Barrett Esophagus : Low-grade Dysplasia

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Image Description

Barrett Esophagus (BE) with Low-grade Dysplasia: The biopsies with low-grade dysplasia show atypical cytologic features and resemble tubular adenomas of colon. There is only minimal or no surface maturation, i.e. the cytologic atypia of the basal crypt glands is also seen in the surface epithelium. There is glandular overcrowding; however, lamina propria is still identifiable between glands. There is mild to moderate architectural distortion.

The glands are lined by cells with elongated hyperchromatic nuclei, increased nuclear:cytoplasmic ratio, maintained nuclear polarity, and increased mitoses. There is nuclear membrane irregularity. Nucleoli are not prominent. There may be some nuclear stratification. In the presence of inflammation, biopsies with features of low-grade dysplasia are perhaps better classified as indefinite for dysplasia.

There is considerable uncertainty about the rate of progression of LGD to adenocarcinoma, given the high degree of interobserver variation in the diagnosis of LGD. The reported rate is about 20% in 5 years.

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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