Letter: incidence rates of Barrett's oesophagus and oesophageal adenocarcinoma in the UK and the Netherlands

ObjectivesStandards for Barrett’s oesophagus (BO) surveillance in the UK are outlined in the British Society of Gastroenterology (BSG) guidelines. This study aimed to assess the quality of current surveillance delivery compared with a dedicated service.DesignAll patients undergoing BO surveillance between January 2016 and July 2017 at a single National Health Service district general hospital were included. Patients had their endoscopy routed to a dedicated BO endoscopy list or a generic service list. Prospective data were analysed against the BSG guidelines and also compared with each patient’s prior surveillance endoscopy.Results361 patients were scheduled for surveillance of which 217 attended the dedicated list, 78 attended the non-dedicated list and 66 did not have their endoscopy. The dedicated list adhered more closely to the BSG guidelines when compared with the non-dedicated and prior endoscopy, respectively; Prague classification (100% vs 87.3% vs 82.5%, p<0.0001), hiatus hernia delineation (100% vs 64.8% vs 63.3%, p<0.0001), location and number of biopsies recorded (99.5% vs 5.6% vs 6.9%, p<0.0001), Seattle protocol adherence (72% vs 42% vs 50%, p<0.0001) and surveillance interval adherence (dedicated 100% vs prior endoscopy 75%, p<0.0001). Histology results from the dedicated and non-dedicated list cohorts revealed similar rates of intestinal metaplasia (79.8% vs 73.1%, p=0.12) and dysplasia/oesophageal adenocarcinoma (4.3% vs 2.6%, p=0.41).ConclusionsThe post-BSG guideline era of BO surveillance remains suboptimal in this UK hospital setting. A dedicated service appears to improve the accuracy and consistency of surveillance care, although the clinical significance of this remains to be determined.

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Dietary factors and the risks of oesophageal adenocarcinoma and Barrett's oesophagus

Nutrition Research Reviews ◽

10.1017/s0954422410000132 ◽

2010 ◽

Vol 23 (2) ◽

pp. 230-246 ◽

Cited By ~ 58

Author(s):

Ai Kubo ◽

Douglas A. Corley ◽

Christopher D. Jensen ◽

Rubinder Kaur

Keyword(s):

Risk Factors ◽

Fruits And Vegetables ◽

Epidemiological Studies ◽

Incidence Rates ◽

Dietary Factors ◽

Barrett’S Oesophagus ◽

Oesophageal Adenocarcinoma ◽

Barrett's Oesophagus ◽

Dark Green ◽

Demographic Distribution

Incidence rates for oesophageal adenocarcinoma have increased by over 500 % during the past few decades without clear reasons. Gastro-oesophageal reflux disease, obesity and smoking have been identified as risk factors, although the demographic distribution of these risk factors is not consistent with the demographic distribution of oesophageal adenocarcinoma, which is substantially more common among whites and males than any other demographic groups. Numerous epidemiological studies have suggested associations between dietary factors and the risks of oesophageal adenocarcinoma and its precursor, Barrett's oesophagus, though a comprehensive review is lacking. The main aim of the present review is to consider the evidence linking dietary factors with the risks of oesophageal adenocarcinoma, Barrett's oesophagus, and the progression from Barrett's oesophagus to oesophageal adenocarcinoma. The existing epidemiological evidence is strongest for an inverse relationship between intake of vitamin C, β-carotene, fruits and vegetables, particularly raw fruits and vegetables and dark green, leafy and cruciferous vegetables, carbohydrates, fibre and Fe and the risk of oesophageal adenocarcinoma and Barrett's oesophagus. Patients at higher risk for Barrett's oesophagus and oesophageal adenocarcinoma may benefit from increasing their consumption of fruits and vegetables and reducing their intake of red meat and other processed food items. Further research is needed to evaluate the relationship between diet and the progression of Barrett's oesophagus to oesophageal adenocarcinoma. Evidence from cohort studies will help determine whether randomised chemoprevention trials are warranted for the primary prevention of Barrett's oesophagus or its progression to cancer.

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Faculty Opinions recommendation of Oesophageal adenocarcinoma and prior diagnosis of Barrett's oesophagus: a population-based study.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718338089.793493545 ◽

2014 ◽

Author(s):

Hugh Barr

Keyword(s):

Population Based ◽

Barrett’S Oesophagus ◽

Oesophageal Adenocarcinoma ◽

Population Based Study ◽

Barrett's Oesophagus

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Faculty Opinions recommendation of Evolution of oesophageal adenocarcinoma from metaplastic columnar epithelium without goblet cells in Barrett's oesophagus.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.726037417.793519451 ◽

2016 ◽

Author(s):

Noam Harpaz ◽

Alexandros Polydorides

Keyword(s):

Goblet Cells ◽

Barrett’S Oesophagus ◽

Oesophageal Adenocarcinoma ◽

Columnar Epithelium ◽

Barrett's Oesophagus

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Multitrait genetic association analysis identifies 50 new risk loci for gastro-oesophageal reflux, seven new loci for Barrett’s oesophagus and provides insights into clinical heterogeneity in reflux diagnosis

Gut ◽

10.1136/gutjnl-2020-323906 ◽

2021 ◽

pp. gutjnl-2020-323906

Author(s):

Jue-Sheng Ong ◽

Jiyuan An ◽

Xikun Han ◽

Matthew H Law ◽

Priyanka Nandakumar ◽

...

Keyword(s):

Risk Factors ◽

Multiple Testing ◽

Association Studies ◽

Barrett’S Oesophagus ◽

Oesophageal Reflux ◽

Oesophageal Adenocarcinoma ◽

Specific Gene ◽

Genome Wide Association Studies ◽

Disease Heterogeneity ◽

Barrett's Oesophagus

ObjectiveGastro-oesophageal reflux disease (GERD) has heterogeneous aetiology primarily attributable to its symptom-based definitions. GERD genome-wide association studies (GWASs) have shown strong genetic overlaps with established risk factors such as obesity and depression. We hypothesised that the shared genetic architecture between GERD and these risk factors can be leveraged to (1) identify new GERD and Barrett’s oesophagus (BE) risk loci and (2) explore potentially heterogeneous pathways leading to GERD and oesophageal complications.DesignWe applied multitrait GWAS models combining GERD (78 707 cases; 288 734 controls) and genetically correlated traits including education attainment, depression and body mass index. We also used multitrait analysis to identify BE risk loci. Top hits were replicated in 23andMe (462 753 GERD cases, 24 099 BE cases, 1 484 025 controls). We additionally dissected the GERD loci into obesity-driven and depression-driven subgroups. These subgroups were investigated to determine how they relate to tissue-specific gene expression and to risk of serious oesophageal disease (BE and/or oesophageal adenocarcinoma, EA).ResultsWe identified 88 loci associated with GERD, with 59 replicating in 23andMe after multiple testing corrections. Our BE analysis identified seven novel loci. Additionally we showed that only the obesity-driven GERD loci (but not the depression-driven loci) were associated with genes enriched in oesophageal tissues and successfully predicted BE/EA.ConclusionOur multitrait model identified many novel risk loci for GERD and BE. We present strong evidence for a genetic underpinning of disease heterogeneity in GERD and show that GERD loci associated with depressive symptoms are not strong predictors of BE/EA relative to obesity-driven GERD loci.

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