Resolution of remodeling in eosinophilic esophagitis correlates with epithelial response to topical corticosteroids.

摘要: Eosinophilic esophagitis (EE) is a disease of increasing prevalence and diagnosed if esophageal histology demonstrates >15 epithelial eosinophils per high power field (hpf), especially in the context acid blockade to exclude gastroesophageal reflux (GERD) (1–3). Patients may present with dysphagia, vomiting, abdominal pain, or poor growth most significant complication stricture formation requiring repeated dilation (1, 4, 7). Subepithelial fibrosis has been described adult pediatric EE patients, those who complain dysphagia (5–8). Our previous studies demonstrated that remodeling occurs lamina propria (LP) esophagus patients concurrent strictures as compared normal controls children GERD (5). Subepithelial accompanied by increased numbers TGFβ-positive expression TGFβ signaling transcription factor, phosphorylated Smad2/3 (pSmad2/3) (5, 6). In addition, associated an number activated blood vessels expressing VCAM-1 subepithelial space Whether LP changes are influenced therapies such topical corticosteroids not systematically assessed patients. Currently, utilize eosinophil resolution major diagnostic criterion for therapeutic response. The fluticasone budesonide have 50–80% overall inflammation clinical symptoms 9–11). However, difference among do respond corticosteroid therapy reported. We therefore hypothesized subjects eosinophilia following would be more likely than did demonstrate eosinophilic inflammation. obtained all biopsy samples, it important determine whether epithelium (obtained biopsies) correlates As current involves esophagogastroduodenescopy (EGD) biopsy, relationship between features course, even young children, can determined. In this study, we treatment swallowed decreases severity (LP vascular activation) mediators (TGFβ1 pSmad2/3) but response therapy. pilot SNP promoter correlate