Barrett Esophagus : Neg for Dysplasia

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Image Description

The following diagnostic categories are used in the context of Barrett esophagus (BE).

Negative for Dysplasia
Indefinite for Dysplasia
Positive for Low-grade Dysplasia
Positive for High-grade Dysplasia
Intramucosal Carcinoma

Negative for Dysplasia: This image shows BE, negative for dysplasia. There is normal surface maturation from the basal glands to the top. The nuclei in the basal portion are slightly larger and more hyperchromatic than those at the surface. Overall, there is no cytologic atypia. The nuclei have smooth contours. Nucleoli are not enlarged. Nuclear polarity is maintained throughout the glands. Some degree of nuclear stratification, a few mitoses in the basal glands, and a few dysmorphic goblet cells are acceptable.

The glandular architecture is uniform. There is abundant lamina propria separating the glands (i.e. no overcrowding). In the presence of ulceration, erosion, or acute inflammation, there may be reparative changes. The nuclei may become enlarged and hyperchromatic with prominent nucleoli, but should still maintain smooth contours. Surface maturation should be normal. There may be some loss of surface mucin.

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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