for an interview by press time.

SOURCE: http://bit.ly/2iKQ1xb

Gastroenterology 2016.