17,35–37 In general, EoE appears to follow a chronic or relapsing course, and complete resolution of the disease is thought to be uncommon.35,36 Observational studies have suggested that a progression of symptoms is common in untreated EoE.5,36,38 Straumann et al. reported findings on 30 treated adult patients reviewed clinically for up to 11.5 years.37 Patients had often developed long-term sequelae, including dysphagia,39 strictures25,26 or crêpe-paper mucosa.40,41 That retrospective study may, however, have been biased towards more severe disease in a tertiary specialist center. Although cases

of Barrett’s esophagus have been reported in patients with EoE, there does not appear to be an increased incidence of esophageal adenocarcinoma.42,43 The diagnosis of EoE requires gastroscopic Y-27632 concentration examination and esophageal biopsy.1 Typically, the endoscopic changes are found along the entire length of the esophagus and not limited to the lower third. Endoscopic CP-690550 cost features include linear furrowing (Fig. 2), mucosal fragility, rings (“trachealization”) and diffuse narrowing of the lumen.44–50 White mucosal plaques are a common feature, reflecting fibrinous exudate due to epithelial eosinophilic inflammation51 (Fig. 3). Importantly, a macroscopically normal esophageal appearance does

not rule out EoE. The First International Gastrointestinal Eosinophilic Research Symposium (FIGERS) guidelines1 recommend that biopsies should always be taken from several sites along the length of the esophagus (upper, mid and lower esophagus) in order to help delineate findings against reflux esophagitis, which typically only affects the lower esophagus.1 However, there is to date no consensus on the exact number and location of biopsies required for a reliable diagnosis of EoE. By definition, biopsies from stomach and duodenum are normal in EoE. Current clinical practice for the allergic evaluation of patients with EoE selleckchem mainly relies on skin prick testing (SPT) as the use

of food-specific serum IgE has not been standardized. Spergel et al.52,53 have defined the diagnostic accuracy of SPT in children with EoE. These findings may be able to guide targeted elimination diets, particularly if patients are only sensitized to a small number of food allergens. Given the limited access to SPT, some gastroenterologists have used empirical elimination diets in children.54 Aeroallergens also appear to be involved in the pathogenesis, although it is often difficult to ascertain to what extent inhalant sensitization specifically contributes in the etiology of EoE. Atopy patch testing (APT) aims to assess cellular responses to epicutaneous exposure of food allergens (Fig. 4). The food allergen is applied to the skin for 48 h under an occlusive dressing (12 mm Finn chambers). The skin findings are read at 72 h. A positive patch test is characterized by erythema, papule formation and localized induration or edema.