EoE often presents with difficulty swallowing, food impaction, stomach pains, regurgitation or vomiting, and decreased appetite.

In addition, young children with EoE may present with feeding difficulties and poor weight gain.

[8] The antigenic exposure is thought to stimulate the esophageal epithelial cells to release the inflammatory cytokines IL-33 and thymic stromal lymphopoietin, which attract and activate Th2 helper T-cells.

[8] Eosinophils are inflammatory cells that release a variety of chemical signals which inflame the surrounding esophageal tissue.

This results in the signs and symptoms of pain, visible redness on endoscopy, and a natural history that may include stricturing.

[9] At a tissue level, EoE is characterized by a dense infiltrate with white blood cells of the eosinophil type into the epithelial lining of the esophagus.

[3] The diagnosis of EoE is typically made based on the combination of symptoms and findings from diagnostic testing.

Prior to the development of the EE Diagnostic Panel, EoE could only be diagnosed if gastroesophageal reflux did not respond to a six-week trial of twice-a-day high-dose proton-pump inhibitors (PPIs) or if a negative ambulatory pH study ruled out gastroesophageal reflux disease (GERD).

[5][14] Endoscopic mucosal biopsy remains the gold standard diagnostic test for EoE and is required to confirm the diagnosis.

If no specific allergenic food or agent is present, a trial of the six-food elimination diet (SFED) can be pursued.

Four- or even two-group exclusion diets may be less difficult to follow and reduce the need for many endoscopies if the response to the limited restriction is good.

[17][19] The elemental diet demonstrates a high rate of response (almost 90% in children, 70% in adults), with a rapid relief of symptoms associated with histological remission.

This diet involves using amino acid-based liquid formulas for 4-6 wk, followed by the histological evaluation of response.

If no eosinophils are present in the repeat biopsy, the diagnosis is either acid-mediated GERD with eosinophilia or non-GERD PPI-responsive EoE with an unknown mechanism.

The goals of therapy for treating EoE are to improve the patient's symptoms and reduce the number of eosinophils on biopsy.

The patient should be informed that after dilation, they might experience chest pain and, in addition, risk of esophageal perforation and bleeding.

Long-standing, untreated disease may result in esophageal remodeling, leading to strictures, Schatzki ring and, eventually, achalasia.

[25] Risk factors for EoE include autoimmune conditions such as, inflammatory bowel disease and rheumatoid arthritis.

[32] In addition to gender (male predominance) and race (mainly a disease of Caucasian individuals), established risk factors for EoE include atopy and other allergic conditions.

A study comparing active EoE children to non-EoE children found an altered microbiome due to a positive correlation between a relatively high abundance of Haemophilus and disease activity seen through an increasing Eosinophilic Esophagitis Endoscopic Reference Score and Eosinophilic Esophagitis Histologic Scoring System (q value = 5e-10).

Measuring the relative abundance of specific taxa in children’s salivary microbiome could serve as a noninvasive marker for eosinophilic esophagitis.