EFFECTS OF HELICOBACTER-PYLORI ON GASTRITIS, PENTAGASTRIN-STIMULATED GASTRIC-ACID SECRETION, AND MEAL-STIMULATED PLASMA GASTRIN-RELEASE IN THE ABSENCE OF PEPTIC-ULCER DISEASE

Objective: There is strong evidence accumulating that chronic infectio n with Helicobacter pylori (H. pylori) interferes with inhibitory path ways of the regulation of acid secretion. The increase in maximum acid output (MAO), and the increase in the sensitivity of the parietal cel l to gastrin commonly observed in patients suffering from duodenal ulc er disease (DU), however, remains largely unexplained. Insufficient ev idence is available concerning how these parameters are influenced by H. pylori infection in patients not suffering from peptic ulcer diseas e (PUD) and how they are related to H. pylori-induced gastritis. The a im of this study was to compare basal gastric acid secretion (BAO), MA O, and the sensitivity of the parietal cell to gastrin in H. pylori-po sitive and H. pylori-negative patients not suffering from PUD, and to study the relationship with their individual postprandial gastrin rele ase and the degree of gastric antral and corpus gastritis. Methods: H. pylori status was assessed by CLO test and histology (two biopsies ea ch from the antrum and the corpus) in 14 H. pylori-positive and 16 H. pylori-negative nonulcer patients of comparable age, weight and gender . Gastritis score was assessed by a pathologist, who was unaware of th e acid secretary data. Following determination of BAG, the relation of pentagastrin and gastric acid secretion was established with a cumula tive pentagastrin dose response curve far the dose range 0.03- 6.0 mu g/kg(-1) h(-1) and MAO (V-max) and pentagastrin sensitivity (ED50) wer e determined. Basal and postprandial gastrin release was measured by r adioimmunoassay. Results: There was a significant higher gastritis sco re in the H. pylori-positive compared with the H. pylori-negative subj ects. The dose response curves of the pentagastrin stimulated gastric acid secretion were not different between H. pylori-positive and H. py lori-negative groups. No correlation was seen between the gastritis sc ore, basal acid output (BAO) peak acid output (PAO), maximum acid outp ut (MAO), ED50 values and the plasma gastrin values. There was, howeve r, a considerable larger variation of the PAO and MAO data of the H. p ylori-infected subjects and >50% of the respective data was above or b elow the relatively low range of the respective values of the noninfec ted subjects. Conclusions: H. pylori-induced gastritis does not regula rly enhance maximum acid output in nonulcer patients, nor does it modi fy the sensitivity of the parietal cell to gastrin. H. pylori infectio n is thus unlikely to be directly responsible for an increase of these parameters in DU disease. Our data support, however, the concept that chronic H. pylori infection can either enhance or attenuate maximum a cid secretory capacity in certain subgroups of patients. (Am J Gastroe nterol 1998;93:1277-1285. (C) 1998 by Am. Coll. of Gastroenterology).