Barrett Esophagus : Treatment

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Treatment of Barrett Esophagus (BE): The treatment modalities become more complex once dysplasia is definitively diagnosed. The treatment will differ by institution, but most patients with dysplasia are treated with endoscopic eradication therapy (EET), in the form of ablation, resection, or both.

Ablative techniques directly destroy the dysplastic tissue using photochemical energy (photoablation), cold temperatures (cryoablation), or radiofrequency energy (radioablation).

Resection techniques are more invasive and involve removal of tissue from the esophagus. These methods include endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD), which involve injection of a submucosal lifting agent to elevate the lesion. Once the lesion is lifted, a diathermic snare or endoscopic knife is used to excise it. The tissue is sent to pathology for evaluation.

Esophagectomy for Barrett Esophagus: High-grade dysplasia in BE used to be routinely treated with esophagectomy. It is no longer the preferred method due to associated high morbidity and mortality and the development of less radical approaches; although it remains a valid option in selected cases. It may be considered in patients where dysplastic mucosa cannot be eradicated by endoscopic mucosal resection or in patients with very long segments of Barrett mucosa that have multifocal dysplasia.

About this image: High-grade dysplasia in BE (higher magnification of the previous image). The glands are irregular in shape. There is marked variation in nuclear size and shape with piling up of nuclei. There is nuclear hyperchromasia, high N:C ratios, prominent nucleoli and increased mitotic activity as well. When viewed at low magnification, the dysplastic areas stand out due to their basophilia and loss of mucus.

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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