The gastric acid pocket is attenuated in H. pylori infected subjects
ObjectiveGastric 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.DesignWe studied 31 H. pylori positive and 28 H. pylori negative volunteers, matched for age,...
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Published in | Gut Vol. 66; no. 9; pp. 1555 - 1562 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
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BMJ Publishing Group LTD
01.09.2017
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ISSN | 0017-5749 1468-3288 1468-3288 |
DOI | 10.1136/gutjnl-2016-312638 |
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Abstract | ObjectiveGastric 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.DesignWe 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.ResultsUnder 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.ConclusionsIn population volunteers, H. pylori positives have reduced intragastric acidity which most markedly affects the postprandial acid pocket. |
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AbstractList | Gastric acid secretory capacity in different anatomical regions, including the postprandial acid pocket, was assessed in
positive and negative volunteers in a Western population.
We studied 31
positive and 28
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
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
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
positives. The
positives had a lower density of parietal and chief cells compared with
negatives in 10 of the 11 gastric locations (p<0.05). 17/31 of the
positives were CagA-seropositive and showed a more marked reduction in intragastric acidity and increased mucosal inflammation.
In population volunteers,
positives have reduced intragastric acidity which most markedly affects the postprandial acid pocket. 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.OBJECTIVEGastric 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.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.DESIGNWe 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.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.RESULTSUnder 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.In population volunteers, H. pylori positives have reduced intragastric acidity which most markedly affects the postprandial acid pocket.CONCLUSIONSIn population volunteers, H. pylori positives have reduced intragastric acidity which most markedly affects the postprandial acid pocket. ObjectiveGastric 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.DesignWe 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.ResultsUnder 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.ConclusionsIn population volunteers, H. pylori positives have reduced intragastric acidity which most markedly affects the postprandial acid pocket. |
Author | Ballantyne, Stuart A Mitchell, David R McColl, Kenneth E L Derakhshan, Mohammad H Orange, Clare Going, James J Wirz, Angela A |
Author_xml | – sequence: 1 givenname: David R surname: Mitchell fullname: Mitchell, David R email: kenneth.mccoll@glasgow.ac.uk organization: Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK – sequence: 2 givenname: Mohammad H surname: Derakhshan fullname: Derakhshan, Mohammad H email: kenneth.mccoll@glasgow.ac.uk organization: Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK – sequence: 3 givenname: Angela A surname: Wirz fullname: Wirz, Angela A email: kenneth.mccoll@glasgow.ac.uk organization: Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK – sequence: 4 givenname: Clare surname: Orange fullname: Orange, Clare email: kenneth.mccoll@glasgow.ac.uk organization: Department of Pathology, School of Medicine, University of Glasgow, Glasgow, UK – sequence: 5 givenname: Stuart A surname: Ballantyne fullname: Ballantyne, Stuart A email: kenneth.mccoll@glasgow.ac.uk organization: Department of Clinical Radiology, NHS Greater Glasgow and Clyde, Glasgow, UK – sequence: 6 givenname: James J surname: Going fullname: Going, James J email: kenneth.mccoll@glasgow.ac.uk organization: Institute of Cancer Sciences, University of Glasgow, Glasgow, UK – sequence: 7 givenname: Kenneth E L surname: McColl fullname: McColl, Kenneth E L email: kenneth.mccoll@glasgow.ac.uk organization: Section of Gastroenterology, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27663505$$D View this record in MEDLINE/PubMed |
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Keywords | GASTRIC ACID SECRETION GASTRIC PARIETAL CELL GASTRITIS HELICOBACTER PYLORI |
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Snippet | ObjectiveGastric acid secretory capacity in different anatomical regions, including the postprandial acid pocket, was assessed in Helicobacter pylori positive... Gastric acid secretory capacity in different anatomical regions, including the postprandial acid pocket, was assessed in positive and negative volunteers in a... Gastric acid secretory capacity in different anatomical regions, including the postprandial acid pocket, was assessed in Helicobacter pylori positive and... |
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SubjectTerms | Acidity Acids Biopsy Biopsy - methods Body mass index Disease Endoscopy Esophageal Sphincter, Lower - metabolism Esophageal Sphincter, Lower - pathology Esophagogastric Junction - metabolism Esophagogastric Junction - pathology Esophagus Female Gastric Acidity Determination Gastric cancer Gastric juice Gastric Mucosa - metabolism Gastritis - etiology Gastritis - metabolism Gastritis - pathology Gastroenterology Helicobacter Infections - complications Helicobacter Infections - metabolism Helicobacter Infections - microbiology Helicobacter Infections - pathology Helicobacter pylori Helicobacter pylori - isolation & purification Humans Infections Male Manometry - methods Middle Aged Mucosa Mucous membrane Population Population studies Pressure Research Design Rodents Sphincter Stomach Stomach - pathology Ulcers United Kingdom |
Title | The gastric acid pocket is attenuated in H. pylori infected subjects |
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