It refers to an abnormal change of the cells of the terminal portion of the esophagus (tube for food). I am modifying the esophageal lining.
In Barrett’s esophagus, the healthy esophageal epithelium is replaced by metaplastic cylindrical cells, thought to be the result of damage from prolonged exposure of the esophagus to the reflux gastroesophageal reflux disease.
The inherent risk of progression of Barrett’s esophagus to adenocarcinoma of the esophagus has been established.
Signs and symptoms
The classic image of a patient with Barrett’s esophagus is a middle-aged white male (55 years old) with a chronic history of gastroesophageal reflux, for example, heartburn, acid regurgitation, and, occasionally, dysphagia.
Some patients, however, deny having any symptoms.
The following techniques are used in the diagnosis and evaluation of Barrett’s esophagus:
Esophagogastroduodenoscopy (EGD): the procedure of choice to diagnose Barrett’s esophagus.
Biopsy: the diagnosis of this condition requires confirmation of biopsies of specialized intestinal metaplasia in the esophagus.
Ultrasonography: When high-grade dysplasia or cancer is found in surveillance endoscopy, endoscopic ultrasound is recommended to evaluate surgical resectability
The diagnosis of Barrett’s esophagus does not lead to a specific therapy. Little evidence supports the assumption that antisecretory agents or antireflux surgery prevent the onset of adenocarcinoma or lead to regression of the condition.
Currently, the indications for medical therapy in controlling Barrett’s esophagus of symptoms and healing of the esophageal mucosa are the same as for gastroesophageal reflux.
Treatment of Barrett’s esophagus
Once Barrett’s esophagus has been identified, patients should undergo periodic surveillance endoscopy to identify histologic markers that increase the risk of cancer (dysplasia) or cancer at an earlier stage and is amenable to treatment.
Dysplasia is the best histological marker for cancer risk. Treatment options for high-grade dysplasia include the following:
- Surgical endoscopy, with intensive biopsy at 3-month intervals until the cancer is detected.
- Endoscopic ablation in most major medical centers, ablation is the first-line therapy.
- Surgical resection
The pharmacological treatment for Barrett’s esophagus should be like gastroesophageal reflux.
Although most authorities agree that the treatment should use a proton pump inhibitor (PPI) instead of an H2 receptor antagonist due to the relative acid insensitivity of patients with Barrett’s esophagus.
Although PPIs are better than H2 receptor antagonists for reducing gastric acid secretion, the evidence for whether PPIs induce regression of Barrett’s esophagus remains inconclusive.
Surgery: In addition to acid, the reflux of pancreatic and biliary secretions into the esophagus has been implicated in the pathogenesis of Barrett’s esophagus. Because medications effectively reduce only the acid component in reflux, surgical treatment may have an advantage.
However, although studies have shown that surgery effectively controls the symptoms of gastroesophageal reflux, the results concerning the regression of Barrett’s esophagus are inconclusive.
There is no good evidence to indicate that surgical therapy provides regression in Barrett’s esophagus.
Therefore, antireflux surgery, such as Nissen fundoplication, is not indicated for eradicating Barrett’s esophagus. Still, it is reasonable for appropriate patients who want surgery to control the symptoms of gastroesophageal reflux.
The evidence is still insufficient to recommend surgery on medical treatment to reduce cancer risk in Barrett’s esophagus.
Although the regression of the characteristics associated with cancer risk seems to be more common after the surgical intervention than medical therapy.
Diet: The data are inconclusive regarding the relationship between Barrett’s esophagus and dietary intake of fruit, fat, and red / processed meat, although information on vegetables in the diet may reduce the risk.
Therefore, the diet for patients with Barrett’s esophagus is recommended for patients with gastroesophageal reflux. Patients should avoid the following:
- Fried or fatty foods
- Carbonated drinks.
- Citrus or juices
- Aspirin and other non-steroidal anti-inflammatory drugs.
Patients should also reduce portion sizes at mealtime, eat at least three (03) hours before bedtime, raise the head of the bed 6 inches, lose weight (if overweight), and stop smoking.
Barrett’s esophagus is well recognized as a complication of gastroesophageal reflux disease. Prolonged exposure of the esophagus to reflux can erode the esophageal mucosa, promote the infiltration of inflammatory cells and ultimately cause epithelial necrosis.
It is believed that this chronic damage promotes the replacement of healthy esophageal epithelium by metaplastic cylindrical cells of Barrett’s esophagus. Why only some people with gastroesophageal reflux develop Barrett’s esophagus is unclear.
The definition of Barrett’s esophagus has evolved considerably in the last 100 years. In 1906, Tileston, a pathologist, described several patients with “peptic ulcer of the esophagus,” in which the epithelium around the ulcer looked much like the one typically found in the stomach.
For the next four decades, the debate focused on the anatomical origin of this mucosal anomaly.
Many researchers, including Barrett in his treatise published in 1950, supported the view that this ulcerous, spinal-shaped organ was the stomach tied inside the chest by a congenitally short esophagus.
In 1953, Allison and Johnstone argued that the columnar organ was more likely esophagus because the intrathoracic region lacked a peritoneal covering, contained submucosal and muscle glands characteristic of the esophagus, and could harbor islands of squamous cells within the columnar segment.
In 1957, Barrett agreed and suggested that the condition that bears his name would be called “lower esophagus lined by columnar epithelium.”
For the next two decades, descriptions of the histology of Barrett’s esophagus varied considerably from the fundic-type epithelium that secretes acid to the intestinal-type epithelium with goblet cells.
Finally, in 1976, Paull et al. published a report on the histological spectrum of Barrett’s esophagus in which they used the manometric guide for their biopsies.
The patients in the study had one or a combination of 3 types of the columnar epithelium; that is, a type of gastric fundus, a kind of union, and a distinctive type of intestinal metaplasia that the researchers called “specialized columnar epithelium.”
This specialized intestinal metaplasia, complete with goblet cells, has become the sine qua non condition for diagnosing the disease.
However, while the study by Paull et al. clarifies the nature of the histological lesion, the endoscopic definition of Barrett’s esophagus has continued to change. Many people believed that the distal esophagus could contain a specific region of the columnar mucosa.
In addition, determining the exact location of the esophagogastric junction in patients with Barrett’s esophagus is often tricky. To avoid false-positive diagnoses, the researchers selected arbitrary lengths of the esophagus with cylindrical lines to establish a diagnosis for their studies.
Finally, the endoscopists of the community accepted this practice, and the biopsy of the so-called distal normal distal columnar esophagus was avoided.
Convincing evidence indicates that specialized intestinal metaplasia, the characteristic histologic lesion of Barrett’s esophagus, predisposes to dysplasia and cancer, regardless of the endoscopic location.
Therefore, the definition of Barrett’s esophagus is currently the finding of specialized intestinal metaplasia anywhere within the tubular esophagus.
The average age of patients with Barrett’s esophagus is 55-65 years. The condition occurs in a 2 to 1 ratio of male to female, with men representing more than 80% of the cases.
Some studies indicate a higher prevalence of smoking, alcohol consumption, and obesity in people with the disease.
Estimates of the prevalence of this condition vary considerably and range from 0.9 to 10% of the adult population in general.
In a study of 120 young patients (range, 16-19 years, mean age, 16.5 ± 1.4 years) treated for esophageal atresia, Barrett’s esophagus was associated with oesophageal atresia without fistula, previous multiple antireflux surgeries, esophageal dilatation, suspected Barrett’s esophagus in endoscopy and histological esophagitis.
Barrett esophagus prognosis
The most significant morbidity associated with Barrett’s esophagus is the development of adenocarcinoma in the esophagus.