HELICOBACTER-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 developes wi th time into atrophic gastritis in approximately one third of infected subjects. Gastritis may affect the gastric antrum, both antrum and co rpus or, occasionally, corpus alone. Acid secretion and local acidity are factors which are considered to influence the ecology and flourish ing of H. pylori infection in the stomach, and can, therefore, also mo dulate the evolution of gastritis into topographically dissimilar subt ypes. In the present study, we analysed whether there occurs an associ ation 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 (greater than or equal to 30 mmol/hr) and lowest among those with a low PAO (<30 mml/hr). Furthermo re, the mean score of chronic corpus gastritis was significantly (P<0. 01) lower in those with PAO less than or equal to 19 mmol/hr than amon g those with PAO greater than or equal to 40 mmol/hr. We conclude that the intensity of chronic inflammation (gastritis) in the corpus mucos a is inversely related to PAO. This supports the hypothesis that acid output may affect the course of H. pylori gastritis and can modulate t he topographic distribution of gastritis in the stomach.