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Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations

BACKGROUND: Hypergastrinaemia occasionally indicates the presence of a gastrinoma. However it is much more commonly associated with various benign causes including proton pump inhibitor (PPI) use, Helicobacter pylori infection and/or atrophic gastritis. The extent to which these factors interact to...

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Autores principales: Veysey-Smith, Reuben, Moore, Andrew R., Murugesan, Senthil V., Tiszlavicz, Laszlo, Dockray, Graham J., Varro, Andrea, Pritchard, D. Mark
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8637328/
https://www.ncbi.nlm.nih.gov/pubmed/34867785
http://dx.doi.org/10.3389/fendo.2021.741887
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author Veysey-Smith, Reuben
Moore, Andrew R.
Murugesan, Senthil V.
Tiszlavicz, Laszlo
Dockray, Graham J.
Varro, Andrea
Pritchard, D. Mark
author_facet Veysey-Smith, Reuben
Moore, Andrew R.
Murugesan, Senthil V.
Tiszlavicz, Laszlo
Dockray, Graham J.
Varro, Andrea
Pritchard, D. Mark
author_sort Veysey-Smith, Reuben
collection PubMed
description BACKGROUND: Hypergastrinaemia occasionally indicates the presence of a gastrinoma. However it is much more commonly associated with various benign causes including proton pump inhibitor (PPI) use, Helicobacter pylori infection and/or atrophic gastritis. The extent to which these factors interact to influence fasting serum gastrin concentrations remains incompletely understood. MATERIALS AND METHODS: Fasting serum gastrin concentrations were measured by radioimmunoassay in 1,400 patients attending for diagnostic oesophagogastro-duodenoscopy. After exclusions, 982 patients were divided into four groups and their results analysed. We compared gastrin concentrations in normal patients (no H. pylori infection, no PPI use and no histological evidence of gastric preneoplasia (n=233)), with those in patients who were taking regular PPIs (H. pylori negative with no gastric preneoplasia (n=301)), patients who had active H. pylori infection but no gastric preneoplasia (n=164) and patients with histologically confirmed gastric preneoplasia (n=284). RESULTS: Median fasting gastrin concentration in the normal group was 20pM and was significantly increased in PPI users (46pM, p<0.0001), patients with active H. pylori infection (27pM, p<0.0001), and patients with antral (25pM, p<0.01) or corpus (48pM, p<0.0001) gastric preneoplasia. PPI use resulted in further significant increases in fasting serum gastrin concentrations in patients who were infected with H. pylori (50pM, n=56) or who had antral gastric preneoplasia (53pM, n=87), but did not significantly alter serum gastrin concentrations in patients with corpus preneoplasia (90pM, n=66). CONCLUSIONS: PPI use, H. pylori infection and atrophic gastritis all caused significant elevations of median fasting gastrin concentrations. However, several patients who had potential risk factors for hypergastrinaemia still demonstrated fasting serum gastrin concentrations within the normal range.
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spelling pubmed-86373282021-12-03 Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations Veysey-Smith, Reuben Moore, Andrew R. Murugesan, Senthil V. Tiszlavicz, Laszlo Dockray, Graham J. Varro, Andrea Pritchard, D. Mark Front Endocrinol (Lausanne) Endocrinology BACKGROUND: Hypergastrinaemia occasionally indicates the presence of a gastrinoma. However it is much more commonly associated with various benign causes including proton pump inhibitor (PPI) use, Helicobacter pylori infection and/or atrophic gastritis. The extent to which these factors interact to influence fasting serum gastrin concentrations remains incompletely understood. MATERIALS AND METHODS: Fasting serum gastrin concentrations were measured by radioimmunoassay in 1,400 patients attending for diagnostic oesophagogastro-duodenoscopy. After exclusions, 982 patients were divided into four groups and their results analysed. We compared gastrin concentrations in normal patients (no H. pylori infection, no PPI use and no histological evidence of gastric preneoplasia (n=233)), with those in patients who were taking regular PPIs (H. pylori negative with no gastric preneoplasia (n=301)), patients who had active H. pylori infection but no gastric preneoplasia (n=164) and patients with histologically confirmed gastric preneoplasia (n=284). RESULTS: Median fasting gastrin concentration in the normal group was 20pM and was significantly increased in PPI users (46pM, p<0.0001), patients with active H. pylori infection (27pM, p<0.0001), and patients with antral (25pM, p<0.01) or corpus (48pM, p<0.0001) gastric preneoplasia. PPI use resulted in further significant increases in fasting serum gastrin concentrations in patients who were infected with H. pylori (50pM, n=56) or who had antral gastric preneoplasia (53pM, n=87), but did not significantly alter serum gastrin concentrations in patients with corpus preneoplasia (90pM, n=66). CONCLUSIONS: PPI use, H. pylori infection and atrophic gastritis all caused significant elevations of median fasting gastrin concentrations. However, several patients who had potential risk factors for hypergastrinaemia still demonstrated fasting serum gastrin concentrations within the normal range. Frontiers Media S.A. 2021-11-18 /pmc/articles/PMC8637328/ /pubmed/34867785 http://dx.doi.org/10.3389/fendo.2021.741887 Text en Copyright © 2021 Veysey-Smith, Moore, Murugesan, Tiszlavicz, Dockray, Varro and Pritchard https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Veysey-Smith, Reuben
Moore, Andrew R.
Murugesan, Senthil V.
Tiszlavicz, Laszlo
Dockray, Graham J.
Varro, Andrea
Pritchard, D. Mark
Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations
title Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations
title_full Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations
title_fullStr Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations
title_full_unstemmed Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations
title_short Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations
title_sort effects of proton pump inhibitor therapy, h. pylori infection and gastric preneoplastic pathology on fasting serum gastrin concentrations
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8637328/
https://www.ncbi.nlm.nih.gov/pubmed/34867785
http://dx.doi.org/10.3389/fendo.2021.741887
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