Barrett's esophagus

Barrett's esophagus is an acquired condition resulting from severe esophageal mucosal injury. It still remains unclear why some patients with gastroesophageal reflux disease develop Barrett's esophagus whereas others do not. The diagnosis of Barrett's esophagus is established if the squamocolumnar junction is displaced proximal to the gastroesophageal junction and if intestinal metaplasia is detected by biopsy. Despite this seemingly simple definition, diagnostic inconsistencies remain a problem, especially in distinguishing short segment Barrett's esophagus from intestinal metaplasia of the gastric cardia. Barrett's esophagus would be of little importance were it not for its well-recognized association with adenocarcinoma of the esophagus. The incidence of esophageal adenocarcinoma continues to increase and the 5-year survival rate for this cancer remains dismal. However, cancer risk for a given patient with Barrett's esophagus is lower than previously estimated. Current strategies for improved survival in patients with esophageal adenocarcinoma focus on cancer detection at an early and potentially curable stage. This can be accomplished either by screening more patients for Barrett's esophagus or with endoscopic surveillance of patients with known Barrett's esophagus. Current screening and surveillance strategies are inherently expensive and inefficient. New techniques to improve the efficiency of cancer surveillance are evolving rapidly and hold the promise to change clinical practice in the future. Treatment options include aggressive acid suppression, antireflux surgery, chemoprevention, and ablation therapy, but there is still no clear consensus on the optimal treatment for these patients.     

Barrett's esophagus

Barrett's esophagus is an acquired metaplastic abnormality in which the normal stratified squamous epithelium lining of the esophagus is replaced by an intestinal-like columnar epithelium. While in itself a benign and asymptomatic disorder, the clinical importance of this relatively common condition relates to its role as a precursor lesion to esophageal adenocarcinoma, the incidence of which has dramatically increased in Western populations in recent years. Although known to arise as a consequence of chronic gastroesophageal reflux, the cellular and molecular mechanisms underlying development Barrett's esophagus and its progression to cancer remain unclear.     

Screening for Barrett's esophagus

Screening and surveillance for Barrett's esophagus have been proposed as strategies for preventing deaths from esophageal adenocarcinoma. A meaningful discussion on the cost efficacy of screening and surveillance for Barrett's esophagus requires a reasonable estimate of the risk of esophageal cancer in this condition. The primary goal of endoscopic screening for individuals with gastroesophageal reflux disease is to identify patients with Barrett's esophagus who will benefit from an intervention to prevent cancer. There is also indirect evidence to suggest that surveillance for Barrett's esophagus may be beneficial. However, there is much debate over the efficacy of these diagnostic procedures. In the absence of definitive data, investigators have used computer models to study the cost effectiveness of screening and surveillance for Barrett's esophagus. It is important for physicians to recognize that such models do not provide a single, definitive answer.     

Biomarkers of Barrett's esophagus

Barrett's esophagus is the strongest risk for esophageal adenocarcinoma(EAC). Metaplasia in patients with BE may progress to dysplasia and then invasive carcinoma. Well-defined diagnostic, progressive, predictive, and prognostic biomarkers are needed to identify the presence of the disease, estimate the risk of malignant transformation, and predict the therapeutic outcome and survival of EAC patients. There are many predictive and prognostic markers that lack substantial validation, and do not allow stratification of patients with gastroesophageal reflux disease in clinical practice for outcome and effectiveness of therapy. In this short review we summarize the current knowledge regarding possible biomarkers, focusing on the pathophysiologic mechanisms to improve prognostic and therapeutic approaches.     

Barrett's esophagus in childhood

This study describes the clinical, radiologic, esophageal function test, endoscopic, and histologic findings of Barrett's esophagus in 11 children aged 6-14 yr. All had long-standing symptoms of gastroesophageal reflux, which had begun in the first year of life in 10 of the 11. Eight of the 11 patients had mid or upper esophageal strictures and 10 of the 11 required fundoplication. Most patients had low lower esophageal sphincter pressures and abnormal pH probe studies. Only 6 of the 11 children had the characteristic pink-red appearance of the mucosa at endoscopy. Fifty endoscopic biopsy specimens taken at multiple levels in the esophagus contained columnar-lined epithelium above the gastroesophageal junction. Five of the patients had specialized (intestinal-type) epithelium as part of the histologic spectrum. The clinical expression of Barrett's esophagus in children is similar to that in adults except that strictures appear to be more common in children, and the endoscopic appearance of the mucosa is not always typical in color. As in adults, gastroesophageal reflux appears to be the etiology. In children beyond infancy, Barrett's esophagus is the most common indication for antireflux surgery at our institution. Biopsy specimens should be taken from multiple levels in the esophagus to avoid overdiagnosis and to establish the diagnosis with certainty.     

Barrett's esophagus complicating scleroderma

Two patients with scleroderma whose esophageal involvement was associated with long-standing reflux esophagitis were found to also have Barrett's esophagus. Since Barrett's esophagus is a premalignant condition, these patients with scleroderma should be considered at high risk for the development of adenocarcinoma of the esophagus.     

Dysplasia in Barrett's esophagus

Summary In a retrospective histological study, resected specimens obtained from 23 patients with adenocarcinoma in Barrett's esophagus (Group I) and endoscopic multiple (step) biopsis from 38 patients without carcinoma in Barrett's esophagus (Group II) were investigated for dysplastic changes. Dysplasia was most frequently found in the type of mucosa comprising intestinal metaplasia. There seem to be two pathways to dysplasia in Barrett's esophagus. In Group I dysplasia was found in 18 out of 23, and in Group II in 2 out of 38 patients. In Barrett's esophagus, dysplasia may be considered not only a precursor of carcinoma, but also a marker for coexisting carcinoma.Presented at the 1984 meeting of the American Gastroenterological Association May 20–23, New Orleans, La., USA     

Barrett's esophagus and achalasia

Two unusual cases of achalasia with endoscopic and histologic documentation of Barrett's esophagus are presented. One patient had Barrett's esophagus at the time of initial endoscopy for achalasia, before any treatment. The other patient developed specialized columnar epithelia in the esophagus after treatment with pneumatic dilation. Each patient had evidence of low-grade dysplasia. Including these two patients, 30 cases of Barrett's esophagus in patients with achalasia have been reported in the literature. In 73% (22 of 30) of the cases, Barrett's esophagus was detected after esophagomyotomy. In 20% (6 of 30) of the cases of achalasia and Barrett's esophagus, adenocarcinoma developed. The current two cases are unusual because Barrett's esophagus in achalasia generally develops from gastroesophageal reflux after esophagomyotomy. No other patients have been reported to develop Barrett's esophagus after pneumatic dilation alone. Patients with achalasia and Barrett's esophagus may be at a particularly high risk for developing dysplasia and adenocarcinoma.     

Endotherapy for Barrett's esophagus

Endotherapy is now the mainstay of therapy for Barrett's associated neoplasia. The approach should begin with confirmation of neoplasia by a gastrointestinal pathologist, patient counseling, and appropriate endoscopic work up. Detailed examination with high-resolution white light endoscopy is the most important tool for detection of neoplasia. Further validation studies are needed for many enhanced imaging modalities before being recommended as part of the standard work up and assessment of patients with Barrett's esophagus (BE). Endoscopic mucosal resection is required for any visible lesion in the setting of dysplasia for accurate histological diagnosis. The remainder of the epithelium may be treated with resection or ablative therapy, followed by adequate surveillance. Patients with nondysplastic Barrett's require further risk stratification before incorporation of ablative therapy for this population. The future will fortify the endoscopic role in Barrett's with validation trials for endoscopic assessment, further long-term results for each of the treatment modalities, potential risk stratification for patients with BE, and improved guidelines for surveillance after therapy.     

Barrett's esophagus: a review

Barrett's esophagus may be defined as a columnar epithelium-lined distal esophagus. As a frequently recognized complication of gastroesophageal reflux, Barrett's esophagus has become a diagnosis of general clinical concern. Factors governing the development of this complication in patients with gastroesophageal reflux are unknown but may be congenitally determined in part. When symptoms are present, they are due to the complications of reflux, such as esophagitis, stricture, ulcer, or bleeding. Barrett's esophagus may be suspected on the basis of results of a barium meal test, endoscopy, or isotope scanning. Iodine staining at endoscopy or manometrically guided biopsy helps to localize the abnormal mucosal segment. The diagnosis is proved by biopsy. The columnar epithelium of Barrett's esophagus has a malignant predisposition, and, once the diagnosis is made, periodic endoscopy, with biopsy and cytologic study, is indicated. The treatment of Barrett's esophagus is directed toward objective cessation of gastroesophageal reflux. In refractory cases, antireflux surgery improves symptoms and complications from reflux, but the columnar epithelium generally persists along with its malignant potential. It is not known whether effective antireflux treatment will lower the incidence of adenocarcinoma.