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Pathology · Digestive System Diseases

Barrett's esophagus

Barrett's esophagus

Barrett's esophagus is an acquired pathological condition characterized by mucosal epithelial metaplasia. The pathology is distinguished by the replacement of stratified squamous epithelium with glandular epithelium, forming areas of intestinal metaplasia above the Z-line.

Key markerFoci of intestinal metaplasia and presence of goblet cells
Macroscopic appearanceTongue-like projections of epithelium above the Z-line
Main riskHigh probability of malignant transformation and development of adenocarcinoma
Molecular factorsOverexpression of Bcl-2, Rab11, telomerase and COX-2 activation
3 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Definition and endoscopic criteria

This disease represents an acquired zone of epithelial metaplasia. The pathological lesion is located circularly above the lower boundary of the esophagogastric junction, known as the Z-line, and extends proximally for three centimeters or more.

During endoscopic examination, the areas of altered glandular epithelium have a characteristic red color and distinctly stand out against the pale, pinkish unchanged stratified squamous epithelium of the esophagus. Visually, these areas resemble "flame-like tongues".

Histological picture and origin

Microscopic examination reveals a combination of two types of epithelium: glandular epithelium of the gastric type is located adjacent to normal squamous epithelium. The key diagnostic feature is intestinal metaplasia, accompanied by the appearance of cytological markers — goblet cells.

The sources of stem cells triggering cell lineages are considered to be multipotent cells of the basal layer of the squamous epithelium or elements located in the excretory ducts of cardiac glands. Chronic inflammation transforms the microenvironment, which begins to regulate the proliferation and differentiation of stem elements toward metaplasia.

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Malignant pathogenesis and molecular stages

The most dangerous clinical course is considered to be incomplete intestinal metaplasia with active secretion of sulfomucins, which stain black with the iron diamine and alcian blue reaction. Malignancy is based on the following processes:

  1. Genetic instability: chromosomal aberrations, mutations, and loss of heterozygosity of alleles (DCC, APC), as well as inactivation of anti-oncogenes (CDKN2, p53).
  2. Epimutations: reversible shifts in the activity of genes responsible for cell division.
  3. Biochemical shifts: overexpression of the anti-apoptotic protein Bcl-2 and the protein Rab11, which transmits proliferative signals.
  4. Enzymatic activation: activation of telomerase, which induces cellular immortalization, as well as nitric oxide synthase and type 2 cyclooxygenase.

As a result of the accumulation of genetic defects and suppression of apoptosis, esophageal adenocarcinoma develops.

Briefly: answers to topical questions

What types of metaplasia exist in Barrett's esophagus besides intestinal?

In addition to intestinal metaplasia, gastric-type metaplasia occurs in Barrett's esophagus. The pathogenesis of the disease shows a strict sequence of changes: against the background of chronic esophagitis, areas of specialized gastric epithelium initially appear. Only after this does the intestinal epithelium with goblet cells form, the presence of which is an obligate histological sign of this precancerous condition. Glandular epithelium of the gastric type is located adjacent to the normal stratified squamous epithelium of the esophagus.

How is Barrett's esophagus classified according to the length of the affected segment?

Barrett's esophagus is diagnosed via EGD and evaluated according to the Prague criteria. The cited sources indicate the following criteria and signs: the zone of epithelial metaplasia is located circularly above the lower border of the esophagogastric junction (Z-line) and extends proximally for 3 cm or more. Foci of metaplastic epithelium are visualized as "flame-like tongues" located above the Z-line and are clearly visible against the pale pink unchanged stratified squamous epithelium of the esophagus.

What diseases and risk factors are the root cause of the development of Barrett's esophagus?

Barrett's esophagus is described in the sources as a complication of GERD and a condition associated with chronic esophagitis. With prolonged exposure of gastroesophageal refluxate to the esophageal mucosa, inflammatory, dystrophic, erosive-ulcerative, and metaplastic changes develop in the stratified squamous epithelium. Chronic inflammation alters the microenvironment, and the altered microenvironment regulates the proliferation and differentiation of stem cells toward metaplasia.

Risk factors for Barrett's esophagus indicated in the sources:

  • long-standing GERD;
  • male sex;
  • obesity;
  • age over 50 years.
How to memorize

Barrett's is "flame-like tongues" of intestinal metaplasia with goblet cells leading to adenocarcinoma.

Class and exam questions

What are the main endoscopic and histological signs of Barrett's esophagus?

Endoscopically, red foci in the form of flame-like tongues extending proximally from the Z-line by 3 cm or more are determined. Histologically, intestinal metaplasia with the mandatory presence of goblet cells is revealed.

Why is Barrett's esophagus considered a precancerous condition?

The condition is associated with a high risk of developing adenocarcinoma. Pathogenesis includes genetic instability, anti-oncogene mutations, telomerase activation, and suppression of apoptosis against the background of incomplete intestinal metaplasia.

What staining methods are used to diagnose specialized epithelium?

Standard hematoxylin and eosin staining is used to reveal the structure, as well as the iron diamine reaction combined with alcian blue to detect sulfomucins in goblet and columnar cells.

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What else to study on this topic

  • Chronic esophagitis and changes in connective tissue papillae
  • Stem cells and the cellular origin of cell lineages
  • Epimutations and decreased expression of contact inhibition proteins (cadherins)
  • Molecular biological pathways of adenocarcinoma progression according to C. Bernstein
  • Benign esophageal tumors: papilloma and its histological structure

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