Eosinophilic Gastritis: A Rare Cause of Non Healing Chronic Antral Ulcer

Abstract

Purpose: Gastric ulcers are highly unusual manifestation of eosinophilic gastroenteritis (EG). We describe a rare case of a non healing gastric ulcer occurring in patient with EG. Methods: 63-year-old male underwent follow up EGD for non healing antral ulcer. At the time of EGD, he was taking oral prednisone 60 mg for acute contact dermatitis. Prior EGD findings were ringed esophagus, 1 cm antral ulcer and gastritis and duodenitis. He was first referred to us with low ferritin (20) without GI symptoms. No history of NSAIDs/ ASA usage, smoking, cocaine or alcohol abuse. Biopsies revealed chronic inflammation in esophagus with marked eosinophilic infiltration (> 25 eosinophil /HPF) and moderate eosinophilia with chronic inflammation in antrum and duodenum; H. pylori was not seen on gastric biopsies; no malignancy or granulomas present. Special stain for CMV was negative. Patient was treated with PPI twice a day followed by additional sucralfate twice a day. Normal CBC with differential; ESR & CRP, IgE and gastrin were normal; negative stool for ova & parasites. Normal colonoscopy with negative random biopsies. Follow-up EGD showed partially healing 5 mm antral ulcer with scattered surrounding erosions compared with prior EGD. There were a markedly reduced number of eosinophils on biopsies. Results: Fortuitously, this patient was placed on steroid for a dermatologic condition prior to his repeat EGD with findings of significant healing of gastric ulcer and resolution of eosinophilic infiltration. Conclusion: EG is defined as a disorder that selectively affects the gastrointestinal tract with eosinophilic inflammation in the absence of known causes for eosinophilia, e.g., drug reactions, parasitic infections, malignancy. Clinical manifestations of disease depend on site of histologic involvement: 1) Diarrhea, iron deficiency anemia and protein-losing enteropathy in predominant mucosal disease; 2) obstruction/ motility disorder in predominant muscle layer disease; 3) ascites in predominant serosal disease. The cause of EG is unknown and the pathogenesis is poorly understood. Typical endoscopic findings in mucosal disease include nodular or polypoid gastric mucosa, erythema, or erosions; ulcer formation is unusual. The definitive finding of Eosinophilic Esophagitis (EE) in our patient supports the diagnosis of eosinophilic gastritis as the cause of our patient's gastric ulcer. The role of food allergy as a stimulus to EG has not been as clearly defined as in EE. It is conceivable that this is not one, but several disorders that manifest as similar histologic end points. Steroids are the mainstay of therapy in patients who fail to respond to dietary manipulation.