Factors Influencing The Development of Barrett's Epithelium in The Esophageal Remnant Postesophagectomy

O’Riordan, J M; Tucker, Olga; Byrne, P. J.; McDonald, G. S. A.; Ravi, N; Keeling, P. W. N.; Reynolds, John V.

doi:10.1111/j.1572-0241.2004.04057.x

Cited by 81 publications

(73 citation statements)

References 22 publications

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“…NSAIDs inhibit COX-2, which can be activated by proinflammatory cytokines, including interleukin-1h (IL-1h) and tumor necrosis factor-a (TNF-a), following mucosal injury. Overexpression of IL-1h has been reported in patients with esophagitis, Barrett's esophagus, and esophageal adenocarcinoma (42), and overexpression of TNF-a has been reported in patients with Barrett's esophagus (43). Exposure of the distal esophagus to acid reflux and components of bile reflux has been associated with the activation of COX-2 (44)(45)(46).…”

Section: Nsaids and Esophageal Adenocarcinomamentioning

confidence: 99%

Nonsteroidal Anti-inflammatory Drugs and the Esophageal Inflammation-Metaplasia-Adenocarcinoma Sequence

Anderson

Johnston²,

Watson³

et al. 2006

Cancer Research

107

108

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Observational studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of esophageal adenocarcinoma, but it is not known at what stage they may act in the esophageal inflammation-metaplasia-adenocarcinoma sequence. In an all-Ireland case-control study, we investigated the relationship between the use of NSAIDs and risk of reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. Patients with esophageal adenocarcinoma, long-segment Barrett's esophagus and population controls were recruited from throughout Ireland. Esophagitis patients were recruited from Northern Ireland only. Data were collected on known and potential risk factors for esophageal adenocarcinoma and on the use of NSAIDs, including aspirin, at least 1 year before interview. Associations between use of NSAIDs and the stages of the esophageal inflammationmetaplasia-adenocarcinoma sequence were estimated by multiple logistic regression. In total, 230 reflux esophagitis, 224 Barrett's esophagus, and 227 esophageal adenocarcinoma and 260 population controls were recruited. Use of aspirin and

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Section: Nsaids and Esophageal Adenocarcinomamentioning

confidence: 99%

Nonsteroidal Anti-inflammatory Drugs and the Esophageal Inflammation-Metaplasia-Adenocarcinoma Sequence

Anderson

Johnston²,

Watson³

et al. 2006

Cancer Research

107

108

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“…Barrett’s esophagus has been reported to arise de novo in patients who have previously undergone gastric pull-up esophagectomy [126,127,128,129,130,131]. In this procedure, the normal squamous epithelium of the cervical esophagus is interposed to the acid secreting mucosa of the gastric body.…”

Section: Development Of Columnar Mucosa After Esophagectomymentioning

confidence: 99%

The Spectrum of Motor Function Abnormalities in Gastroesophageal Reflux Disease and Barrett’s Esophagus

et al. 2009

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Barrett’s esophagus has traditionally been regarded as the most severe end of the spectrum of gastroesophageal reflux disease and is of great clinical importance in view of the association with esophageal adenocarcinoma. Studies have documented high levels of esophageal acid exposure in Barrett’s esophagus. Various pathogenetic mechanisms underlie this phenomenon. These include abnormalities in esophageal peristalsis, defective lower esophageal sphincter pressures, gastric dysmotility and bile reflux. Whilst these factors provide evidence for an acquired cause of Barrett’s esophagus, an underlying genetic predisposition cannot be ruled out. Although the past decade has brought about many new discoveries in the pathogenesis of Barrett’s esophagus, it has also added further controversy to this complex disorder. A detailed analysis of the gastrointestinal motor abnormalities occurring in Barrett’s esophagus follows, with a review of the currently available literature and an update on this condition that continues to be of interest to the gastroenterologist.

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“…Some reports even consider that reflux symptoms actually have no value in predicting the existence of reflux-related injury in esophageal remnant (15,22). Notably, 16% of patients in our longitudinal study developed metaplasia in the remnant esophagus, the prevalence was much less than that in western countries (20,23). We previously investigated the difference of mucosal damage in the esophageal remnant after esophagectomy and gastric interposition between Chinese and Canadian population, revealing that Canadian population was more sensitive to the gastroesophageal reflux damage compared to Chinese population, which might be attributed to the different genetic backgrounds (24).…”

Section: Discussionmentioning

confidence: 62%

“…Gastroesophageal reflux is a common complication after esophagectomy and esophagogastrostomy, which could eventually result in damage to esophageal remnant. Several studies have reported that esophagectomy with gastric pull-up would increase the development of esophagitis and also Barrett's epithelium (19)(20)(21). Therefore, esophagectomy with gastric interposition may represent a good in vivo model for the pathogenesis of GERD.…”

Section: Discussionmentioning

confidence: 99%

Longitudinal study of esophageal mucosal damage after esophagectomy and gastric interposition: relationship between reflux-related mucosal injury and Notch signaling

et al. 2017

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Background: Esophagectomy with gastric interposition could serve as a good human reflux model to study the molecular pathogenesis of esophageal mucosal damage induced by gastroesophageal reflux. This study was to investigate the role of Notch signaling in reflux injury of esophageal mucosa. Results: Forty-four out of 48 patients completed four follow-ups. Injuries of esophageal remnant confirmed by endoscopical and histological examinations were both more often with a longer postoperative period (P<0.05). The mRNA expression levels of Notch1 and Hes1 were decreased in a time-dependent manner after operation (P<0.001). Notch1 and Hes1 mRNA levels were significantly higher in normal squamous mucosa than in esophagitis, and higher in esophagitis than in metaplasia (P<0.05). Immunohistochemical study also demonstrated a similar protein expression pattern. Samples with endoscopic evidence of mucosal damage exhibited lower expression of Notch1 mRNA levels as compared to biopsies without visualized damage (P=0.035).Conclusions: This is the first longitudinal study on Notch signaling in human esophagectomy model, our preliminary findings suggest decreased Notch signaling might be involved in the development of mucosa damage caused by gastroesophageal reflux.

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Factors Influencing The Development of Barrett's Epithelium in The Esophageal Remnant Postesophagectomy

Cited by 81 publications

References 22 publications

Nonsteroidal Anti-inflammatory Drugs and the Esophageal Inflammation-Metaplasia-Adenocarcinoma Sequence

Nonsteroidal Anti-inflammatory Drugs and the Esophageal Inflammation-Metaplasia-Adenocarcinoma Sequence

The Spectrum of Motor Function Abnormalities in Gastroesophageal Reflux Disease and Barrett’s Esophagus

Longitudinal study of esophageal mucosal damage after esophagectomy and gastric interposition: relationship between reflux-related mucosal injury and Notch signaling

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