Barrett Esophagus : Clinical

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Image Description

Clinical Features: The columnar epithelium of Barrett esophagus (BE) by itself causes no symptoms. Patients are usually diagnosed during endoscopic evaluation for gastroesophageal reflux disease (GERD). BE is found in almost 10% of patients with symptomatic GERD. Most patients are middle-aged or older adults (avg. age 55 years) with a chief complaint of heartburn.

BE is sometimes seen in children in association with cystic fibrosis (which can cause gastroesophageal reflux) or following chemotherapy. In addition to the history of GERD, other risk factors associated with the development of BE include white race, male gender, age > 50, hiatal hernia, tobacco use, and central obesity.

This endoscopic view with narrow band imaging (NBI) is from the same case as the previous image. The columnar epithelium lining the distal esophagus is clearly delineated as dark brown mucosa against normal squamous epithelium which appears greenish. Further discussion of NBI is in slide 4.

Image courtesy of: Pramod Malik, MD; used with permission.

About the Disease

Barrett esophagus (BE) is a metaplastic replacement of the stratified squamous epithelium of the distal esophagus with columnar epithelium containing goblet cells. US definition requires intestinal metaplasia. In Japan and the UK, goblet cells are not required for the diagnosis. BE is a preneoplastic lesion and increases the risk for esophageal adenocarcinoma (EAC). BE is found in about 5-10% of individuals with symptomatic gastroesophageal reflux disease. It is more common white males with a median age at diagnosis of 55 years. Diagnosis requires both endoscopic and histologic findings. At endoscopy, Barrett mucosa appears orange-pink (salmon colored) and velvety in contrast to pale pink glossy squamous mucosa. In short-segment and long-segment BE, metaplastic epithelium lines < 3 cm or ≥ 3 cm of the distal esophagus respectively. Biopsies are classified as neg. for dysplasia, indefinite for dysplasia, and positive for LGD or HGD. Patients with non-neoplastic BE develop LGD at the rate of 4.3% per year, and HGD at the rate of 0.9% per year. The rate of progression to cancer within 5 years is 20% with LGD and 50% with HGD. Abnormalities in CDKN2A and TP53 may indicate higher risk of progression. Treatment of BE without dysplasia consists of proton pump inhibitors. Patients undergo surveillance endoscopy every 3-5 years. BE with dysplasia can be treated with endoscopic ablation or resection techniques. References:Iacobuzio-Donahue, C. A. & Montgomery E. (2012). Gastrointestinal and Liver Pathology - 2nd Edition. Feldman, M., Friedman, L. S., & Brandt, L. J. (2020). Sleisenger & Fordtran's Gastrointestinal & Liver Disease - 11th Edition. Arnold C, Lam-Hamlin D, and Montgomery E. (2019). Atlas of Gastrointestinal Pathology : A Pattern Based Approach to Neoplastic Biopsies - First Edition. Odze & Goldblum Surgical Pathology of the GI Tract, Liver, Biliary Tract and Pancreas (2014). 3rd edition. Goldblum, J. R. et al (2018). Rosai and Ackerman's Surgical Pathology - Eleventh Edition.

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