Barrett's Esophagus and Prevention of Esophageal Adenocarcinoma: A Literature Review

Abstract

Barrett's esophagus (BE) is an acquired metaplastic condition in which the normal stratified squamous epithelium of the distal esophagus is replaced by specialized columnar epithelium, often associated with intestinal metaplasia. This alteration is strongly linked to gastroesophageal reflux disease and is the primary recognized precursor to esophageal adenocarcinoma (EAC). Although only a subset of individuals with BE progresses to neoplasia, the presence of dysplasia—particularly high-grade dysplasia—is a significant marker of progression. This review aims to analyze key aspects regarding the pathophysiology, risk factors, diagnosis, risk stratification, endoscopic surveillance, and current strategies for preventing EAC in individuals with BE. A narrative literature review was conducted, searching for international guidelines, clinical trials, observational studies, and systematic reviews available in bibliographic databases, with an emphasis on publications indexed in PubMed and documents from the American College of Gastroenterology (ACG), American Gastroenterological Association (AGA), and European Society of Gastrointestinal Endoscopy (ESGE). The literature demonstrates that neoplastic progression is multifactorial, depending on the interplay between clinical characteristics, the extent of the metaplastic segment, the presence and grade of dysplasia, sex, age, obesity, smoking, and other factors. Proton pump inhibitor therapy is a key component of clinical management, while endoscopic eradication therapy plays a central role in cases of confirmed dysplasia and superficial neoplasia. Endoscopic surveillance remains important, although the magnitude of its impact on mortality is still a subject of debate. Emerging strategies include biomarkers, artificial intelligence systems, advanced imaging techniques, and personalized risk prediction models. It is concluded that the prevention of esophageal adenocarcinoma in patients with Barrett's esophagus should be individualized, combining reflux control, modification of risk factors, appropriate histopathological assessment, risk-stratified endoscopic surveillance, and early treatment of dysplastic or neoplastic lesions.