Rationale for eradication of Helicobacter pylori infection in duodenal ulcer disease.

Helicobacter pylori is presently considered a major factor predisposing to the development of duodenal ulceration. The risk of duodenal disease is increased up to 15-fold in patients with H pylori-associated gastritis compared with individuals without H pylori infection. This magnitude of risk with H pylori infection is higher than that of any other known or postulated factor contributing to duodenal ulcer formation. To reclassify duodenal ulcer disease from simply being an acid-related disease to being an infectious disease may appear radical, but no questions remain concerning the essential role of H pylori in this disease. The sequence of events in the development of duodenal ulceration is based on strong circumstantial evidence. The steps by which H pylori interacts with the duodenal mucosa in forming duodenal ulcers may be as follows: 1) H pylori infection of the antral mucosa alters gastric physiology, with an increase in gastrin release and a consequent increase in gastric acid secretion. 2) The increased acid load of the bulbar-duodenal mucosa is responsible for the induction of gastric metaplasia. 3) Gastric metaplasia in the duodenal mucosa can be colonized by H pylori resulting in chronic duodenitis. 4) The interaction of H pylori with the metaplastic gastric epithelium leads to weakening of the normal mucosal integrity. At this point, a variety of factors related to H pylori itself, the host response, or the superimposition of factors such as smoking or stress may ultimately lead to ulcer formation. 5) From clinical observations, it is well established that treatment of H pylori infection without concomitant effects on acid secretion is effective in healing duodenal ulcers. More importantly, eradication of H pylori significantly reduces duodenal ulcer relapse rates. Data from clinical trials strongly suggest that H pylori eradication may cure duodenal ulcer disease.