2004
DOI: 10.1016/j.prp.2004.04.002
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Effects of duodenogastric reflux on gastrin cells, somatostatin cells and serotonin cells in human antral gastric mucosa

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Cited by 6 publications
(7 citation statements)
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“…24 However, prior studies have suggested that endoscopy has decreased accuracy and a lower positive predictive value when compared to other methods, such as hepatobiliary scintigraphy, further contributing to the missed diagnosis. 6,[29][30][31] The prevalence of motility disorders was similar to those seen in previous studies of functional dyspepsia, with approximately one third of patients showing delayed gastric emptying. 2,32 The lack of significant delay in gastric emptying, especially in the BG group suggests that a primary gastric emptying/motility problem is unlikely to be an important mechanism and that excess duodenogastric bile reflux is the key driver for this problem.…”
Section: Discussionsupporting
confidence: 74%
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“…24 However, prior studies have suggested that endoscopy has decreased accuracy and a lower positive predictive value when compared to other methods, such as hepatobiliary scintigraphy, further contributing to the missed diagnosis. 6,[29][30][31] The prevalence of motility disorders was similar to those seen in previous studies of functional dyspepsia, with approximately one third of patients showing delayed gastric emptying. 2,32 The lack of significant delay in gastric emptying, especially in the BG group suggests that a primary gastric emptying/motility problem is unlikely to be an important mechanism and that excess duodenogastric bile reflux is the key driver for this problem.…”
Section: Discussionsupporting
confidence: 74%
“…NSAID-induced chemical gastropathy is however indistinguishable from BG histologically, and is clearly one limitation that may contribute to the under recognition of BG. 29 Another limitation is that most endoscopists may not recognize or document duodenogastric bile reflux. We used the presence of bile in the stomach as an endoscopic marker for duodenogastric reflux, as it can be easily identified during endoscopy.…”
Section: Discussionmentioning
confidence: 99%
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“…One possible explanation could be that DRG, which damages the gastric mucosa by bile acids and pancreatic phospholipase A2, leads to peptic ulcers 20 21 . In addition, some animal studies demonstrated that DGR suppresses somatostatin concentrations and increases intragastric gastrin and acid secretion 18 22 23 24 25 26 . Therefore, DGR may be considered a factor in the pathogenesis of gastric and duodenal ulcers as suggested by some researchers 18 30 31 .…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, studies demonstrated that DGR may suppress the somatostatin concentration that is produced by the alkaline nature or pancreatic component of the reflux, which subsequently results in hypersecretion of acid and hypergastrinemia 18 22 23 24 . DGR may therefore be considered a common factor in the pathogenesis of gastric and duodenal ulcers 23 24 25 26 .…”
mentioning
confidence: 99%