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Barrett's esophagus
Last reviewed: 23.04.2024
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Barrett's esophagus is an acquired condition that is one of the complications of gastroesophageal or duodenogastroesophageal reflux disease, which develops as a result of replacement of the destroyed multilayer squamous epithelium of the lower esophagus with cylindrical epithelium, which leads to a predisposition to the development of adenocarcinoma of the esophagus or cardia (BD Starostin, 1997). ).
The disease was first described by the British surgeon Barrett in 1950.
Barrett's esophagus is recorded in 8-10% of adults (Phillips, 1991).
What causes Barrett's esophagus?
The main causes of the development of Barrett's esophagus are gastroesophageal or duodenogastroesophageal reflux disease and diaphragmatic hernia.
The pathogenesis of Barrett's esophagus BD Starostin (1997) considers as follows.
As a result of a long-term GERD, the normal multilayer squamous epithelium of the esophagus mucosa undergoes destruction under the influence of aggressive factors of gastric juice (hydrochloric acid, pepsin), bile acids, pancreatic enzyme trypsin. Conjugated bile acids cause damage to the mucosa of the esophagus at pH 2.0-3.0, unconjugated bile acids and trypsin - at pH 7.0.
The destroyed normal multilayer epithelium of the esophagus is replaced by a cylindrical epithelium, which is more resistant to hydrochloric acid, pepsin and duodenal contents. The primary source for Barrett's specialized cylindrical epithelium are multipotent stem cells located in the glands of the esophagus. They migrate to the exposed surface of the esophagus, replace the multilayer squamous epithelium and then these immature cells are transformed (differentiated) into the cylindrical epithelium.
In the future, the phenomena of dysplasia of the cylindrical epithelium may develop and a neoplastic progression begins which is associated with three types of cell cycle disorders: mobilization of cells from G0 into the G1 phase; loss of control of the transition of the G1 phase to the S phase; accumulation of cells in the C2 phase. An important stage in the neoplastic profession is the loss of regulation of the transition of the G1 phase to the S phase.
This process regulates the suppressor gene P53 located on the short arm of chromosome 17. The loss of normal functioning of the P53 gene promotes the development of chromosomal mutations, epithelial dysplasia and tumor progression. The impairment of the function of the P53 gene was found in adenocarcinomas originating in the Barrett's esophagus, in the areas of dysplasia of the cylindrical epithelium and even in the metaplastic cylindrical epithelium without signs of dysplasia.
Symptoms of Barrett's esophagus
It was established that replacing the multilayer epithelium of the esophagus cylindrical with the Barrett esophagus does not cause any specific symptoms. Cylindrical 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 others, the symptoms of GERD are poorly expressed.
Barrett's esophagus has no pathognomonic symptoms; symptoms of Barrett's esophagus correspond to GERD. However, it should be remembered that a long history of GERD and age of patients correlate with the presence of metaplasia in the Barrett esophagus.
How is Barrett's esophagus diagnosed?
Barrett's esophagus is diagnosed on the basis of 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 may be superficial or penetrating);
- hernia of the esophageal opening of the diaphragm in 80-90% of patients;
- mesh pattern of the esophagus mucosa.
Fibroesophagogastroduodenoscopy
FGDS is the main method of diagnosing Barrett's esophagus. Cylindrical epithelium (Barrett's epithelium) in the case of FGD has the appearance of a velvet-like (velvet) mucosa of red color, which distally imperceptibly passes into the usual mucous membrane of the proximal part of the stomach, and proximally into squamous epithelium of the esophagus of pink color. In 90% of patients, diaphragmatic hernia is also determined, and in all - the phenomenon of esophagitis of different degrees of severity.
To confirm the diagnosis of Barrett's esophagus, histological examination of biopsies of the esophagus mucosa is performed. Barrett's esophagus is possible if at least one of the multiple biopsy specimens reveals a cylindrical epithelium, regardless of the extent of its location. Biopsy specimens should be taken from four quadrants starting in the gastroesophageal junction and proximally every 1-2 cm.
The specialized cylindrical epithelium has a villous surface and crypts lined with slime-prismatic and goblet cells. Goblet cells contain acidic mucin (a mixture of sialomucins and sulphomucins). The prismatic cells are located between the goblets and resemble colonocytes. Detecting also enteroendocrine cells that produce glucagon, cholecystokinin, secretin, neurotensin, serotonin, penkreatic polypeptide, somatostatin).
Immunohistochemical study reveals in the altered mucosa at Barrett's esophagus a sucrasoisomaltase - a specific marker of Barrett's epithelium.
Chromaesophagoscopy
Chromaesophagoscopy is based on the fact that examination of the esophagus is performed after preliminary introduction into the esophagus of toluidine blue, indigo carmine or methylene blue. These dyes stain the metaplastic mucosa and leave the normal sections of the mucosa of the esophagus uncolored.
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Esophagomanemegria and 24-hour pH monitoring
Ezofagomanometry reveals a decrease in pressure in the lower esophageal sphincter. 24-hour intraosophageal pH monitoring reveals a prolonged decrease in the intrasophageal pH.
Radioisotope study
To confirm the diagnosis of Barrett's esophagus, a radioisotope scan with technetium-99 tons is performed. The degree of accumulation of the isotope correlates with the prevalence of the cylindrical epithelium.
What do need to examine?
What tests are needed?