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The role of acid inhibition in Helicobacter pylori eradication

Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments...

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Autores principales: Scott, David R., Sachs, George, Marcus, Elizabeth A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: F1000Research 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957631/
https://www.ncbi.nlm.nih.gov/pubmed/30023042
http://dx.doi.org/10.12688/f1000research.8598.1
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author Scott, David R.
Sachs, George
Marcus, Elizabeth A.
author_facet Scott, David R.
Sachs, George
Marcus, Elizabeth A.
author_sort Scott, David R.
collection PubMed
description Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments of H. pylori infection rely on acid suppression in combination with at least two antibiotics. The role of acid suppression in eradication therapy has been variously attributed to antibacterial activity of proton pump inhibitors directly or through inhibition of urease activity or increased stability and activity of antibiotics. Here we discuss the effect of acid suppression on enhanced replicative capacity of H. pylori to permit the bactericidal activity of growth-dependent antibiotics. The future of eradication therapy will rely on improvement of acid inhibition along with current antibiotics or the development of novel compounds targeting the organism’s ability to survive in acid.
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spelling pubmed-49576312018-07-17 The role of acid inhibition in Helicobacter pylori eradication Scott, David R. Sachs, George Marcus, Elizabeth A. F1000Res Review Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments of H. pylori infection rely on acid suppression in combination with at least two antibiotics. The role of acid suppression in eradication therapy has been variously attributed to antibacterial activity of proton pump inhibitors directly or through inhibition of urease activity or increased stability and activity of antibiotics. Here we discuss the effect of acid suppression on enhanced replicative capacity of H. pylori to permit the bactericidal activity of growth-dependent antibiotics. The future of eradication therapy will rely on improvement of acid inhibition along with current antibiotics or the development of novel compounds targeting the organism’s ability to survive in acid. F1000Research 2016-07-19 /pmc/articles/PMC4957631/ /pubmed/30023042 http://dx.doi.org/10.12688/f1000research.8598.1 Text en Copyright: © 2016 Scott DR et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Scott, David R.
Sachs, George
Marcus, Elizabeth A.
The role of acid inhibition in Helicobacter pylori eradication
title The role of acid inhibition in Helicobacter pylori eradication
title_full The role of acid inhibition in Helicobacter pylori eradication
title_fullStr The role of acid inhibition in Helicobacter pylori eradication
title_full_unstemmed The role of acid inhibition in Helicobacter pylori eradication
title_short The role of acid inhibition in Helicobacter pylori eradication
title_sort role of acid inhibition in helicobacter pylori eradication
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957631/
https://www.ncbi.nlm.nih.gov/pubmed/30023042
http://dx.doi.org/10.12688/f1000research.8598.1
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