It refers to an abnormal change of the cells of the terminal portion of the esophagus (tube for food). 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 of 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 for the diagnosis of 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 the control of 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 that is 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 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 the same as for 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 have been found to be 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 are effective in reducing only the acid component in reflux, surgical treatment may have an advantage.
However, although studies have shown that surgery is effective in controlling the symptoms of gastroesophageal reflux, the results with respect to 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 the eradication of Barrett’s esophagus, but it is certainly reasonable for appropriate patients who want surgery to control the symptoms of gastroesophageal reflux.
With regard to reducing the risk of cancer in Barrett’s esophagus, the evidence is still insufficient to recommend surgery on medical treatment.
Although the regression of the characteristics associated with the risk of cancer 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 intake of vegetables in the diet may reduce the risk.
Therefore, the diet for patients with Barrett’s esophagus is the same 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 normally found in the stomach.
The debate for the next 4 decades 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, in fact, 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 will be called “lower esophagus lined by columnar epithelium.”
For the next 2 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 1 or a combination of 3 types of columnar epithelium; that is, a type of gastric fundus, a type 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 the diagnosis of the condition.
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 normal region of the columnar mucosa.
In addition, determining the exact location of the esophagogastric junction in patients with Barrett’s esophagus is often difficult. To avoid false positive diagnoses, the researchers selected arbitrary lengths of 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 eosophageal atresia without fistula, previous multiple antireflux surgery, 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.
The majority of patients with this condition will not develop esophageal cancer , and the risk of progression to esophageal adenocarcinoma is estimated at approximately 0.5% per year in patients without dysplasia in the initial surveillance biopsies.