Risk of Malignant Progression in Barrett's Esophagus Patients: Results from a Large Population-Based Study

Bhat, Shivaram; Coleman, Helen; Yousef, Fouad; Johnston, Brian T.; McManus, Damian; Gavin, Anna; Murray, Liam

doi:10.1093/jnci/djr203

Cited by 647 publications

(552 citation statements)

References 34 publications

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“…However, not all studies have corroborated this fi nding ( 12 ). Although DNA content abnormalities appear to be comparable in both metaplastic epithelium without goblet cells compared with metaplastic epithelium with goblet cells, other studies suggest that cancer most commonly occurs in columnar metaplasia with goblet cells compared with columnar metaplasia without goblet cells ( 11,13,14 ). Even if the rate of EAC is markedly higher in CLE containing IM, another complicating factor is sampling error leading to misclassifi cation of IM-containing CLE as non-IM CLE.…”

Section: Summary Of Evidencementioning

confidence: 99%

“…Data substantiating a chemopreventive eff ect in the setting of BE are sparse. In part, this paucity of data refl ects the low rate of progression to neoplasia in BE ( 65,136 ), making intervention studies diffi cult to perform. In addition, patients who might have previously been considered for chemoprevention, such as those with BE and LGD, are now considered for endoscopic ablative therapy, making the pool of patients who would gain markedly from a chemopreventive agent even smaller.…”

Section: Summary Of Evidencementioning

confidence: 99%

“…If such irregularity is detected, the next step in the management of that patient should be EMR or endoscopic submucosal dissection, both for therapeutic benefi t and to allow staging of the lesion ( 145,146 ). Although than previously believed ( 68,136,148 ). Given the low rate of progression in these patients, the low but real rate of complications of endoscopic therapy ( 149 ), and the costs associated with its delivery ( 150 ), ablative therapy cannot be recommended in patients with nondysplastic BE.…”

Section: Summary Of Evidencementioning

confidence: 99%

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ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

Shaheen

Falk

Iyer

et al. 2016

American Journal of Gastroenterology

1,323

1,409

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Recent population studies suggest that gastroesophageal refl ux disease (GERD) is increasing in prevalence, both in the United States and worldwide ( 1,2 ). Th e diagnosis of GERD is associated with a 10-15% risk of Barrett's esophagus (BE), a change of the normal squamous epithelium of the distal esophagus to a columnar-lined intestinal metaplasia (IM). Risk factors associated with the development of BE include long-standing GERD, male gender, central obesity ( 3 ), and age over 50 years ( 4,5 ). Th e goal of a screening and surveillance program for BE is to identify individuals at risk for progression to esophageal adenocarcinoma (EAC), a malignancy that has been increasing in incidence since the 1970s ( 6,7 ).Th e purpose of this guideline is to review the defi nition and epidemiology of BE, available screening modalities for BE detection, rationale and methods for surveillance, and available treatment modalities including medical, endoscopic, and surgical techniques. In order to evaluate the level of evidence and strength of recommendations, we used the GRADE (Grading of Recommendations Assessment, Development and Evaluation) system ( 8 ). Th e level of evidence ranged from "high" (implying that further research was unlikely to change the authors' confi dence in the estimate of the eff ect) to "moderate" (further research would be likely to have an impact on the confi dence in the estimate of eff ect) to "low" (further research would be expected to have an important impact on the confi dence in the estimate of the eff ect and would be likely to change the estimate) or "very low" (any estimate of eff ect is very uncertain). Th e strength of a recommendation was graded as "strong" when the desirable eff ects of an intervention clearly outweighed the undesirable eff ects and as "conditional" when there was uncertainty about the tradeoff s. We used meta-analyses or systematic reviews when available, followed by clinical trials and cohort and case-control studies. In order to determine the level Barrett's esophagus (BE) is among the most common conditions encountered by the gastroenterologist. In this document, the American College of Gastroenterology updates its guidance for the best practices in caring for these patients. These guidelines continue to endorse screening of high-risk patients for BE; however, routine screening is limited to men with refl ux symptoms and multiple other risk factors. Acknowledging recent data on the low risk of malignant progression in patients with nondysplastic BE, endoscopic surveillance intervals are attenuated in this population; patients with nondysplastic BE should undergo endoscopic surveillance no more frequently than every 3-5 years. Neither routine use of biomarker panels nor advanced endoscopic imaging techniques (beyond high-defi nition endoscopy) is recommended at this time. Endoscopic ablative therapy is recommended for patients with BE and high-grade dysplasia, as well as T1a esophageal adenocarcinoma. Based on recent level 1 evidence, endoscopic ablative therapy is ...

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Section: Summary Of Evidencementioning

confidence: 99%

Section: Summary Of Evidencementioning

confidence: 99%

Section: Summary Of Evidencementioning

confidence: 99%

See 1 more Smart Citation

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

Shaheen

Falk

Iyer

et al. 2016

American Journal of Gastroenterology

1,323

1,409

View full text Add to dashboard Cite

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“…[34] The updated practice guidelines published in 2011 by the American Gastrointestinal Association (AGA) state that intestinal-type epithelium (SIM) is the only type of esophageal columnar epithelium that clearly predisposes a patient to malignancy [35]. In a subgroup analysis by status in BE, the incidence of EAC in patients with SIM in BE at an index biopsy was 0.23 % patient-years (pyrs) (95 % confidence interval [CI] 0.18-0.29 % per year), and the risk of cancer was significantly higher in patients with SIM than in patients whose first biopsies did not show SIM (0.04 % per year, 95 % CI 0.02-0.08 % per year) [43].…”

Section: Sim (Goblet Cells) and Carcinogenesismentioning

confidence: 99%

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

Watari

Oshima

Fukui

et al. 2013

Clin J Gastroenterol

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Barrett's esophagus (BE) is a premalignant condition of esophageal adenocarcinoma (EAC). Although the incidence of BE has risen rapidly in the West, it is rare in Asia despite a recent increase in the prevalence of gastroesophageal reflux disease. Controversies over the definition of BE are presented because most cases show shortsegment BE, especially ultra-short BE, in Asia. Here we review possible risk factors for the development of EAC, particularly possible roles of ethnicity, specialized intestinal metaplasia (SIM), BE length, and environmental factors, such as Helicobacter pylori infection and obesity. Additionally, we summarize recent studies on the effect of chemoprevention including proton pump inhibitors, nonsteroidal anti-inflammatory drugs or aspirin in order to reduce the risk of neoplastic progression in BE patients. Although substantial knowledge of risk factors of dysplasia/EAC in BE is shown, the risk for neoplastic development may be influenced by geographic variation, study population, the presence or absence of SIM or dysplasia at baseline, and the small number of BE patients investigated. Recently, the efficiency of surveillance for BE patients has been discussed from the standpoint of cost-effectiveness. It may be too difficult to draw conclusions because no randomized clinical trials of BE surveillance have been performed.

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“…Some studies indicate that the chances of identifying goblet cells are related to the length of Barrett's, location of the biopsies (more goblet cells in proximal esophagus), number of biopsies, patient age and gender, being more common in men [1]. Most interest has focussed on those patients with an endoscopically visible columnar lined epithelium containing intestinal metaplasia since this is the form most clearly associated with malignancy with an annual progression rate estimated to be in the region of 0.3-0.4% per annum [2,3]. However, recent studies comparing goblet and non-goblet containing metaplastic epithelium have shown that both types demonstrate the same frequency of DNA content abnormalities [4,5], suggesting that the gastric form is not entirely benign.…”

mentioning

confidence: 99%

Do Transcription Factors Hold the Key to Understanding the Development of Barrett’s Esophagus?

Fitzgerald

2012

Dig Dis Sci

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Barrett's esophagus is a complex metaplasia which can occur as a pure gastric or intestinal histopathological phenotype but more commonly occurs as a mosaic comprising gastric and intestinal forms. Intestinal metaplasia is typified by the presence of goblet cells seen on light microscopy. Some studies indicate that the chances of identifying goblet cells are related to the length of Barrett's, location of the biopsies (more goblet cells in proximal esophagus), number of biopsies, patient age and gender, being more common in men [1]. Most interest has focussed on those patients with an endoscopically visible columnar lined epithelium containing intestinal metaplasia since this is the form most clearly associated with malignancy with an annual progression rate estimated to be in the region of 0.3-0.4% per annum [2,3]. However, recent studies comparing goblet and non-goblet containing metaplastic epithelium have shown that both types demonstrate the same frequency of DNA content abnormalities [4,5], suggesting that the gastric form is not entirely benign.The molecular and cell biological process by which Barrett's esophagus arises is poorly understood. The emerging theories include trans-differentiation from a mature esophageal keratinocyte or altered differentiation of an esophageal or submucosal stem cell [6]. More recently it has been suggested that Barrett's may occur from expansion of an embryological remnant [7]. Whichever theory is correct, all appear to depend on the activation of transcription factors to alter the cell fate. To date most effort has focussed on the homeobox genes Cdx1 and 2 which, in contrast to the dramatic effect observed when ectopically expressed in the murine stomach [8], fail to induce intestinalisation when over-expressed in the esophagus. Other transcription factors examined have included Hedgehog [9] and another critical signalling molecule in embryonic development called BMP4 [10], which have generally failed to induce phenotypic intestinalisation and in particular goblet cells.The aim of this paper was therefore to explore whether the helix-loop-helix transcription factor Math1/Atoh1, which is required for the differentiation of the three secretory cell lineages in the intestine (enteroendocrine, Paneth and goblet cells), could induce intestinalisation of an esophageal cell line. In order to explore this Kong et al. [11] first confirmed earlier reports that this gene is over-expressed in Barrett's esophageal tissues [12]. RNA expression levels in endoscopic biopsies were found to be at a highly variable level (from 10-to 1,000-fold), but the levels were always in excess of that found in paired normal esophageal biopsies. It is unfortunate that no matching histology was available for these Barrett's samples, since as noted in the discussion, it is likely that this variation in RNA expression levels correlated with the goblet cell numbers which are known to be heterogeneous in this epithelium. This is a methodological point worth noting since many studies in the Barrett's field are...

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Risk of Malignant Progression in Barrett's Esophagus Patients: Results from a Large Population-Based Study

Abstract: We found the risk of malignant progression among patients with BE to be lower than previously reported, suggesting that currently recommended surveillance strategies may not be cost-effective.

Cited by 647 publications

References 34 publications

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

Do Transcription Factors Hold the Key to Understanding the Development of Barrett’s Esophagus?

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