LAUSR

First and foremost, we would like to thank the authors for their interest in our paper and their valuable comments and discussion. Of course, we would like to reply to some of the remarks made. The authors have claimed a lack of details regarding the preoperative cohort and diagnostic criteria that were used in our study. However, we did provide information on how diagnostics were run preoperatively in this update [1], of course, in less detail than in the previously published study [2]. The article includes information on patient demographics as well as information on patients’ surgeries before sleeve gastrectomy (SG). In addition, preoperative gastroscopies ensured that patients neither had hiatal hernias, reflux, or Barrett’s esophagus (BE). Next, we would like to address the issue of BE diagnosis. For the diagnosis of BE, we used the guidelines set by the American Gastroenterology Association (AGA), which are in turn based on the Seattle biopsy protocol for endoscopic surveillance of BE. According to these guidelines, we used white light endoscopy and sampled four-quadrant biopsies every 1–2 cm along the columnar-lined esophagus, starting from the endoscopic esophagogastric junction. Additionally, seemingly neoplastic areas were biopsied as well [3–5]. BE diagnosis according to the AGA guidelines is rather strict in that for BE to be diagnosed biopsies always need to contain intestinal metaplasia and goblet cells, which is the method used at the Clinical Institute for Pathology of the Vienna Medical University [6, 7]. However, not all gastroenterological societies are equally as strict with BE diagnosis (e.g., the British Society of Gastroenterology define BE as: B(...) an oesophagus in which any portion of the normal distal squamous epithelial lining has been replaced by metaplastic columnar epithelium, which is clearly visible endoscopically (≥1cm) above the GOJ [gastro-oesophageal junction, note] and confirmed histopathologically from oesophageal biopsies^) [8]. Thus, we consider an overdiagnosis unlikely. Further, the authors have questioned the recommendations we made in terms of postoperative care for SG patients based on the results of our study: screenings for BE at intervals of 5 years and of 12 months in case BE was diagnosed. We would like to argue here that this is a very specific situation—SG patients seem to develop reflux and BE long-term, as found not only by us but also by Mandeville et al. (47.8% de novo reflux after 8.5 years) [9] or Genco et al. (17.2% of BE after 4.8 years!) [10]. Therefore, we recommend gastroscopies for SG patients at 5-year intervals based on the results of a number of recent long-term studies that found high reflux rates after SG in order to detect the ramifications of reflux at an early stage. Different to reflux in non-SG patients, reflux after SG seems to intensify over time [9, 11]. Hence, the situation of reflux-triggered BE after SG may not be comparable to BE in non-SG patients and progression of BE might be faster or more aggressive than in non-SG patients. Furthermore, we suggest annual gastroscopies for patients with BE after SG—who constitute only a small group so far—as the trigger for BE has not been eliminated [1]. Besides, we consider data gained from gastroscopies as scientifically highly interesting—they may, after all, contribute to a better understanding of BE progression after SG in the long term. As a final point, we would like to reiterate that we do consider a conversion to Roux-en-Y gastric bypass (RYGB) the best option for patients with reflux and/or BE after SG— despite the considerable doubts expressed by the authors. Two studies have recently confirmed RYGB as an apt method for BE patients. Andrew et al. have presented BE regression in * Gerhard Prager [email protected]