The gastric acid pocket is attenuated inH. pyloriinfected subjects.
Gastric acid secretory capacity in different anatomical regions, including the postprandial acid pocket, was assessed inHelicobacter pyloripositive and negative volunteers in a Western population.



We studied 31H. pyloripositive and 28H. pylorinegative 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, theH. pyloripositives 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 inH. pyloripositives 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 inH. pyloripositives. TheH. pyloripositives had a lower density of parietal and chief cells compared withH. pylorinegatives in 10 of the 11 gastric locations (p<0.05). 17/31 of theH. pyloripositives were CagA-seropositive and showed a more marked reduction in intragastric acidity and increased mucosal inflammation.



In population volunteers,H. pyloripositives have reduced intragastric acidity which most markedly affects the postprandial acid pocket.
Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
David R
DR
Mitchell
Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
Mohammad H
MH
Derakhshan
Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
Angela A
AA
Wirz
Department of Pathology, School of Medicine, University of Glasgow, Glasgow, UK.
Clare
C
Orange
Department of Clinical Radiology, NHS Greater Glasgow and Clyde, Glasgow, UK.
Stuart A
SA
Ballantyne
Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
James J
JJ
Going
Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
Kenneth E L
KEL
McColl
D001706:Biopsy / Q000379:methods; D049630:Esophageal Sphincter, Lower / Q000378:metabolism / Q000473:pathology; D004943:Esophagogastric Junction / Q000378:metabolism / Q000473:pathology; D005260:Female; D005745:Gastric Acidity Determination; D005753:Gastric Mucosa / Q000378:metabolism*; D005756:Gastritis / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008365:Manometry / Q000379:methods; D008875:Middle Aged; D012107:Research Design; D013270:Stomach / Q000473:pathology; D006113:United Kingdom
GASTRIC ACID SECRETION; GASTRIC PARIETAL CELL; GASTRITIS; HELICOBACTER PYLORI