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Original article
The gastric acid pocket is attenuated in H. pylori infected subjects
  1. David R Mitchell1,
  2. Mohammad H Derakhshan1,
  3. Angela A Wirz1,
  4. Clare Orange2,
  5. Stuart A Ballantyne3,
  6. James J Going4,
  7. Kenneth E L McColl1
  1. 1Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK
  2. 2Department of Pathology, School of Medicine, University of Glasgow, Glasgow, UK
  3. 3Department of Clinical Radiology, NHS Greater Glasgow and Clyde, Glasgow, UK
  4. 4Institute of Cancer Sciences, University of Glasgow, Glasgow, UK
  1. Correspondence to Professor Kenneth E L McColl, Institute of Cardiovascular and Medical Sciences, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK; kenneth.mccoll{at}glasgow.ac.uk

Abstract

Objective Gastric acid secretory capacity in different anatomical regions, including the postprandial acid pocket, was assessed in Helicobacter pylori positive and negative volunteers in a Western population.

Design We studied 31 H. pylori positive and 28 H. pylori 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.

Results Under fasting conditions, the H. pylori 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 H. pylori 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 H. pylori positives. The H. pylori positives had a lower density of parietal and chief cells compared with H. pylori negatives in 10 of the 11 gastric locations (p<0.05). 17/31 of the H. pylori positives were CagA-seropositive and showed a more marked reduction in intragastric acidity and increased mucosal inflammation.

Conclusions In population volunteers, H. pylori positives have reduced intragastric acidity which most markedly affects the postprandial acid pocket.

  • HELICOBACTER PYLORI
  • GASTRIC ACID SECRETION
  • GASTRITIS
  • GASTRIC PARIETAL CELL

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