INTERACTION OF NSAIDS AND HELICOBACTER-PYLORI ON GASTROINTESTINAL INJURY AND PROSTAGLANDIN PRODUCTION - A CONTROLLED DOUBLE-BLIND TRIAL

Background: H. pylori and nonsteroidal antiinflammatory drugs (NSAIDs) are major causes of gastroduodenal injury in man, We assessed the eff ect of daily NSAID ingestion on gastric histology and the interaction of H. pylori infection and NSAID ingestion on gross and histological i njury and prostaglandin production. Methods: Fifty-two healthy volunte ers with normal baseline endoscopy were randomly assigned to receive i dentical-appearing naproxen 500 mg b.d., etodolac 400 mg b.d., or plac ebo b.d. for 4 weeks. The number and size of all erosions and ulcers w ere recorded by endoscopy at weeks 1 and 4, Biopsies taken at baseline , week 1 and week 4 were assessed for H. pylori, histology and gastric prostaglandin E(2) production. Results: No significant changes occurr ed with treatment in any histological feature in the three study group s or in H. pylori positive or negative subsets. Antral inflammation sc ores (scale, 0-6) for the NSAID group were: week 0-1.2+/-0.3; week 1-1 .1+/-0.3; week 4-1.3+/-9.3; fndings of 'chemical gastritis' were not s een. No significant difference in gross gastroduodenal injury (number or total surface area of ulcers or erosions) was seen between H. pylor i positive and negative subjects in the three groups at week 1 or 4. B aseline prostaglandin E(2) production was significantly higher in H. p ylori positive subjects (2398+/-400 vs. 1064+/-255 pg/mg protein) and decreased significantly with 1 week of naproxen in H. pylori positive and negative subjects. Conclusions: NSAID ingestion does not cause dif fuse histological injury. Any diffuse histological injury in the gastr ic mucosa is related to the presence of H. pylori, and this H. pylori- associated gastritis is not altered by NSAID ingestion. Furthermore, t he development of gross gastroduodenal damage with 4 weeks of NSAID us e is not influenced by underlying H. pylori infection.