Question: An 84-year-old man presenting with fatigue was referred for endoscopy owing to anemia. On his esophagogastroduodenoscopy, a segment of Barrett’s esophagus (BE) was seen (Prague classification C2M4). Random biopsies were obtained as per the Seattle protocol. Histology revealed at least one specimen harboring high-grade dysplasia. He had ascending colon adenocarcinoma on colonoscopy. The BE segment was subsequently reassessed using white light, narrow band imaging (NBI), acetic acid chromoendoscopy, and high magnification. In a proximal tongue, there was an area appeared to have an irregular microvasculature. This was presumed to be the dysplastic lesion (Figure A; NBI). A clear demarcation line was noted between the distal nondysplastic segment and the irregular microvasculature of the proximal dysplastic area (Figure B; NBI and near focus). A decision was made to initially resect the BE segment using the endoscopic submucosal dissection (ESD) technique and operate the right-sided colon cancer at the same season in the following weeks. He continued his proton pump inhibitor (PPI) in the interim. While reassessing the lesion before performing ESD 0 month later, the previously identified dysplastic lesion was no longer identified (Figure C; white light). What is the most likely explanation and what is the best way to manage the case? See the Gastroenterology web site () for more information on submitting your favorite image to Clinical Challenges and Images in GI. Further careful examination with NBI and magnification revealed an area of brownish discoloration below re-epithelialized mucosa (Figure D). The area to resect could not be ascertained, but the NBI and magnification images combined with the previously known location of the dysplastic area were used as landmarks to proceed with an ESD (Figure E, F). On histology, the dysplastic BE was buried underneath normal appearing squamous cell epithelium (Figure G; stain: hematoxylin and eosin). The dysplastic glandular proliferation showed focally fused glands formed by atypical, mitotically active epithelial cells without goblet cells. The dysplastic elements did not involve the muscularis mucosae nor the submucosa. This unique case demonstrates that re-epithelialization of a Barrett’s mucosa can occur within a short time interval. While managing BE, endoscopists should be aware of the acceleration of re-epithelization and the potential concealing of dysplastic cells under normal-appearing epithelial tissue such as presented here. Some evidence has shown that acid suppression can lead to this occurrence. A study of 26 patients examining the effect of high-dose lansoprazole on BE found that squamous islands were developed in 77% of the patients by the final visit.1Sampliner R.E. Effect of up to 3 years of high-dose lansoprazole on Barrett’s esophagus.Am J Gastroenterol. 1994; 89: 1844-1848PubMed Google Scholar In the study, squamous re-epithelization and subsequent burying of the dysplasia below the surface could be attributed to high-dose PPI use. It is, thus, paramount to carefully inspect the whole BE segment and beyond its obvious extent, especially in patients on a PPI. Likewise, this observation highlights the utmost importance of careful inspection and precise documentation of the location of dysplasia in BE during endoscopy. Applying advanced imaging techniques in addition to the white light may facilitate the visibility and improve the diagnostic and interventional precision.2Qumseya B. Sultan S. Bain P. et al.ASGE guideline on screening and surveillance of Barrett’s esophagus.GIE Journal. 2019; : 335-359Google Scholar
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