Summary
Hp and NSAID are the most common pathogens in the stomach, but their interaction on gastro- duodenal mucosa has been little studied. Hp infection in humans does not interfere with NSAID-induced gastric ulcer healing by omeprazole, therefore, there is no rationale to eradicate the germ. Hp infection induces COX-2 expression resulting in excessive biosynthesis of gastroprotective prostaglandin (PG), which should in turn counteract NSAID-induced gastropathy and contribute to healing of existing ulcers. Some investigators claim that Hp infection
acts synergistically with NSAID on ulcerogenesis and propose that Hp should be eradicated, particularly at the onset of long-term NSAID therapy. Our studies in about 6500 dyspeptic patients undergoing upper endoscopy and 13C-urea breath test revealed that about 70% of these patients are Hp positive and 31% of these develop
gastro-duodenal ulcers. Of these ulcers, 66% were Hp positive and NSAID negative, 3% – NSAID positive and Hp negative, 8% were both Hp positive and NSAID positive, while 23% ulcers were Hp and NSAID negative. An evidence was obtained for negative interaction
between Hp infection and NSAID on risk of gastro-duodenal ulcers suggesting that Hp may attenuate the peptic ulcerogenesis.
Our results support the concept 1) the interaction between Hp infection and NSAID on gastro- duodenal ulcerations is antagonistic, 2) the Hp and NSAID are independent risk factors for peptic ulcerations in humans, 3) there is no need for the Hp eradication in NSAID-treated
patients, and 4) the rate of ulcer complications (hemorrhage and perforation) remains constant despite the decrease in Hp and ulcer prevalence.

Keywords: Anti-Inflammatory Agents, Non-Steroidal - metabolism, Gastric Acid - metabolism, Gastric Mucosa - drug effects, Gastric Mucosa - microbiology, Helicobacter pylori - metabolism, Models, Biological, Peptic Ulcer - complications, Peptic Ulcer - diagnosis, Peptic Ulcer - microbiology, Risk Factors, Stomach - immunology