nature publishing group ORIGINAL CONTRIBUTIONS ESOPHAGUS 759 © 2013 by the American College of Gastroenterology The American Journal of GASTROENTEROLOGY INTRODUCTION Eosinophilic esophagitis (EoE) is diagnosed in about 6% of patients undergoing upper endoscopy (1). It is a common cause for dysphagia and food impaction (2–5). In children with EoE, symp- toms and histology improve when an elemental diet is adminis- tered, showing the importance of food triggers (6–8). Gonsalves et al (9) recently demonstrated both histologic and symptomatic improvement on a six-food elimination diet in most adult subjects with EoE, suggesting that EoE is substantially triggered by food antigens in adults as well. To our knowledge, there are no prior published studies of an elemental diet in adults with EoE. he goal of this study is to clar- ify to what degree food allergens are responsible for this disease and to determine whether an elemental diet in adults with EoE is a practical, efective treatment for adult EoE. Tissue eosinophil content, a deining feature of EoE, is the main end point, although symptoms, endoscopic features, and mast cell content were also examined. Mast cells are suspected to play an important role in the pathogenesis of EoE (10). METHODS Study design his was a prospective cohort study from 2009 to 2011 at the Uni- versity of Utah Medical Center and Salt Lake Veterans Adminis- tration Medical Center, Salt Lake City, UT, consisting of adults diagnosed with EoE. he study was designed to determine whether adults with EoE would respond to an elemental diet by either histologic or symptomatic criteria. Study end points he main study end point was whether there was a reduction in number of tissue eosinophils on treatment and how quickly this occurred. he speciic end points were set to match those of Gon- salves et al (9) the only other clinical trial of food restriction in adult EoE. A complete histologic response was considered 5 eosinophils/maximal high power ield (hpf). A nearly complete histologic response was 6–10 eosinophils/maximal hpf. A partial histologic response was >10 eosinophils/maximal hpf but less than half the immediate pretreatment eosinophil content. Secondary Elemental Diet Induces Histologic Response in Adult Eosinophilic Esophagitis Kathryn A. Peterson, MD, MSc(Epid) 1 , Kathryn R. Byrne, MD 1 , Laura A. Vinson, MS 1 , Jian Ying, PhD 2 , Kathleen K. Boynton, MD 1 , John C. Fang, MD 1 , Gerald J. Gleich, MD 3 , Douglas G. Adler, MD 1 and Frederic Clayton, MD 4 OBJECTIVES: Elemental diets have not been studied in adults with eosinophilic esophagitis (EoE). The goal of this trial was to assess the efficacy of an elemental diet in adults with EoE. METHODS: A total of 18 adults with EoE were given an elemental diet for 4 weeks, or just 2 weeks if their response was complete. Symptoms and histologic findings, based on biweekly biopsies, were monitored. Six subjects were rebiopsied 2–7 days after resuming a normal diet. RESULTS: After therapy, esophageal tissue eosinophil content decreased from 54 to 10 per maximal high power field ( P = 0.0006). There was complete or nearly complete response ( 10 eosinophils) in 72% of subjects. Mast cell content, parabasal layer thickness, and endoscopic furrows and exudates also significantly decreased. Of the 29 qualified subjects, 11 (38%) failed to adhere to the diet. Several subjects had significant weight loss. Symptoms and endoscopic fixed strictures did not improve. After the subjects resumed a normal diet, the eosinophil content increased substantially in 3–7 days. CONCLUSIONS: While symptoms did not improve and dietary compliance was problematic, there was substantial histologic improvement after 4 weeks on the elemental diet. EoE in adults is substantially triggered by foods. Am J Gastroenterol 2013; 108:759–766; doi:10.1038/ajg.2012.468; published online 5 February 2013 1 Department of Gastroenterology, University of Utah Health Sciences Center , Salt Lake City , Utah, USA; 2 Department of Biostatistics in Family and Preventative Medicine, University of Utah Health Sciences Center, Salt Lake City , Utah, USA; 3 Department of Dermatology, University of Utah Health Sciences Center, Salt Lake City , Utah, USA; 4 Department of Pathology, University of Utah Health Sciences Center , Salt Lake City , Utah, USA. Correspondence: Frederic Clayton, MD, Department of Pathology, University of Utah Health Sciences Center , 50 N Medical Drive, Salt Lake City, Utah 84132, USA. E-mail: fred.clayton@path.utah.edu Received 14 August 2012; accepted 11 December 2012 see related editorial on page 775