Squamous metaplasia
Weight regain can accompany re-emergence of obesity-related comorbidities and, thus, early intervention is important. Although diet, exercise, and behavior modifications are fundamental, they can have limited efficacy. Thus, endoscopic management is important, with specific evaluation for gastrogastric fistulae, pouch dilation, and GJA dilation, all of which can be successfully intervened upon endoscopically. For GJA dilation in particular, APC has been used with promising results.1
In the normal GI tract, the esophagus is lined with squamous epithelium, and the stomach is lined with columnar epithelium. One of the most well-known and well-documented scenarios in which the typical mucosal lining is replaced by abnormal mucosa is Barrett’s esophagus (BE). BE is defined by the replacement of the normal distal squamous epithelial lining with columnar epithelium with a minimum length of 1 cm (tongues or circumferential) containing specialized intestinal metaplasia on histopathologic examination. It is well-documented that treatment of BE with thermal ablation and acid suppression therapy results in re-epithelialization of the esophagus with neosquamous mucosa.2 In contrast with this, in our patients, after we burned the gastric columnar mucosa with APC to treat their dilated GJA, the gastric pouch mucosa has been replaced with squamous epithelium, which we have termed “reverse BE.” To our knowledge, there are no reports of this condition in the literature, nor do we know the precise cause. There is a series of patients without a history of bariatric surgery who developed squamous metaplasia in the proximal gastric cardia.3 The authors hypothesized that this condition may be due to chronic mucosal injury owing to hiatal hernia, reflux, caustic ingestion, chronic gastritis, or pyloric stenosis. We suggest two potential mechanisms for this condition in our patients: 1) extending the ablation to the Z-line on the medial aspect of the pouch may allow for the distal extension of squamous mucosa during the healing process; and 2) acid suppression therapy with proton pump inhibitors after the procedure, in combination with a postoperative decrease in acid production, allows for a shift in the cell proliferation and differentiation in the pouch. Notably, although there are well-defined guidelines for surveillance of BE, owing to the risk of progression to esophageal adenocarcinoma,2 it is unclear what clinical significance this reverse BE may have in the future. It is important to continue to monitor these patients and clarify the natural history of this finding.
References
1. Brunaldi VO, Jirapinyo P, de Moura DTH et al. Endoscopic treatment of weight regain following Roux-en-Y gastric bypass: a systematic review and meta-analysis. Obes Surg. 2018;28:266-76.
2. Weusten B, Bisschops R, Coron E et al. Endoscopic management of Barrett’s esophagus: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement. Endoscopy. 2017;49:191-8.
3. Fass R, Sampliner RE. Extension of squamous epithelium into the proximal stomach: a newly recognized mucosal abnormality. Endoscopy. 2000;32:27-32.
Christopher C. Thompson is a consultant for Boston Scientific and Medtronic, a consultant for and has institutional grants from USGI Medical, Olympus, and Apollo Endosurgery.
ginews@gastro.org