Case Presentation: A 48 year old female with no significant past medical history presented with acute onset of dysphagia, early satiety, nausea /vomiting and epigastric pain. Epigastric pain and non-bloody non-bilious emesis occurred after each meal. Lab work significant for eosinophilia (absolute eosinophil count 2,084/microL, reference < 500/microL ). CT abdomen and pelvis significant for marked distention of a fluid filled stomach and a transition point in the first portion of the duodenum. Supportive treatment with NPO, IV fluids, naso-gastric tube for decompression, anti-emetics for nausea control was provided. EGD and gastric emptying test were normal. Due to persistent symptoms , CT enterography was obtained and concerning for a submucosal or serosal infectious/inflammatory process as potential etiology. Endoscopic ultrasound with fine needle aspiration (EUS- FNA) was performed to assess for infiltrative diseases as cause of the wall thickening. Endosonographic thickening of the submucosal layers of the antrum, pylorus, duodenum was present. All biopsies revealed diffuse eosinophilic infiltration with differential diagnosis now including eosinophilic/allergic gastroenteritis, parasitic infection, drug effect, inflammatory bowel disease, collagen vascular disease, and lymphoproliferative disorders. Patient's diagnosis of eosinophilic gastroenteritis finalized after complete workup of eosinophilia to rule out other etiologies.
Discussion: Eosinophilic gastroenteritis (EGE) is a rare disease- with prevalence of 22 per 100,000 persons. The pathogenesis of EGE is not well understood and clinical features of EGE depend on the location, extent, and layers of eosinophilic infiltration. Patients commonly present with blood eosinophilia (average absolute eosinophil county of 1000 cells/microL), elevated serum immunoglobulin E (IgE), and anemia secondary to iron deficiency and occult gastrointestinal bleeding. Eosinophilic mucosal infiltration presents with symptoms including abdominal pain, nausea, vomiting, early satiety and diarrhea. Deeper submucosal, muscular infiltration presents as dysphagia, regurgitation of undigested foods, intestinal perforation and gastric outlet obstruction. Identification and proper diagnosis for this disease is vital as it can lead to malabsorption, protein-losing enteropathy and failure to thrive.
Conclusions: Eosinophilic gastroenteritis (EGE) should be suspected in a patient with abdominal pain, nausea, vomiting, early satiety, diarrhea, weight loss, or ascites in conjunction with peripheral eosinophilia (eosinophil count >500 eosinophils/microL in the peripheral blood), and/or a history of food allergy or intolerance. EGE diagnosis is based on eosinophilic infiltration of the gastrointestinal tract on biopsy and/or eosinophilic ascitic fluid, lack of involvement of any other organs, and the absence of other etiologies for intestinal eosinophilia.
Treatment includes a six food elimination diet (avoidance of soy, wheat, egg, milk, peanut/tree nuts and fish/shellfish). Glucocorticoid therapy (prednisone 20-40 mg/day) for acute symptom management and transition to oral budesonide has been used for patients with disease in the gastric antrum. Other therapies for refractory disease include ketotifen ( H1 antihistamine, mast cell), montelukast (leukotriene antagonist) , and omalizumab anti-IgE monoclonal antibody.