Helicobacter pylori has repeatedly been shown to be associated with chronic superficial gastritis (CSG), which involves the antrum and the fundus of the stomach (Figure 23-1). Essentially all infected persons develop chronic superficial gastritis and it has clearly been shown worldwide that H pylori is the major cause of this lesion. Most of the patients with H pylori-induced chronic superficial gastritis are asymptomatic. The organisms are present on the luminal surface of mucus-secreting cells and within gastric pits, but do not invade tissue. Colonization of the affected areas of the gastric mucosa may be patchy (heavily colonized areas may be adjacent to those with no colonization). Organisms are generally not present over areas of intestinal metaplasia in the gastric mucosa. This CSG is nearly always present in patients with either gastric or duodenal ulcers. Essentially all patients with duodenal ulcers harbor H pylori in the duodenum. In duodenal ulcer disease, H pylori is associated with gastric metaplasia, but not with normal duodenal mucosa. The association of H pylori infection and gastric metaplasia is highly associated with active duodenitis.
H pylori causes the most common form of chronic gastritis (CSG), and chronic gastritis is a well known risk factor for the development of gastric carcinoma. The epidemiologic characteristics of H pylori infection are similar to those observed in the epidemiology of adenocarcinoma of the stomach. In addition, the development of intestinal metaplasia and atrophic gastritis, two risk factors for gastric cancer, are associated with H pylori infection. All these data and prospective epidemiologic studies indicate that infection of humans with H pylori is causally associated with the risk of developing gastric cancer. H pylori infection also is associated with risk of developing gastric lymphoma.Copyright © 1996
The University of Texas Medical Branch at Galveston