Natural course of Helicobacter pylori gastric infection.

Helicobacter pylori acquisition induces chronic gastritis that affects antrum, corpus or both. In approximately half of the cases, Helicobacter pylori gastritis slowly (years, decades) develops to atrophic gastritis, thereby resulting in severe abnormalities in the function of the stomach. In humans, the appearance of intestinal metaplasia associates with atrophic gastritis (loss of normal antral and/or oxyntic glands), and intestinal metaplasia linearly increases in grade and extent with increasing age and progression of atrophy. Several mechanisms may play in role in the development of atrophic gastritis and intestinal metaplasia; i.e., including genetic liability of the host to destruction of cells and glands, specific cytotoxic strains of Helicobacter pylori, environmental factors other than the bacterial ones, and some functional properties of the stomach, such as output of acid and intragastric acidity. Atrophic and metaplastic alterations may also result from genotoxic and mutagenic injuries which are triggered by the inflammation, or are exogenous.