[Campylobacter pylori: cause of gastritis and ulcer disease?]

Several studies have shown a striking association between the presence of Campylobacter pylori (C.p) in the gastric mucosa and histologically confirmed gastritis and ulcer disease. The microorganism has been found in up to 90% of patients with active chronic antral (type B) gastric ulcer, and in up to 70% of patients with duodenal ulcer. Voluntary ingestion of C.p. by two persons and two epidemic occurrences after apparent C.p. contamination of stomach probes, with demonstration of the bacterium in the mucosa, have shown that C.p. can induce acute gastritis; in one volunteer the acute gastritis progressed to the active chronic form. Eradication of C.p. by antibacterial treatment is associated with resolution of gastritis. Relapse of peptic ulcer is closely related to infection by C.p. The microorganism has important virulence factors allowing it to select an ecological niche below the mucus layer on the gastric mucosa. C.p. exhibits strong mucolytic activity through proteases which could damage the mucus barrier and therefore increase susceptibility to development of gastritis and peptic ulcers; however, the pathogenic impact of C.p. remains unknown. C.p. is diagnosed by histological or microbiological examination of gastric biopsy specimens or by serological techniques. Bismuth salts alone or in combination with antibiotics are effective against C.p., but the efficacy of antimicrobial treatment of gastritis and ulcer disease associated with C.p. has still to be proven by large double-blind placebo-controlled trials. The hitherto published findings do not allow definite evaluation of the pathogenetic significance of C.p. in gastritis and ulcer disease.(ABSTRACT TRUNCATED AT 250 WORDS)