Barrett Esophagus : Dysplasia Assessment

Image 12 of 36

Image Description

Dysplasia Assessment in Barrett Esophagus (BE): Pitfalls

Separation of low-grade dysplasia (LGD) from reactive changes seen in reflux esophagitis can be difficult.
The interobserver agreement for the diagnosis of LGD is less than 50%.
The interobserver agreement is about 85% for the diagnosis of high-grade dysplasia (HGD).
Dysplasia causes only subtle or no endoscopic abnormalities. Recent advances in endoscopy such as narrow band imaging have aided in identification of dysplastic foci during real-time endoscopy.
Dysplasia is often patchy in extent and severity, causing significant sampling errors with the 4-quadrant biopsy approach used by the endoscopists. In older studies of patients who underwent esophagectomy due to a diagnosis of HGD on biopsies, about 13% of cases showed invasive adenocarcinoma that was missed on biopsies.

About this image: Low magnification view of Barrett esophagus. Note the columnar epithelium on the right and cardiac-type glands in the lamina propria. The glands on the left underneath the squamous epithelium have low-grade dysplasia.

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.

Image 12 of 36