The gastric acid pocket is attenuated in <i>H. pylori</i> infected subjects.

Abstract

Gastric acid secretory capacity in different anatomical regions, including the postprandial acid pocket, was assessed in <i>Helicobacter pylori</i> positive and negative volunteers in a Western population. We studied 31 <i>H. pylori</i> positive and 28 <i>H. pylori</i> negative volunteers, matched for age, gender and body mass index. Jumbo biopsies were taken at 11 predetermined locations from the gastro-oesophageal junction and stomach. Combined high-resolution pH metry (12 sensors) and manometry (36 sensors) was performed for 20 min fasted and 90 min postprandially. The squamocolumnar junction was marked with radio-opaque clips and visualised radiologically. Biopsies were scored for inflammation and density of parietal, chief and G cells immunohistochemically. Under fasting conditions, the <i>H. pylori</i> positives had less intragastric acidity compared with negatives at all sensors >1.1 cm distal to the peak lower oesophageal sphincter (LES) pressure (p<0.01). Postprandially, intragastric acidity was less in <i>H. pylori</i> positives at sensors 2.2, 3.3 and 4.4 cm distal to the peak LES pressure (p<0.05), but there were no significant differences in more distal sensors. The postprandial acid pocket was thus attenuated in <i>H. pylori</i> positives. The <i>H. pylori</i> positives had a lower density of parietal and chief cells compared with <i>H. pylori</i> negatives in 10 of the 11 gastric locations (p<0.05). 17/31 of the <i>H. pylori</i> positives were CagA-seropositive and showed a more marked reduction in intragastric acidity and increased mucosal inflammation. In population volunteers, <i>H. pylori</i> positives have reduced intragastric acidity which most markedly affects the postprandial acid pocket.