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 inGut Vol. 66; no. 9; pp. 1555 - 1562
Main Authors Mitchell, David R, Derakhshan, Mohammad H, Wirz, Angela A, Orange, Clare, Ballantyne, Stuart A, Going, James J, McColl, Kenneth E L
Format Journal Article
LanguageEnglish
Published England BMJ Publishing Group LTD 01.09.2017
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ISSN0017-5749
1468-3288
1468-3288
DOI10.1136/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.
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
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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
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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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StartPage 1555
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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