Barrett Esophagus : High-grade Dysplasia

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Image Description

High-grade Dysplasia (HGD) in Barrett Esophagus (BE): The glands have marked cytologic atypia and architectural abnormalities. There is no surface maturation, i.e. the abnormal features of deep basal glands are also present in the surface epithelium. The glands show overcrowding, angulation, branching, or crypt budding. If cytologic features are sufficiently abnormal, glands with lesser degree of architectural distortion may still be classified as HGD.

Cytologic features include: nuclear enlargement and hyperchromasia, irregularity of nuclear membrane, prominent nucleoli, loss of nuclear polarity, and increased mitotic activity. Some glands show nuclear stratification. Other cases have small crowded glands lined by a single layer of highly atypical cells. Inflammation is usually minimal or absent.

Significance of Dysplasia: Patients with non-neoplastic Barret esophagus 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 about 20% with LGD and about 50% with HGD.

Image courtesy of: Phoenix Bell, MD.

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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