Sequelae of eosinophilic esophagitis (EoE) include food impaction and esophageal stricture. Duration of inflammation is a predicted risk factor; however, complications remain unpredictable. Studies using the functional lumen imaging probe (FLIP) have demonstrated decreased distensibility of the esophagus in adult patients with EoE. As the impact of inflammation on the developing esophagus is unknown, we investigated esophageal distensibility in a pediatric cohort to determine the effect of age, ongoing inflammation, and fibrotic features on distensibility.
We conducted a prospective observational study at two tertiary pediatric institutions. Subjects underwent FLIP evaluation during endoscopy to determine distensibility of the esophagus. During stepwise distension, simultaneous intrabag pressure and 16 channels of cross-sectional areas were measured. The minimal diameter at maximal esophageal distention at an intrabag pressure of 40 mm Hg was identified. Distensibility was compared between EoE and non-EoE subjects and between clinical variables within the EoE cohort. Potential confounding variables were identified.
Forty-four non-EoE and 88 EoE subjects aged 3–18 years were evaluated. Age positively correlated with esophageal distensibility in the non-EoE cohort, but this trend was not observed in the EoE population. Subjects with EoE had reduced distensibility even after adjusting for age. Active inflammation (eosinophils >15 eos/high-power field), histological lamina propria fibrosis, and various features of a fibrotic phenotype (stricture, food impaction, circumferential rings on endoscopy) were associated with decreased distensibility within the EoE cohort. FLIP was safe, feasible, and well tolerated.
These findings suggest that remodeling occurs in the pediatric EoE population, warranting early diagnosis and initiation of therapy prior to the onset of disease complications.
1Digestive Health Institute, Gastrointestinal Eosinophilic Diseases Program, Children’s Hospital Colorado, Aurora, Colorado, USA
2Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Mucosal Inflammation Program, University of Colorado School of Medicine, Aurora, Colorado, USA
3Division of Allergy and Immunology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
4Research Institute, The Children’s Hospital Colorado, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, USA
5Department of Pathology and Laboratory Medicine, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
6Department of Pathology and Laboratory Medicine, Gastrointestinal Eosinophilic Diseases Program, Children’s Hospital Colorado, University of Colorado School of Medicine, Aurora, Colorado, USA
7Division of Gastroenterology, Hepatology and Nutrition, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
8Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
Correspondence: Amanda B. Muir, Children’s Hospital Colorado, 13123 E. 16th Avenue, B290, Aurora, Colorado 80045, USAE-mail: email@example.com
Correspondence: Amanda B. Muir, The Children’s Hospital of Philadelphia, 34th and Civic Center Boulevard, Philadelphia, Pennsylvania 19103, USA.firstname.lastname@example.org
SUPPLEMENTARY MATERIAL accompanies this paper at http://links.lww.com/AJG/A551
Received 29 November 2016; accepted 28 March 2017
Guarantors of the article: Amanda B. Muir, MD and Calies Menard-Katcher, MD, MS.
Specific author contributions: Experimental design: C.M.K., A.B.M., A.J.B., J.M.S. and G.T.F.; experimental execution: A.J.B., F.N.A., A.B.M., C.M.K., G.T.F. and C.L.; data analysis and interpretation: P.Z., C.M.K., A.B.M., A.J.B. and G.T.F.; reagents/materials/analysis tool contributions: A.B.M., C.M.K., A.J.B., G.T.F., B.J.W. and K.C., R.V.; manuscript writing/editing: A.B.M., C.M.K., B.J.W., K.C., C.L., G.T.F., J.M.S., P.Z. and R.V.
Financial support: This study was supported by the following NIH Grants: K08DK106444 (A.B.M.), K23DK109263 (C.M.K.), AGA June and Donald AGA Castell Esophageal Clinical Research Award (A.B.M.), NASPGHAN George Ferry Young Investigator Development Award (C.M.K.), and NIH 1K24DK100303 (G.T.F.). CEGIR (U54 AI117804) is part of the Rare Disease Clinical Research Network (RDCRN), an initiative of the Office of Rare Disease Research (ORDR), NCATS, and is funded through collaboration between NIAID, NIDDK, and NCATS (G.T.F., A.B.M., Z.P., K.C., J.S. and C.M.K.) CEGIR is also supported by patient advocacy groups including APFED, CURED and EFC.
Potential competing interests: G.T.F.: EnteroTrack, Royalties recieved from UptoDate. The other authors declare no conflict of interest.