H. pylori corpus gastritis--relation to acid output

H. pylori acquisition is the main cause of chronic gastritis in humans. After acquisition, non-atrophic gastritis appears which develops with time into atrophic gastritis in approximately one third of infected subjects. Gastritis may affect the gastric antrum, both antrum and corpus or, occasionally, corpus alone. Acid secretion and local acidity are factors which are considered to influence the ecology and flourishing of H. pylori infection in the stomach, and can, therefore, also modulate the evolution of gastritis into topographically dissimilar subtypes. In the present study, we analysed whether there occurs an association between the intensity of chronic gastritis (inflammation) of the corpus mucosa and the pentagastrin stimulated peak acid output (PAO) in 94 subjects who had an H. pylori positive, non-atrophic gastritis. It appeared that the mean PAO was significantly higher in subjects who had mild or no chronic corpus gastritis than in those who had severe corpus gastritis. The prevalence of subjects with mild or no gastritis was highest among those with a high PAO ( > or = 30 mmol/hr) and lowest among those with a low PAO ( < 30 mml/hr). Furthermore, the mean score of chronic corpus gastritis was significantly (P < 0.01) lower in those with PAO < or = 19 mmol/hr than among those with PAO > or = 40 mmol/hr. We conclude that the intensity of chronic inflammation (gastritis) in the corpus mucosa is inversely related to PAO. This supports the hypothesis that acid output may affect the course of H. pylori gastritis and can modulate the topographic distribution of gastritis in the stomach.