[What role today for Helicobacter pylori in peptic ulcer?]

Abstract

Helicobacter pylori (H. pylori) and nonsteroidal anti-inflammatory drugs/aspirin (NSAIDs) remain today the main etiologies of duodenal (DU) and gastric (GU) ulcers. In some countries or areas in which prevalence of H. pylori infection has decreased, and probably also in which the consumption of NSAIDs is high, the proportion of ulcers not associated with H. pylori is high. Nevertheless, the proportion of Helicobacter pylori-negative, NSAID-negative ulcers remains low, less than 6% in most studies. Furthermore, this proportion is probably overestimated because the search for the infection and NSAIDs treatments was not always performed properly. Data about characteristics of idiopathic GU (after excluding cancer) are missing. In two studies, Helicobacter pylori-negative, NSAID-negative DU were associated in two thirds to three quarters of the cases with co-morbidities, often severe (cirrhosis, respiratory, renal or cardiac failure, malignancy). Numerous digestive diseases can give a DU, Crohn's disease being probably the most frequent one. Gastric acid hypersecretion, as in H. pylori-positive DU, seems to be the pathogenic factor of idiopathic DU, with increased duodenal acid load. The outcome of idiopathic ulcers has been little studied. There are no reliable data concerning the risk of complications. Therapy is based on proton pump inhibitors at a dosage allowing prolonged healing