Barrett esophagus (BE) is a disease entity characterized by the gradual replacement of stratified squamous epithelium of the distal esophagus with metaplastic columnar epithelium. This transformation of the distal esophagus occurs in response to chronic exposure of the esophageal lining to gastric contents, as seen in gastroesophageal reflux disease (GERD). BE is diagnosed with high-resolution endoscopy and confirmed with biopsy and subsequent histologic examination of suspected tissue.
BE is the only known precursor lesion of esophageal adenocarcinoma. Despite advances in diagnosis, treatment, and surgical technique, the prognosis for patients with esophageal adenocarcinoma remains poor, with a 5-year survival of approximately 17% to 20%.1–3 Given the poor prognosis of this disease, much attention is focused on identifying and treating BE before it progresses to adenocarcinoma.
The diagnosis, screening, surveillance, and treatment of BE have changed rapidly with the advent of new technologic advances in both high-resolution and interventional endoscopy. This chapter provides a brief review of the epidemiology, pathology, screening, and surveillance of BE. It then focuses on the modern treatment of the disease, which is rapidly shifting from surgery to a variety of endoscopic therapies.
GERD is the antecedent condition to BE and affects approximately 16% to 35% of the U.S. population.4 The prevalence of BE in the United States is believed to be 1.5% of the population, increasing to approximately 15% in patients with a long history of reflux symptoms.5 Traditionally, patients with BE are estimated to have between 30- and 125-fold higher relative risk of developing esophageal adenocarcinoma compared to patients without BE.6 The mean reported annual risk of developing esophageal adenocarcinoma in BE patients is 0.5%, although newer evidence from retrospective data suggest this is likely an overestimation, with an annual risk closer to 0.12%. Patients with BE have an 11-fold greater risk of developing esophageal adenocarcinoma than patients without BE.7
The elevated risk of neoplastic transformation in BE with dysplasia has led to more aggressive screening in populations with elevated risk. The increased emphasis on screening has occurred in the context of a rising incidence of esophageal adenocarcinoma, amounting to 2% to 7% per year in the United States over the past 30 years.8 Demographic risk factors known to increase the risk of developing BE include Caucasian race, older age, male gender, family history, chronic reflux symptoms, metabolic syndrome, and central obesity.9
The ideal protocol for population-based screening for BE remains an area of active debate. Although a significant portion of the population suffers from GERD, BE and esophageal adenocarcinoma remain relatively uncommon entities. Even among patients with symptomatic GERD, there are no randomized controlled studies demonstrating the benefit of general screening. Undertaking a broad-based screening program would place a significant burden on the medical system and deliver a low yield, ...