Findings can show different types of strictures or a ringed esophagus that could be caused by EoE.Īn allergist and immunologist should evaluate patients with a history of atopy or food allergy and a diagnosis of EoE. Another common nonspecific finding would be a barium swallow study. There is no diagnostic laboratory test available for EoE, but a mildly elevated serum IgE level is present in patients with EoE. Other histological findings suggestive of EoE include basal cell hyperplasia, elongation of papillae, superficial layering of eosinophils, extracellular eosinophilic granules, and fibrosis of sub-epithelium. The pathological diagnosis of EoE is made when eosinophils are present greater than or equal to 15 per high power field (HPF). Clinicians also should note that some patients may have normal esophagus in upper endoscopy. Įndoscopic findings of EoE include corrugated mucosa, longitudinal mucosal furrows, fixed esophageal rings or trachealization, whitish mucosal plaque or exudate, stricture, superficial mucosa tear upon passing endoscope, diffusely narrow lumen, and mucosal friability giving the appearance of crepe paper. During the endoscopy, biopsies also should be taken from the antrum and duodenum to rule out other possible causes of eosinophilia.

Esophageal biopsies normally should be taken from the proximal, mid, and distal esophagus.

Upper endoscopy with esophageal biopsy also should be done on patients with a presumed diagnosis of GERD who are resistant to optimal proton pump inhibitor (PPI) dose (20 to 40 mg orally twice daily) and duration (8 to 12 weeks). Patients who present with food impaction, dysphagia, and history of atopy should undergo an upper endoscopy evaluation with esophageal biopsy to diagnose EoE.

Ĭlinicians should arrive at the diagnosis of EoE only after positive findings on clinical, endoscopic, and histopathologic examinations. The remodeling of inflamed mucosa can occur with repeated exposure to the antigens, leading to remodeling and fibrosis which clinically manifests as various esophageal dysfunction that includes dysphagia, epigastric pain, dyspepsia, chest pain, and food impaction. It has been reported that a single exposure to airway antigen challenge and cutaneous antigen exposure may lead to recruitment of eosinophils in the esophagus leading to EoE. TGF-B is responsible for remodeling of esophageal mucosa and smooth muscle dysfunction. The other important cytokine involved in the pathogenesis is TGF-B (transforming growth factor-beta), which is released by eosinophils and mast cells recruited after immune activation. Overall, this immunogenic process starts as an allergic response to various environmental antigens, food, or aeroallergens and leads to the inflammation of esophageal mucosa. Eotaxin-3 is overexpressed in the esophageal mucosa in EoE patients. The stimulated Th2 cells activate various proinflammatory cytokines such as IL5, IL13, and IL15, which recruit eosinophils. TSLP stimulates Th2 cells and induces eotaxin-3. This study reported that the gene responsible for EoE was TSLP (thymic stromal lymphopoietin) which is located in the 5q22 region of male X chromosome.

The pioneer study that described the genetic basis for EoE was a study of genome-wide microarray expression profile analysis. There is a strong genetic component involved in the pathogenesis of EoE and a high concordance reported for EoE among family members. EoE occurs as a result of an immunogenic reaction to various antigens which are commonly found in food and air.

Types of endoscopy findings