Eosinophilic esophagitis to unsuspected rare food allergen.

According to the International Gastrointestinal Eosinophilic revealed normal appearance of the esophageal, gastric, and Researchers Consensus, “Eosinophilic esophagitis (EoE) represents a chronic, immune/antigen mediated, esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation.”1 The onset is usually in children and young adults. The presenting symptoms depend on the patient’s age and may include feeding difficulty, vomiting, abdominal pain, dysphagia, and in severe cases, food impaction.1 Adult patients also may complain of heartburn, cough, or choking. The symptoms can be vague and misdiagnosed, often as gastroesophageal reflux disease, with a prolonged course and complications. The correct diagnosis may not be reached until esophageal stricture develops. The diagnosis is based on esophageal endoscopy and biopsy examination revealing at least 15 eosinophils per high-power field.1 In some patients, food hypersensitivity is involved and can be suspected by the medical history or by skin testing (prick or patch) or serum specific immunoglobulin E (IgE) testing. A trial of elimination of the most common causative foods (milk, egg, wheat, soy, peanut/tree nuts, and fish/seafood) without testing has been recently advocated, to be followed by re-introducing those foods one by one to identify the causative food.2e4 We present a case of an adult inwhom the causative food would not have been identified by a trial of an empiric elimination diet or by testing for common foods only. A 58-year-old white man, a university professor, had a history of upper gastrointestinal symptoms for more than 15 years, which had been treated as gastroesophageal reflux disease. He also had allergic rhinitis (treated with antihistamines when needed) and asthma (controlled with inhaled corticosteroids), autoimmune alopecia, and splenectomy for autoimmune thrombocytopenia at 22 years of age. He was initially treated with H2 receptor blockers and then proton-pump inhibitors, with only partial improvement. During the subsequent 6 years, symptoms worsened and reached significant dysphagia. Esophagogastroduodenoscopy showed mild V-line longitudinal furrow in the distal esophagus and reflux esophagitis at the gastroesophageal junction. Results of esophageal biopsies revealed marked esophagitis with increased eosinophils; on average greater than 60/high-power field (hpf; Fig 1A), confirming the diagnosis of EoE. Duodenal and stomach biopsy specimens showed mild to moderate chronic gastritis, but no evidence of celiac sprue or Helicobacter pylori. Swallowed viscous budesonide 0.5 mg daily was prescribed by the gastroenterologist, but it was taken irregularly. Over the next 2 years, he had increased nausea, dyspepsia, and dysphagia. A second esophagogastroduodenoscopy