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Background: Food deserts are low-income census tracts with poor access to supermarkets and are associated with worse outcomes in breast, colon, and a small number of esophageal cancer patients. This study investigated residency in food deserts on readmission rates in a multi-institutional cohort of esophageal cancer patients undergoing trimodality therapy., Methods: A retrospective review of patients who underwent trimodality therapy at 6 high-volume institutions from January 2015 to July 2019 was performed. Food desert status was defined by the United States Department of Agriculture by patient ZIP Code. The primary outcome was 30-day readmission after esophagectomy. Multilevel, multivariable logistic regression was used to model readmission on food desert status adjusted for diabetes, insurance type, length of stay, and any complication, treating the institution as a random factor., Results: Of the 453 records evaluated, 425 were included in the analysis. Seventy-three patients (17.4%) resided in a food desert. Univariate analysis demonstrated food desert patients had significantly increased 30-day readmission. No differences were seen in length of stay, complications, or 30-day mortality. In the adjusted logistic regression model, residing in a food desert remained a significant risk factor for readmission (odds ratio, 2.11; 95% CI, 1.07-4.15). There were no differences in 30-day, 90-day, or 1-year mortality based on food desert status, although readmission was associated with worse 90-day and 1-year mortality., Conclusions: Food desert residence was associated with 30-day readmission after esophagectomy in patients undergoing trimodality treatment for esophageal cancer in this multi-institutional population. Identification of patients residing in a food desert may allow surgeons to focus preventative interventions during treatment and postoperatively to improve outcomes., (Copyright © 2023 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Background: Observational studies demonstrate a protective effect of statins on the development and progression of esophageal adenocarcinoma. The role of statins in the prevention of reflux-induced esophageal changes remains unknown., Aims: Using a mixed gastroduodenal reflux mouse model, we hypothesized that oral administration of simvastatin would attenuate reflux-induced mucosal changes of the distal esophagus., Methods: Human Barrett's (CPB) and esophageal adenocarcinoma (FLO1 and OE19) cells were treated with simvastatin. Cell proliferation and apoptosis were evaluated using the MTS proliferation and annexin V apoptosis assays, respectively. A reflux mouse model was generated by performing a side-to-side anastomosis between the gastroesophageal junction and first portion of the duodenum (duodeno-gastroesophageal anastomosis, DGEA). DGEA mice were fed a standard or simvastatin-containing diet following surgery. Mice were euthanized 6 weeks post-operatively., Results: Simvastatin significantly decreased proliferation and increased apoptosis in all cell lines. Compared to control animals, mice undergoing DGEA who were fed a standard diet demonstrated a fourfold increase in mucosal thickness and significant increase in proliferating cells (p < 0.0001). DGEA mice fed a simvastatin-containing diet had an attenuated response to reflux, with a significant reduction in mucosal hyperplasia and proliferation (p < 0.0001). DGEA mice fed a simvastatin-containing diet demonstrated significant upregulation of procaspase-3 (p = 0.009) and cleaved caspase-3 (p = 0.034) in the distal esophagus., Conclusions: We demonstrate for the first time a reduction in reflux-induced histologic changes of the distal esophagus following oral administration of simvastatin in vivo. These findings identify simvastatin as a potential preventative agent to inhibit the development and progression of reflux-induced esophageal injury., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)