What causes Barrett's esophagus?

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Last updated: December 6, 2025View editorial policy

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What Causes Barrett's Esophagus

Barrett's esophagus is caused by chronic gastroesophageal reflux disease (GERD), where prolonged acid exposure damages the normal squamous epithelium of the distal esophagus, triggering a metaplastic change to columnar epithelium as a protective response. 1

Primary Pathophysiologic Mechanism

The development of Barrett's esophagus follows a specific sequence of injury and repair:

  • Destruction of the normal squamous mucosa is the necessary prerequisite, allowing for reepithelialization of the lower esophagus with metaplastic columnar epithelium 1
  • Acid exposure is the primary destructive agent, though the exact contributions of acid, pepsin, and duodenal refluxate remain incompletely defined 1
  • The healing environment determines the epithelial type: Animal studies demonstrate that damaged esophageal tissue regenerates columnar epithelium when exposed to acid, but regenerates squamous epithelium when exposed to neutral pH 1

Role of Bile and Duodenal Contents

While acid is the primary driver, bile may play a synergistic role:

  • Bile reflux appears more common in patients with Barrett's esophagus compared to those with uncomplicated GERD or control subjects 1
  • Bile reflux parallels increased acid reflux in Barrett's patients, suggesting a combined injurious effect rather than bile acting alone 1
  • The relative contribution of duodenal contents versus acid remains controversial, but evidence suggests they work together 1

Clinical Risk Factors

The following factors increase risk for developing Barrett's esophagus:

  • Chronic GERD symptoms, particularly long-standing (>20 years) and severe reflux 1, 2
  • Male gender (significantly higher prevalence) 2, 3
  • Caucasian race 3
  • Age over 50 years 2, 3
  • Obesity and high body mass index 2, 3
  • Tobacco use 2, 4, 3
  • Hiatal hernia size 2
  • Family history 4

Cellular Origin and Metaplastic Process

The exact cellular origin remains incompletely understood:

  • Columnar cells differ histologically from gastric cardia cells, ruling out simple upward migration of gastric epithelium 1
  • A pluripotential basal cell at the border between squamous and Barrett's mucosa, with features of both columnar and squamous tissue, may be the progenitor of Barrett's epithelium 1
  • The metaplastic change represents an adaptive response to chronic injury, where the more acid-resistant columnar epithelium replaces damaged squamous epithelium 1

Important Clinical Considerations

Most patients with Barrett's esophagus are undiagnosed during life, as autopsy studies reveal far more cases than are clinically detected 4

The severity of reflux symptoms does not reliably predict Barrett's development, as there is only moderate correlation between symptoms and actual esophageal acid exposure 1

Barrett's esophagus patients often have decreased sensitivity to reflux symptoms due to the columnar epithelium being less sensitive than squamous epithelium, leading to underdiagnosis 5

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Esophageal Adenocarcinoma Risk Factors

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Barrett's esophagus: What do we need to know?

Disease-a-month : DM, 2020

Guideline

Barrett's Esophagus Without Dysplasia

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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