Barretts's carcinogenesis

Mukaisho, Ken‐ichi; Kanai, Shunpei; Kushima, Ryoji; Nakayama, Tadanobu; Hattori, Takanori; Sugihara, Hiroyuki

doi:10.1111/pin.12804

Cited by 23 publications

(19 citation statements)

References 122 publications

(225 reference statements)

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“…Bile acids have a carcinogenic effect on esophageal mucosa [17,18]. Potential carcinogenic risk of postoperative bile reflux after OAGB has been proposed numerous times.…”

Section: Discussionmentioning

confidence: 99%

Bile Reflux is a Common Finding in the Gastric Pouch After One Anastomosis Gastric Bypass

et al. 2019

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Introduction Data on postoperative bile reflux after one anastomosis gastric bypass (OAGB) is lacking. Bile reflux scintigraphy (BRS) has been shown to be a reliable non-invasive tool to assess bile reflux after OAGB. We set out to study bile reflux after OAGB with BRS and endoscopy in a prospective series (RYSA Trial). Methods Forty patients (29 women) underwent OAGB between November 2016 and December 2018. Symptoms were reported and upper gastrointestinal endoscopy (UGE) was done preoperatively. Six months after OAGB, bile reflux was assessed in UGE findings and as tracer activity found in gastric tube and esophagus in BRS (follow-up rate 95%). Results Twenty-six patients (68.4%) had no bile reflux in BRS. Twelve patients (31.6%) had bile reflux in the gastric pouch in BRS and one of them (2.6%) had bile reflux also in the esophagus 6 months postoperatively. Mean bile reflux activity in the gastric pouch was 5.2% (1-21%) of total activity. De novo findings suggestive of bile reflux (esophagitis, stomal ulcer, foveolar inflammation of gastric pouch) were found for 15 patients (39.5%) in postoperative UGE. BRS and UGE findings were significantly associated (P = 0.022). Eight patients experienced de novo reflux symptoms at 6 months, that were significantly associated with BRS and de novo UGE findings postoperatively (P = 0.033 and 0.0005, respectively). Conclusion Postoperative bile reflux in the gastric pouch after OAGB is a common finding in scintigraphy and endoscopy. The long-term effects of bile exposure will be analyzed in future reports after a longer follow-up. Trial registration Clinical Trials Identifier NCT02882685

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“…Bile acids have a carcinogenic effect on esophageal mucosa [17,18]. Potential carcinogenic risk of postoperative bile reflux after OAGB has been proposed numerous times.…”

Section: Discussionmentioning

confidence: 99%

Bile Reflux is a Common Finding in the Gastric Pouch After One Anastomosis Gastric Bypass

et al. 2019

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“…Since the esophagogastric junction is located on the dorsal side of the body, when a person lies down in the supine position immediately after eating, the esophagogastric junction is exposed to bile acid reflux. Since bile acids are involved in the onset of Barrett’s esophagus [ 24 , 46 – 48 ] and PACM too is suggested to be associated with Barrett’s esophagus, bile acids may be associated with PACM.…”

Section: Discussionmentioning

confidence: 99%

Development of Pancreatic Acinar Cell Metaplasia During Gastric Repair in a Rat Duodenal Contents Reflux Model

et al. 2020

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Background We previously reported the development of pancreatic acinar cell metaplasia (PACM) in the glandular stomach of a duodenal contents reflux model (reflux model). Aims We aimed to investigate the characteristics and histogenesis of PACM using a reflux model. Methods A reflux model was created using 8-week-old male Wistar rats, which were killed up to 30 weeks postoperatively. Histological examination was performed to analyze the glandular stomach–jejunal anastomosis. Furthermore, electron microscopic images of PACM samples were compared with pancreatic and gastric glands removed from rats that had not undergone surgery. Immunostaining for α-amylase, HIK1083, TFF2, and Ki-67 was performed, and double fluorescent staining was carried out using antibodies against α-amylase and HIK1083, or α-amylase and TFF2. Results In all reflux model rats, PACM was observed proximal to the glandular stomach–jejunal anastomosis, surrounded by pseudopyloric metaplasia. The number of chief cells was decreased in the deep part of the gland, where PACM occurred. Electron microscopy showed that PACM cells had greater numbers of rough endoplasmic reticulum tubules than chief cells, and exhibited pancreatic acinar cell morphology. Upon immunochemical staining, the regenerative foveolar epithelium and part of the pseudopyloric glands stained strongly positive for TFF2, whereas PACM cells were only weakly positive. Double fluorescent staining identified early lesions of PACM in the neck, which were double positive for α-amylase and TFF2, but negative for HIK1083. Conclusions PACM could be induced by duodenal contents reflux. PACM originates from stem cells located in the neck of oxyntic glands during gastric mucosal regeneration.

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“…Chronic exposure of the esophageal mucosa to gastroduodenal fluid (bile salts and hydrochloric acid) causes active and erosive esophagitis, resulting in metaplasia of squamous cells to columnar epithelial cells, and submucosal fibrosis as Barrett's esophagus. It has been shown that chronic gastroesophageal reflux induces Barrett's esophagus according to clinicopathological analyses [5,6] and experimental studies using animal models [7][8][9][10]. Regarding the requirement of goblet cells (intestinal metaplasia) within the columnar-lined mucosa, the global histological definition of Barrett's esophagus is still controversial in Europe, the US, the UK and Japan [5] (Figure 2).…”

Section: Gerd-barrett's Esophagus (Mucosal Remodeling)-adenocarcinomamentioning

confidence: 99%

Proposal for an Organ-Specific Chronic Inflammation–Remodeling–Carcinoma Sequence

2019

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An organ-specific chronic inflammation-remodeling-carcinoma sequence has been proposed, mainly for the alimentary tract. As representative diseases, gastroesophageal reflux disease, chronic gastritis and inflammatory bowel disease (ulcerative colitis and Crohn's disease of the colitis type) were adopted for this discussion. Tissue remodeling is such an important part of tumorigenesis in this sequence that an organ-specific chronic inflammation-remodeling-carcinoma sequence has been proposed in detail. Chronic inflammation accelerates the cycle of tissue injury and regeneration; in other words, cell necrosis (or apoptosis) and proliferation result in tissue remodeling in long-standing cases of inflammation. Remodeling encompasses epithelial cell metaplasia and stromal fibrosis, and modifies epithelial-stromal cell interactions. Further, the accumulation of genetic, epigenetic and molecular changes-as well as morphologic disorganization-also occurs during tissue remodeling. The expression of mucosal tissue adapted to chronic inflammatory injury is thought to occur at an early stage. Subsequently, dysplasia and carcinoma develop on a background of remodeling due to continuous, active inflammation. Accordingly, organ-specific chronic inflammation should be ameliorated or well controlled with appropriate monitoring if complete healing is unachievable.

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Barretts's carcinogenesis

Cited by 23 publications

References 122 publications

Bile Reflux is a Common Finding in the Gastric Pouch After One Anastomosis Gastric Bypass

Bile Reflux is a Common Finding in the Gastric Pouch After One Anastomosis Gastric Bypass

Development of Pancreatic Acinar Cell Metaplasia During Gastric Repair in a Rat Duodenal Contents Reflux Model

Proposal for an Organ-Specific Chronic Inflammation–Remodeling–Carcinoma Sequence

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