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Barrett's esophagus
Medical expert of the article
Last reviewed: 04.07.2025
Barrett's esophagus is an acquired condition that is one of the complications of gastroesophageal or duodenogastroesophageal reflux disease, developing as a result of the replacement of the destroyed multilayered squamous epithelium of the lower part of the esophagus with columnar epithelium, which leads to a predisposition to the development of adenocarcinoma of the esophagus or cardia (B. D. Starostin, 1997).
The disease was first described by the British surgeon Barrett in 1950.
Barrett's esophagus occurs in 8-10% of adults (Phillips, 1991).
What causes Barrett's esophagus?
The main causes of Barrett's esophagus are gastroesophageal or duodenogastroesophageal reflux disease and diaphragmatic hernia.
B. D. Starostin (1997) considers the pathogenesis of Barrett's esophagus as follows.
As a result of long-term GERD, the normal multilayered squamous epithelium of the esophageal mucosa is destroyed by aggressive factors of gastric juice (hydrochloric acid, pepsin), bile acids, and the pancreatic enzyme trypsin. Conjugated bile acids cause damage to the esophageal mucosa at pH 2.0-3.0, unconjugated bile acids and trypsin - at pH 7.0.
The destroyed normal stratified epithelium of the esophagus is replaced by columnar epithelium, which is more resistant to hydrochloric acid, pepsin and duodenal contents. The primary source for Barrett's specialized columnar epithelium are multipotent stem cells located in the glands of the esophagus. They migrate to the exposed surface of the esophagus, replace the stratified squamous epithelium and then these immature cells are transformed (differentiated) into columnar epithelium.
Later, dysplasia of the columnar epithelium may develop and neoplastic progression may begin, which is associated with three types of cell cycle disorders: mobilization of cells from G0 to G1 phase; loss of control over the transition from G1 phase to S phase; accumulation of cells in C2 phase. An important stage of neoplastic progression is the loss of regulation of the transition from G1 phase to S phase.
This process is regulated by the suppressor gene P53, located on the short arm of chromosome 17. Loss of normal P53 function contributes to the development of chromosomal mutations, epithelial dysplasia, and tumor progression. Dysfunction of the P53 gene has been found in adenocarcinomas arising in Barrett's esophagus, in areas of dysplasia of the columnar epithelium, and even in metaplastic columnar epithelium without signs of dysplasia.
Symptoms of Barrett's Esophagus
It has been established that the replacement of the multilayered epithelium of the esophagus with a cylindrical one in Barrett's esophagus does not cause any specific symptoms. Columnar epithelium is less sensitive to pain than the natural squamous epithelium of the esophagus. Therefore, more than 25% of patients with Barrett's esophagus do not have symptoms of gastroesophageal reflux disease (GERD), and in the remaining patients, GERD symptoms are mild.
Barrett's esophagus has no pathognomonic symptoms; the symptoms of Barrett's esophagus correspond to GERD. However, it should be remembered that a long history of GERD and the age of patients correlate with the presence of metaplasia in Barrett's esophagus.
How is Barrett's esophagus diagnosed?
Barrett's esophagus is diagnosed based on instrumental and laboratory data.
X-ray of the esophagus and stomach
The most characteristic radiographic signs of Barrett's esophagus are:
- Barrett's ulcer (it can be superficial or penetrating);
- hernia of the esophageal opening of the diaphragm in 80-90% of patients;
- mesh pattern of the esophageal mucosa.
Fibroesophagogastroduodenoscopy
FGDS is the main diagnostic method for Barrett's esophagus. The cylindrical epithelium (Barrett's epithelium) during FGDS has the appearance of a velvet-like red mucous membrane, which distally imperceptibly passes into the normal mucous membrane of the proximal stomach, and proximally into the squamous epithelium of the esophagus of pink color. In 90% of patients, a diaphragmatic hernia is also determined, and in all - symptoms of esophagitis of varying severity.
To confirm the diagnosis of Barrett's esophagus, a histological examination of biopsies of the esophageal mucosa is performed. Barrett's esophagus is possible if at least one of the multiple biopsies reveals columnar epithelium, regardless of the extent of its location. Biopsies should be taken from four quadrants, starting at the gastroesophageal junction and proximally every 1-2 cm.
The specialized columnar epithelium has a villous surface and crypts lined with mucus-secreting prismatic and goblet cells. Goblet cells contain acidic mucin (a mixture of sialomucins and sulfomucins). Prismatic cells are located between the goblet cells and resemble colonocytes. Enteroendocrine cells producing glucagon, cholecystokinin, secretin, neurotensin, serotonin, pencreatic polypeptide, somatostatin are also found.
Immunohistochemical examination reveals sucraseisomaltase, a specific marker of Barrett's epithelium, in the altered mucosa in Barrett's esophagus.
Chromoesophagososcopy
Chromoesophagoscopic examination is based on the fact that the esophagus is examined after preliminary introduction of toluidine blue, indigo carmine or methylene blue into the esophagus. These dyes stain the metaplastic mucous membrane and leave normal areas of the esophageal mucous membrane unstained.
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Esophagomanomegry and 24-hour pH monitoring
Esophagomanometry reveals a decrease in pressure in the lower esophageal sphincter. 24-hour intraesophageal pH monitoring reveals a prolonged decrease in intraesophageal pH.
Radioisotope research
To confirm the diagnosis of Barrett's esophagus, radioisotope scanning with technetium-99t is performed. The degree of accumulation of the isotope correlates with the prevalence of columnar epithelium.
What do need to examine?
How to examine?
What tests are needed?