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Clinical impact of microbiome in patients with decompensated cirrhosis
Cirrhosis is an increasing cause of morbidity and mortality. Recent studies are trying to clarify the role of microbiome in clinical exacerbation of patients with decompensated cirrhosis. Nowadays, it is accepted that patients with cirrhosis have altered salivary and enteric microbiome, characterize...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6141334/ https://www.ncbi.nlm.nih.gov/pubmed/30228776 http://dx.doi.org/10.3748/wjg.v24.i34.3813 |
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author | Oikonomou, Theodora Papatheodoridis, George V Samarkos, Michael Goulis, Ioannis Cholongitas, Evangelos |
author_facet | Oikonomou, Theodora Papatheodoridis, George V Samarkos, Michael Goulis, Ioannis Cholongitas, Evangelos |
author_sort | Oikonomou, Theodora |
collection | PubMed |
description | Cirrhosis is an increasing cause of morbidity and mortality. Recent studies are trying to clarify the role of microbiome in clinical exacerbation of patients with decompensated cirrhosis. Nowadays, it is accepted that patients with cirrhosis have altered salivary and enteric microbiome, characterized by the presence of dysbiosis. This altered microbiome along with small bowel bacterial overgrowth, through translocation across the gut, is associated with the development of decompensating complications. Studies have analyzed the correlation of certain bacterial families with the development of hepatic encephalopathy in cirrhotics. In general, stool and saliva dysbiosis with reduction of autochthonous bacteria in patients with cirrhosis incites changes in bacterial defenses and higher risk for bacterial infections, such as spontaneous bacterial peritonitis, and sepsis. Gut microbiome has even been associated with oncogenic pathways and under circumstances might promote the development of hepatocarcinogenesis. Lately, the existence of the oral-gut-liver axis has been related with the development of decompensating events. This link between the liver and the oral cavity could be via the gut through impaired intestinal permeability that allows direct translocation of bacteria from the oral cavity to the systemic circulation. Overall, the contribution of the microbiome to pathogenesis becomes more pronounced with progressive disease and therefore may represent an important therapeutic target in the management of cirrhosis. |
format | Online Article Text |
id | pubmed-6141334 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-61413342018-09-18 Clinical impact of microbiome in patients with decompensated cirrhosis Oikonomou, Theodora Papatheodoridis, George V Samarkos, Michael Goulis, Ioannis Cholongitas, Evangelos World J Gastroenterol Editorial Cirrhosis is an increasing cause of morbidity and mortality. Recent studies are trying to clarify the role of microbiome in clinical exacerbation of patients with decompensated cirrhosis. Nowadays, it is accepted that patients with cirrhosis have altered salivary and enteric microbiome, characterized by the presence of dysbiosis. This altered microbiome along with small bowel bacterial overgrowth, through translocation across the gut, is associated with the development of decompensating complications. Studies have analyzed the correlation of certain bacterial families with the development of hepatic encephalopathy in cirrhotics. In general, stool and saliva dysbiosis with reduction of autochthonous bacteria in patients with cirrhosis incites changes in bacterial defenses and higher risk for bacterial infections, such as spontaneous bacterial peritonitis, and sepsis. Gut microbiome has even been associated with oncogenic pathways and under circumstances might promote the development of hepatocarcinogenesis. Lately, the existence of the oral-gut-liver axis has been related with the development of decompensating events. This link between the liver and the oral cavity could be via the gut through impaired intestinal permeability that allows direct translocation of bacteria from the oral cavity to the systemic circulation. Overall, the contribution of the microbiome to pathogenesis becomes more pronounced with progressive disease and therefore may represent an important therapeutic target in the management of cirrhosis. Baishideng Publishing Group Inc 2018-09-14 2018-09-14 /pmc/articles/PMC6141334/ /pubmed/30228776 http://dx.doi.org/10.3748/wjg.v24.i34.3813 Text en ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
spellingShingle | Editorial Oikonomou, Theodora Papatheodoridis, George V Samarkos, Michael Goulis, Ioannis Cholongitas, Evangelos Clinical impact of microbiome in patients with decompensated cirrhosis |
title | Clinical impact of microbiome in patients with decompensated cirrhosis |
title_full | Clinical impact of microbiome in patients with decompensated cirrhosis |
title_fullStr | Clinical impact of microbiome in patients with decompensated cirrhosis |
title_full_unstemmed | Clinical impact of microbiome in patients with decompensated cirrhosis |
title_short | Clinical impact of microbiome in patients with decompensated cirrhosis |
title_sort | clinical impact of microbiome in patients with decompensated cirrhosis |
topic | Editorial |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6141334/ https://www.ncbi.nlm.nih.gov/pubmed/30228776 http://dx.doi.org/10.3748/wjg.v24.i34.3813 |
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