Intraluminal pH and Goblet Cell Density in Barrett’s Esophagus

Theodorou, Dimitrios; Ayazi, Shahin; DeMeester, Steven R.; Zehetner, Joerg; Peyré, Christian G.; Grant, Kimberly S.; Augustin, Florian; Oh, Daniel S.; Lipham, John C.; Chandrasoma, Parakrama; Hagen, Jeffrey A.; DeMeester, Tom R.

doi:10.1007/s11605-011-1776-3

Cited by 36 publications

(24 citation statements)

References 20 publications

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“…Intestinal phenotypes are found more proximally at the squamo-columnar junction, whereas cardiac and oxyntocardiac gland phenotypes are proportionally more common around the gastroesophageal junction [28][29][30] compared to the biopsies collected from the gastro-esophageal junction, with a clear stepwise gradient in between 29 . The density of glands containing intestinal differentiation correlates with the pH gradient along the BE segment; the less acidic the local average pH (closer to the squamo-columnar junction) the higher the proportion of glands with goblet cell differentiation 31 .…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Insights Into the Pathophysiology of Esophageal Adenocarcinoma

2018

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Although researchers have identified genetic alterations that contribute to development of esophageal adenocarcinoma, we know little about features of patients or environmental factors that mediate progression of chronic acid biliary reflux to Barrett's esophagus and cancer. Increasing our understanding of the mechanisms by which normal squamous epithelium progresses to early-stage invasive cancer will help formulate rational surveillance guidelines and allow us to divest resources away from patients at low risk of malignancy. We review the cellular and genetic alterations that occur during progression of Barrett's esophagus, based on findings from clinical studies and mouse models of disease. We review the features of the luminal and mucosal microenvironment of Barrett's esophagus that promote, in a small proportion of patients, development of esophageal adenocarcinoma. Markers of clonal evolution can be used to determine patient risk for cancer and set surveillance intervals.

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Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Insights Into the Pathophysiology of Esophageal Adenocarcinoma

2018

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“…There is evidence that goblet cells preferentially appear near the neo-SCJ 5 and their density is higher in the proximal third of CLE. 6 However, as far as we know, there are no data supporting differences between biopsies from the SCJ or from just below the Zline, as we have systematically performed, 2 in the assessment of IM. It is clear from our study that proton pump inhibitors used in the clinical setting do not prevent IM development.…”

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confidence: 84%

Letter: cancer risk among persons with columnar‐lined oesophagus – authors’ reply

Pereira

Chaves

2012

Aliment Pharmacol Ther

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SIRS, We thank Lenglinger and co-workers for their comments regarding our study.1 Our data clearly show that columnar-lined oesophagus (CLE) with only cardiac (CM) and oxintocardiac mucosa (OCM) cannot be considered free from cancer risk, as the majority of patients will develop intestinal metaplasia (IM) over time. 2However, the magnitude of this risk remains unknown. Bhat et al.3 reported a five-fold reduction (0.07 vs. 0.36) in the combined annual incidence of cancer or high-grade dysplasia in CLE without IM in comparison to CLE with IM in the index endoscopy, but Kelty et al. found no difference. 4 We agree with the need for larger multi-centric studies, but strict inclusion criteria are needed to minimise the problem of sampling error in IM assessment. From our data, we cannot either support or deny the hypothesis of Chandrasoma 5 that both OCM and IM develop from CM, but we can hypothesise that OCM is an early event, when compared with IM. Lenglinger suggests that biopsies from the squamocolumnar junction (SCJ) have the highest yield for the detection of IM. There is evidence that goblet cells preferentially appear near the neo-SCJ 5 and their density is higher in the proximal third of CLE. 6 However, as far as we know, there are no data supporting differences between biopsies from the SCJ or from just below the Zline, as we have systematically performed, 2 in the assessment of IM. It is clear from our study that proton pump inhibitors used in the clinical setting do not prevent IM development.2 Oberg reported a 10.3-fold decrease in the risk of developing IM in patients with an efficient anti-reflux surgical procedure, 7 but 20% of them developed IM during follow-up. We have no data on the efficiency of surgical procedures performed in our cohort. 2 ACKNOWLEDGEMENTThe authors' declarations of personal and financial interests remain unchanged from those in the original article.

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“…15, 21 In a recent study, Theodorou and colleagues reported that the density of goblet cells correlated directly with an esophageal luminal pH gradient, suggesting that goblet cell differentiation is pH dependent and may be due to the effects of pH on bile acid dissociation. 22 …”

Section: Definition and Diagnostic Criteria Of Barrett’s Esophagusmentioning

confidence: 99%

Barrett’s Esophagus

Naini¹,

Souza²,

Odze

2016

American Journal of Surgical Pathology

131

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This review provides a summary of our current understanding of, and the controversies regarding, the diagnosis, pathogenesis, histopathology, and molecular biology of Barrett's esophagus (BE) and associated neoplasia. Barrett's esophagus is defined as columnar metaplasia of the esophagus. There is worldwide controversy regarding the diagnostic criteria of BE, mainly with regard to the requirement to histologically identify goblet cells in biopsies. Patients with BE are at increased risk for adenocarcinoma which develops via a metaplasia-dysplasia-carcinoma sequence. Surveillance of patients with BE relies heavily on the presence and grade of dysplasia. However, there are significant pathologic limitations and diagnostic variability in evaluating dysplasia, particularly with regard to the more recently recognized unconventional variants. Identification of non-morphology based biomarkers may help risk stratification of BE patients and this is a subject of ongoing research. Due to recent achievements in endoscopic therapy, there has been a major shift in the treatment of BE patients with dysplasia or intramucosal cancer, away from esophagectomy and towards endoscopic mucosal resection and ablation. The pathologic issues related to treatment and its complications are also discussed in this review article.

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Intraluminal pH and Goblet Cell Density in Barrett’s Esophagus

Abstract: Patients with BE have a goblet cell gradient that correlates directly with an esophageal luminal pH gradient. This suggests that goblet cell differentiation is pH dependent and likely due to the effect of pH on bile acid dissociation.

Cited by 36 publications

References 20 publications

Insights Into the Pathophysiology of Esophageal Adenocarcinoma

Insights Into the Pathophysiology of Esophageal Adenocarcinoma

Letter: cancer risk among persons with columnar‐lined oesophagus – authors’ reply

Barrett’s Esophagus

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