Barrett's Esophagus

Iascone, C

doi:10.1001/archsurg.1983.01390050027005

Cited by 255 publications

(19 citation statements)

References 12 publications

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“…Several studies have documented lower mean basal LES pressures in patients with Barrett’s esophagus compared to patients with uncomplicated GERD (fig. 1a) [8,9,10,11,12,13,14,15,16]. However, when patients with Barrett’s esophagus are compared to patients with severe reflux esophagitis only, no significant differences in LES pressures were noted [17,18,19,20].…”

Section: Lower Esophageal Sphinctermentioning

confidence: 99%

“…Barham et al [45] reported even longer acid clearance time in patients with reflux strictures. When compared to patients with all degrees of reflux esophagitis but without Barrett’s esophagus, patients with Barrett’s esophagus had longer acid clearance times [8, 18, 19] and increased numbers of reflux episodes [8, 19]. …”

Section: Esophageal Dysmotilitymentioning

confidence: 99%

“…In view of the evidence showing impaired esophageal peristalsis and longer esophageal clearance times in patients with severe reflux esophagitis and Barrett’s esophagus, it is not surprising that these patients are subjected to the highest levels of esophageal acid exposure [8, 54, 55]. Nevertheless, whether esophageal peristaltic dysfunction is a primary defect independent of mucosal changes, or arises from reflux-induced mucosal injury with resultant esophageal dysmotility is still a matter of controversy.…”

Section: Esophageal Dysmotilitymentioning

confidence: 99%

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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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Section: Lower Esophageal Sphinctermentioning

confidence: 99%

Section: Esophageal Dysmotilitymentioning

confidence: 99%

Section: Esophageal Dysmotilitymentioning

confidence: 99%

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

et al. 2009

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“…As a group, patients with Barrett's esophagus have a very low lower-esophageal sphincter pressure (23), making recognition of the end of the esophagus difficult. The proximal margin of the gastric folds within a hiatal hernia when the distal esophagus is deflated serves as a marker for the end of the esophagus and the location of the esophagogastric junction (24).…”

Section: The Diagnosis Of Barrett's Esophagus Requires Systematic Biomentioning

confidence: 99%

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Sampliner

1998

The American Journal of Gastroenterology

105

110

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“…Comparative studies have reported that persons with BE have less prevalent reflux symptoms than those with GERD alone. 65, 66 …”

Section: Biology Of Early Barrett’s Esophagusmentioning

confidence: 99%

Early events during neoplastic progression in Barrett's esophagus

Reid

2011

CBM

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SUMMARY Advances in genomic analysis and sequencing, transcriptomics and proteomics are rapidly increasing our understanding of the complexity, redundancies and heterogeneity among cancers. Challenges to risk stratification, prevention and early detection will become great if, as expected, EA has similar complexity compared to other cancers. Discovery of very large possible combinations of biomarkers for BE risk assessment for progression to EA may overwhelm the translational research process for biomarker validation. One approach for risk stratification and early detection would be to search for fundamental biomarkers of progression, such as mutation rate, generation of diversity and clonal expansions. However, our previous studies and others have reported that low density STR biomarkers combined with DNA content flow cytometry could stratify patients into clinically relevant risk groups to manage the cancer risk for five years into the future reasonably well.117 With new SNP based technology and larger cohort studies with greater sample sizes, there is promise to achieve better biomarkers for EA risk stratification and early detection for clinical use because genome-wide measures of chromosome instability and 17pLOH have shown promise in all prospective studies. Such a platform could be readily adapted to risk stratification and evolutionary biomarkers of progression, including measures of clonal diversity and expansions.

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Barrett's Esophagus

Cited by 255 publications

References 12 publications

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

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

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Early events during neoplastic progression in Barrett's esophagus

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