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Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa

AIMS: To evaluate association between duodenogastric reflux and early gastric mucosal changes before and after the cholecystectomy procedure. MATERIALS AND METHODS: Patients were evaluated with preoperative and postoperative endoscopy and endoscopic biopsy. Demographic and clinical characteristics,...

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Autores principales: Mercan, Erdinc, Duman, Ugur, Tihan, Deniz, Dilektasli, Evren, Senol, Kazim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5108731/
https://www.ncbi.nlm.nih.gov/pubmed/27917345
http://dx.doi.org/10.1186/s40064-016-3641-z
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author Mercan, Erdinc
Duman, Ugur
Tihan, Deniz
Dilektasli, Evren
Senol, Kazim
author_facet Mercan, Erdinc
Duman, Ugur
Tihan, Deniz
Dilektasli, Evren
Senol, Kazim
author_sort Mercan, Erdinc
collection PubMed
description AIMS: To evaluate association between duodenogastric reflux and early gastric mucosal changes before and after the cholecystectomy procedure. MATERIALS AND METHODS: Patients were evaluated with preoperative and postoperative endoscopy and endoscopic biopsy. Demographic and clinical characteristics, histological parameters, presence of duodenogastric reflux, and Updated Sydney scores were noted. RESULTS: A total of fifty patients who obeyed the follow-up were enrolled into the study. Median age of the patients was 43 years (range 25–84). Male–female ratio was 0.51 (17/33). Duodenogastric reflux % and Updated Sydney scores before and after cholecystectomy were 24 (48%) versus 39 (78%) and 2.38 ± 2.21 versus 3.46 ± 3.05, respectively (p = 0.001, p < 0.000). Mucosal inflammation degree showed significant increase in 15 (30%) patients, decrease in 7 (14%) patients and equality in 28 (56%) patients (p = 0.037). Neutrophil activation degree was significantly higher in 21 (42%) patients, lower in 5 (10%) patients after the surgery (p = 0.005). Postoperative glandular atrophy degree was also higher in 13 (26%) patients and equal in 37 (74%) patients (p = 0.001). Pre- and postoperative degree of intestinal metaplasia and H. pylori density did not any show significant difference (p = 0.157, p = 0.248, respectively).There were significant positive correlation between postoperative H. pylori infection and mucosal activity, inflammation, atrophy and intestinal metaplasia. CONCLUSION: Cholecystectomy is a potent inducer of pathologic duodenogastric reflux. Early onset of duodenogastric reflux and underlying H. pylori gastritis cause early gastric mucosal injury following cholecystectomy procedure by interacting collectively.
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spelling pubmed-51087312016-12-02 Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa Mercan, Erdinc Duman, Ugur Tihan, Deniz Dilektasli, Evren Senol, Kazim Springerplus Research AIMS: To evaluate association between duodenogastric reflux and early gastric mucosal changes before and after the cholecystectomy procedure. MATERIALS AND METHODS: Patients were evaluated with preoperative and postoperative endoscopy and endoscopic biopsy. Demographic and clinical characteristics, histological parameters, presence of duodenogastric reflux, and Updated Sydney scores were noted. RESULTS: A total of fifty patients who obeyed the follow-up were enrolled into the study. Median age of the patients was 43 years (range 25–84). Male–female ratio was 0.51 (17/33). Duodenogastric reflux % and Updated Sydney scores before and after cholecystectomy were 24 (48%) versus 39 (78%) and 2.38 ± 2.21 versus 3.46 ± 3.05, respectively (p = 0.001, p < 0.000). Mucosal inflammation degree showed significant increase in 15 (30%) patients, decrease in 7 (14%) patients and equality in 28 (56%) patients (p = 0.037). Neutrophil activation degree was significantly higher in 21 (42%) patients, lower in 5 (10%) patients after the surgery (p = 0.005). Postoperative glandular atrophy degree was also higher in 13 (26%) patients and equal in 37 (74%) patients (p = 0.001). Pre- and postoperative degree of intestinal metaplasia and H. pylori density did not any show significant difference (p = 0.157, p = 0.248, respectively).There were significant positive correlation between postoperative H. pylori infection and mucosal activity, inflammation, atrophy and intestinal metaplasia. CONCLUSION: Cholecystectomy is a potent inducer of pathologic duodenogastric reflux. Early onset of duodenogastric reflux and underlying H. pylori gastritis cause early gastric mucosal injury following cholecystectomy procedure by interacting collectively. Springer International Publishing 2016-11-14 /pmc/articles/PMC5108731/ /pubmed/27917345 http://dx.doi.org/10.1186/s40064-016-3641-z Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Research
Mercan, Erdinc
Duman, Ugur
Tihan, Deniz
Dilektasli, Evren
Senol, Kazim
Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa
title Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa
title_full Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa
title_fullStr Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa
title_full_unstemmed Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa
title_short Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa
title_sort cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5108731/
https://www.ncbi.nlm.nih.gov/pubmed/27917345
http://dx.doi.org/10.1186/s40064-016-3641-z
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