Summary: Background: The frequency of eosinophilic oesophagitis (EoE) occurrence is escalating. Current diagnostic criteria recently proposed for the disease, determine that previous estimates of incidence and prevalence are outdated.Aim: To gauge the current incidence and prevalence of EoE by performing a systematic review of population‐based studies.Methods: Three electronic databases were searched from their inception dates to September 2018. A total of 2386 documents were screened; 29 studies reported on the prevalence and incidence of EoE in the general population.Results: The pooled prevalence of EoE was 34.4 cases per 100 000 inhabitants (95% CI, 23.1‐47.5), and was higher for adults (42.2; 95% CI, 31.1‐55) than for children (34; 95% CI, 22.3‐49.2). The pooled EoE incidence rates were 6.6/100 000 person‐years (95% CI, 3‐11.7) in children and 7.7/100 000 (95% CI, 1.8‐17.8) in adults. No differences were found between North American and European studies using varied sources of data (insurance and administrative databases compared to hospital‐bases case series). Subgroup analysis according to risk of bias did not change results significantly. A steady rise in EoE incidence and prevalence rates was observed over time, comparing studies conducted under subsequent definitions for EoE. No significant publication bias was found.Conclusions: In a systematic review and meta‐analysis, we found a sharp increase, higher than previous estimates, in the incidence and prevalence of EoE in population based studies. Results from studies carried out in developed countries show broad consistency and provide evidence of increasing pooled prevalence and incidence of EoE rates over time.

Eosinophilic esophagitis (EoE) is a chronic, Th2-inflammatory disease of the esophagus that can severely affect food intake. Currently, diagnosis and assessing response to treatment of EoE is highly invasive and requires endoscopy with esophageal biopsies. Finding non-invasive and accurate biomarkers is important for improving patient well-being. Unfortunately, EoE is usually accompanied by other atopies, which make it difficult to identify specific biomarkers. Providing an update of circulating EoE biomarkers and concomitant atopies is therefore timely. This review summarizes the current knowledge in EoE blood biomarkers and two of its most common comorbidities, bronchial asthma (BA) and atopic dermatitis (AD), focusing on dysregulated proteins, metabolites, and RNAs. It also revises the current knowledge on extracellular vesicles (EVs) as non-invasive biomarkers for BA and AD, and concludes with the potential use of EVs as biomarkers in EoE.

Background: Eosinophilic esophagitis (EoE) is a chronic non‐IgE‐mediated allergic disease of the esophagus. An unbiased proteomics approach was performed to investigate pathophysiological changes in esophageal epithelium. Additionally, an RNAseq‐based transcriptomic analysis in paired samples was also carried out.Methods: Total proteins were purified from esophageal endoscopic biopsies in a cohort of adult EoE patients (n = 25) and healthy esophagus controls (n = 10). Differentially accumulated (DA) proteins in EoE patients compared to control tissues were characterized to identify altered biological processes and signaling pathways. Results were also compared with a quantitative proteome dataset of the human esophageal mucosa. Next, results were contrasted with those obtained after RNAseq analysis in paired samples. Finally, we matched up protein expression with two EoE‐specific mRNA panels (EDP and Eso‐EoE panel).Results: A total of 1667 proteins were identified, of which 363 were DA in EoE. RNA sequencing in paired samples identified 1993 differentially expressed (DE) genes. Total RNA and protein levels positively correlated, especially in DE mRNA‐proteins pairs. Pathway analysis of these proteins in EoE showed alterations in immune and inflammatory responses for the upregulated proteins, and in epithelial differentiation, cornification and keratinization in those downregulated. Interestingly, a set of DA proteins, including eosinophil‐related and secreted proteins, were not detected at the mRNA level. Protein expression positively correlated with EDP and Eso‐EoE, and corresponded with the most abundant proteins of the human esophageal proteome.Conclusions: We unraveled for the first time key proteomic features involved in EoE pathogenesis. An integrative analysis of transcriptomic and proteomic datasets provides a deeper insight than transcriptomic alone into understanding complex disease mechanisms.

Eosinophilic esophagitis (EoE) has arisen as a common disorder in current clinical and endoscopic gastroenterology practice. Areas covered: A comprehensive review of the literature to summarize and update different aspects related with the use of endoscopy in the diagnostic workout and treatment of pediatric and adult EoE patients is conducted. Expert commentary: Endoscopic features in EoE are frequently subtle, so were inadverted in some initial reports of the disease. Literature has described a wide number of EoE-associated features, systematized in the EREFS classification, which standardized the grade and severity of exudates, rings, edema, furrows, and strictures. The insufficient reliability of these features to predict eosinophilic inflammation still makes biopsies essential in diagnosing or monitoring EoE. EoE causes half of the food impactions requiring endoscopy; food impaction leads to EoE diagnosis in up to half of cases. Long term consequences of EoE include esophageal remodeling leading to strictures and narrowing, thus impairing symptoms and needs dilation. Recognizing the risks from dilation in EoE required carrying out a safe technique to avoid the high complication rate reported in the early literature. Endoscopic dilation should be considered in patients with esophageal narrowing and dysphagia/food impaction unresponsive to diet or drugs-based anti-inflammatory treatment.

Eosinophilic esophagitis (EoE) is a chronic, progressive, type 2 inflammatory disease with increasing global prevalence. An eosinophil-predominant inflammation that permeates the epithelium and deeper esophageal layers characterizes the disease. Several cytokines, mainly derived from inflammatory T-helper 2 (Th2) cells and epithelial cells, are involved in perpetuating inflammatory responses by increasing surface permeability and promoting tissue remodeling characterized by epithelial–mesenchymal transition (EMT) and collagen deposition. This leads to esophageal strictures and narrow caliber esophagi, which are proportional a patient’s age and untreated disease length. Pathophysiological mechanisms leading to EoE have been described in recent years, and transforming growth factor beta (TGF)-beta have been involved in fibrotic phenomena in EoE. However, evidence on the dependence of these phenomena on TGF-beta is scarce and contradictory. This review provides state-of-the art knowledge on intimate mechanisms of esophageal fibrosis in EoE and its clinical consequences.