Barrett Esophagus : Introduction

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Image Description

Introduction: Barrett esophagus (BE) is a metaplastic change characterized by replacement of the normal stratified squamous epithelium of the distal esophagus with columnar epithelium containing goblet cells (intestinal metaplasia). It is named after Norman Barrett, an Australian surgeon who described it in 1950's.

BE arises secondary to chronic gastroesophageal reflux disease (GERD), in which acid refluxes from the stomach into the lower esophagus. Over time, the acid-damaged squamous epithelium is replaced by columnar epithelium which is better equipped to handle an acidic environment through its mucin secretions and tight junctions.

The columnar epithelium by itself causes no symptoms. The presence of BE is a risk factor for the development of dysplasia and ultimately, esophageal adenocarcinoma (EAC). The pathogenesis of BE remains unknown.

This endoscopic image shows a small patch of orange-pink (salmon-colored) mucosa in the distal esophagus. When < 3cm of metaplalstic epithelium lines the distal esophagus (as in this case), it is categorized as short-segment BE.

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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