Challenges and updates in the management of eosinophilic esophagitis

Abstract

Eosinophilic esophagitis (EE) is a chronic T helper cell-2 mediated inflammatory condition and is considered as a primary cause of dysphagia and foregut symptoms. There are many challenges regarding the treatment options of EE. Different therapeutic approaches are best at meeting different endpoints. There are unresolved questions such as whether the goal for treatment should be to control esophageal eosinophilia and inflammation or to achieve symptomatic improvement. Still, proton pump inhibitors are used in differential diagnosis, along with their anti-inflammatory and anti-acid properties. Conducted trials continue to recommend the use of topical corticosteroids and empiric food elimination diets as first-line therapeutic modalities. The growing knowledge on the pathogenesis of EE has allowed further progression of encouraging targeted biologic therapies. However, the guidelines for EE management should be updated accordingly in the coming years, including fast evolving data on non-invasive diagnostic strategies, new treatment modalities, and the long-term prognosis of the disease.

Eosinophilic Esophagitis and Achalasia: Two Distinct Nosologic Entities or a Possible Etiopathogenic Association?

“…The pathogenesis of EoE seems to be the result of a complex interaction between various factors such as genetic background, environmental causes, and antigenic stimuli [2]. Exposure to allergens triggers the antigen presentation and differentiation of T helper 2 cells secreting interleukins (IL-4, IL-5, and IL-13).…”

“…Exposure to allergens triggers the antigen presentation and differentiation of T helper 2 cells secreting interleukins (IL-4, IL-5, and IL-13). These cytokines further overexpress other mediators such as chemokine ligand 26/eotaxin-3 and the upregulation of periostin in epithelial cells and fibroblasts [2]. Desmoglein, calpain, and filaggrin along with recruitment and stimulation of eosinophils lead to disruption of the epithelial barrier of the esophagus.…”

“…Desmoglein, calpain, and filaggrin along with recruitment and stimulation of eosinophils lead to disruption of the epithelial barrier of the esophagus. Eosinophils may also release IL-9 affecting mast cells [2]. The pathophysiological mechanism also involves propagation of basophils and plasma cells rich in IgG4 which are found in the lamina propria [2].…”

“…Although EoE mainly refers to people between 20 and 40 years old, all age-groups may be affected. EoE shows a male predominance, with a male-to-female ratio of 3:1 [2, 3]. The most recent definition of EoE applies to patients with specific symptoms such as dysphagia and food impaction who concurrently show marked eosinophilic inflammation in endoscopic esophageal specimens [histologically a peak count of 15 eosinophils per high-power field (hpf) of esophageal biopsy tissue] [2, 4, 5].…”

“…Even though dysphagia is a common, initially presenting symptom in patients with EoE, its etiology remains unclear [2]. Anatomic abnormalities such as strictures can only be found in a small proportion of patients with EoE, raising the possibility that there may be an underlying esophageal motility disorder [2]. Published literature regarding associations between esophageal motility disorders and EoE is limited.…”