Many adults with EE present with dysphagia or food impactions and subsequently are found to have an esophageal stricture requiring multiple esophageal dilatations for treatment. Esophageal subepithelial fibrosis has been found in the adult literature in patients with EE. Chehade et al evaluated distal esophageal biopsy specimens in children with EE, eosinophilic gastroenteritis, gastroesophageal reflux disease, and controls for the presence of increased collagen deposition indicative of fibrosis. They found that fibrosis was present in 57% of patients with EE, of which 42% had symptoms of dysphagia and 80% had food impactions. The degree of fibrosis was not associated with eosinophil count but was associated with eosinophilic degranulation (10). Upon degranulation, eosinophils release major basic protein (MBP) and transforming growth factor (TGF-β). MBP changes smooth muscle contractility by blocking M2 muscarinic receptors therefore changing the motility of the esophagus. TGF-β is believed to cause an increase in the production of the extracellular matrix and smooth muscle hypertrophy and hyperplasia leading to esophageal thickening and fibrosis. TGF-β is a key growth factor that increases fibroblasts and subsequent fibrosis in the lung as well. Corticosteroids have been shown to reverse esophageal remodeling, but no large clinical trials have evaluated the treatment of esophageal fibrosis related to EE. To quote Aceves and Ackerman: "[f]ibrosis likely contributes to multiple clinical aspects of EE, including dysphagia symptoms, disease chronicity, and stricture formation." Fibrosis is measured in esophageal tissue by evaluating the amount of collagen that is deposited. Trichrome stains specifically for collagen (11).