Barrett’s esophagus (BE) is a peptic ulcer in the lower esophagus, often associated with stricture, caused by the presence of columnar-lined epithelium. The columnar-lined epithelium may contain functional mucous cells, parietal cells, or chief cells in the esophagus instead of the normal squamous cell epithelium. The presence of specialized intestinal metaplasia (SIM) with goblet cells confirms the diagnosis of BE.

The incidence is divided into two subtypes: long-segment Barrett’s esophagus (LSBE) and short-segment Barrett’s esophagus (SSBE). In LSBE, the incidence is reported to be 0.3% to 2% of the entire population, but 8% to 20% in patients with gastroesophageal reflex disease (GERD). In the United States, the incidence is 376:100,000, predominately in Caucasian males. In SSBE, the incidence is reported to be 5% to 30%.

BE is a complication of GERD. Patients who develop BE usually have a combination of symptoms. Prolonged esophageal acid fixation produces erosive esophagitis. The pH of the refluxate, combined with the duration of contact with the esophageal mucosa, determines the degree of mucosal injury. Prolonged exposure erodes the esophageal mucosa, promotes inflammatory cellular infiltrates, and can culminate in epithelial necrosis. The damage and necrosis lead to replacement of the damaged tissue with metaplastic columnar cells, the origin of which is not understood. Patients with LSBE generally have longer durations of reflux symptoms, severe combined patterns of reflux (in both supine and erect positions), and low pressure at the lower esophageal sphincter (LES). LSBE patients are less sensitive to direct acid exposure to the esophagus. SSBE patients have a greater sensitivity to direct acid exposure to the esophagus, shorter duration of reflux, and only upright (erect) reflux.