HELICOBACTER-PYLORI COLONIZATION DENSITY AND GASTRIC-ACID OUTPUT IN NONULCER DYSPEPSIA AND DUODENAL-ULCER DISEASE

Background. The pattern of intragastric Helicobacter pylori colonizati on and its density may be determined by parietal cell function. H. pyl ori bacterial products san inhibit gastric acid secretion from the par ietal cell. The aim of this investigation was to study the relationshi p between acid output and intragastric H. pylori distribution and colo nization density in duodenal ulcer (DU) and non-ulcer subjects. The st udy included 14 patients with active DU, 10 with inactive DU and 10 no n-ulcer dyspeptics. Methods. Acid output studies in response to fastin g and maximal pentagastrin stimulation, basal (BAO) and peak (PAO) aci d outputs were calculated. A quantitative assessment of H. pylori colo nization density in biopsies from five sites of the gastroduodenum in the active ulcer group, and from the antrum in inactive duodenal ulcer and non-ulcer groups. Results. There were negative correlations betwe en total gastroduodenal bacterial colonization density and, PAO (r - 0 .87, p = 0.0025) and BAO (r - 0.635, p < 0.02) in the active ulcer gro up. There were negative correlations between antral H. pylori coloniza tion density and PAO in the active duodenal ulcer (r - 0.7449, p < 0.0 1) and non-ulcer (r - 0.5837, p < 0.1) groups but not in the inactive duodenal ulcer group (r - 0.1869, p > 0.2). Conclusions. An equilibriu m is reached between gastroduodenal H. pylori colonization density and gastric acid secretory capacity in active duodenal ulcer disease. It is hypothesized that thresholds of bacterial load and acid secretory c apacity, in combination, are required for active ulceration in DU dise ase.