Abstract

G A A b st ra ct s major basic protein. These genetic products have not been previously used to differentiate between the two phenotypes of EoE. Methods We prospectively entered patients from 2012 who presented to the USF Joy McCann Swallowing Center. Informed consent was obtained to acquire 6 additional biopsies from the proximal and distal esophagus. These tissue samples were stored in an EoE tissue bank. EoE phenotype was classified as time of their first endoscopy by luminal diameter. Fibrostenotic disease was defined as a luminal diameter less than 17 mm based on resistance to passage of the smallest diameter bougie and inflammatory as 17 mm or above. Expression analysis of the complete genome using the Affymetrix U133 Plus 2.0 array was then performed to compare fibrostenotic to inflammatory phenotypes. Results Ten patients with EoE (4 fibstenotic and 6 inflammatory) were evaluated by gene expression microarray analysis. Inflammatory EoE was used as control during analysis. A total of 54,676 probe sets representing the entire transcriptome were analyzed. Of these, 825 were genes that had a greater than 2-fold difference and an ANOVA p-value of <.05. (Figure 1). The genes previously reported in the pediatric population, including TGF-beta 1, IL-15, eotaxin-3, TSLP, periostin, and MBP, did not demonstrate a significant difference. Discussion Following microarray analysis of 10 patients with EoE, subtle differences were seen between the two groups, but not in genes that have been associated with the disease previously. The majority of genes reviewed did not have a significant difference between the two phenotypes. This may be because factors contributing to fibrostenotic EoE disease are not genetic, but rather due to duration of the chronic eosinophilic inflammation.

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