Barrett’s esophagus is a change that occurs in the lining of the esophagus in response to chronic acid injury. About 10% of patients with gastroesophageal reflux disease (GERD), develop Barrett’s esophagus. When Barrett’s esophagus develops, the inner layer of tissue in the esophagus transforms from normal tissue (called squamous cell epithelium) into tissue that looks more like the small intestine (columnar epithelium with intestinal metaplasia), which is customized to withstand acid that is constantly flushing down from the stomach. While this new intestine-type tissue in the esophagus may be more resistant to inflammation and ulceration from acid exposure, it also unfortunately carries a higher risk of developing cancer.

Because of this increased cancer risk, patients with Barrett’s esophagus should undergo some regimen of endoscopic surveillance. The goal of endoscopic surveillance is to identify the development of pre-cancerous change, called dysplasia, within the segment of Barrett’s tissue. Detecting dysplasia enables pursuit of endoscopic interventions for eradication of the abnormal tissue before actual cancer may develop.

Of course, to do proper surveillance for dysplasia, one must first know that Barrett’s esophagus is present and the need for surveillance exists. In general, an initial endoscopy for screening for Barrett’s esophagus is not necessary in all patients with a history of reflux. A combination of specific risk factors may indicate a role for screening endoscopy, however, including age > 50, male gender, Caucasian race, chronic GERD/reflux symptoms, obesity, family history of Barrett’s esophagus or esophageal adenocarcinoma in a first degree relative, or tobacco use. Following screening, if Barrett’s esophagus is confirmed in a patient, the frequency of endoscopy surveillance to detect pre-cancerous change should generally be every 3 to 5 years in patients without a history of dysplasia. Patients with a long-segment of Barrett’s may warrant more frequent surveillance.

Barrett’s esophagus is the primary risk factor for esophageal adenocarcinoma, the most common type of esophageal cancer. Fortunately, while patients with Barrett’s esophagus may have approximately 30 times the risk of esophageal cancer as those without, the overall or absolute risk of cancer is still low. The rate of cancer developing in patients with Barrett’s esophagus is currently estimated to be about 1 out of 250 to 1 out of 400 patients per year. Thus, while the presence of Barrett’s esophagus plus development of dysplasia is an indication for endoscopic eradication therapy, the presence of Barrett’s esophagus without dysplasia only warrants surveillance, since the risks of endoscopic treatment (such as bleeding or esophageal injury) outweigh the small reduction in cancer risk.

Once Barrett’s esophagus has developed, acid reduction therapies may reduce the risk of progression to cancer. Prior analysis has supported that proton pump inhibitors (PPIs) may reduce the risk of development of high-grade dysplasia or esophageal adenocarcinoma by ~ 70%. The definitive role of acid suppression therapy, however, needs further clarification with additional research. While some guidelines recommend routine PPI treatment in all patients with Barrett’s, others suggest the need for PPI treatment only for the purpose of controlling reflux symptoms. Anti-reflux endoscopic and surgical procedures are available for patients with continued reflux symptoms despite PPI therapy.



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