Prevention of nonsteroidal anti-inflammatory drug-induced small-intestinal injury by prostaglandin: a pilot randomized controlled trial evaluated by capsule endoscopy.

BACKGROUND

There is no known preventive agent against nonsteroidal anti-inflammatory drug (NSAID) induced small-intestinal injury.

OBJECTIVE

To evaluate by capsule endoscopy whether coadministration of prostaglandin (PG) can prevent small-intestinal damage induced by short-term NSAID treatment.

DESIGN

Single-blind, randomized, controlled trial.

SETTING

All procedures were performed at Nippon Medical School.

SUBJECTS

Thirty-four healthy male volunteers.

METHODS

All subjects were randomly assigned to 2 groups: an NSAID-control group, who underwent NSAID (diclofenac sodium, 25 mg 3 times daily) and omeprazole (20 mg once daily) treatment, and an NSAID-PG group, who received PG (misoprostol, 200 microg 3 times daily) in addition to the same NSAID-omeprazole treatment. Eligible subjects, 15 per group, underwent capsule endoscopy before and 14 days after treatment.

MAIN OUTCOME MEASUREMENTS

The number of mucosal breaks at capsule endoscopy.

RESULTS

NSAID treatment significantly increased the mean (SD) number of mucosal breaks per subject, from a basal level of 0.1 +/- 0.3 up to 2.9 +/- 6.3 lesions in the NSAID-control group (P = .012). In contrast, there was no significant change in the mean number of mucosal breaks before and after PG cotreatment (P = 0.42). Thus, the mean number of posttreatment mucosal breaks per subject was significantly higher in the NSAID-control group than in the NSAID-PG group (P = .028). There was a significant increase in the percentage of subjects in the NSAID-control group, with at least 1 mucosal break after treatment (from 6.7% to 53.3%), whereas there was no change in the incidence of mucosal breaks in the NSAID-PG group, which remained at 13.3%. (P = .002).

LIMITATIONS

Single-center, open-label study.

CONCLUSIONS

PG cotherapy reduced the incidence of small-intestinal lesions induced by a 2-week administration of diclofenac sodium.