1912 Chronic Non-Healing Gastric Ulcer Caused by Eosinophilic Gastroenteritis

Abstract

INTRODUCTION: Eosinophilic gastroenteritis (EG) occurs when eosinophils (eos) infiltrate the gastrointestinal (GI) tract leading to GI dysfunction. The prevalence of EG is 2.5 cases per 100,000 people in the US. The diagnosis is confirmed by histology with >20 eos per HPF. Common manifestations include abdominal pain, nausea, vomiting, and malabsorption. Ulcers are rarely seen in EG. CASE DESCRIPTION/METHODS: We describe a case of a 23 year old female with history of asthma presented with one month of severe epigastric pain, nausea and vomiting. Her pain was constant and exacerbated by eating. She took NSAIDs for 14 days without relief but denied melena, hematochezia, and hematemesis. She had no history of food intolerances, travel, smoking or alcohol use. Vitals and exam were unremarkable except for epigastric tenderness without rebound or guarding. Initial work up revealed WBC 8.0 K/UL with 16.7% eos, Hb 11.9 g/dL, MCV 80.6 fL, and ferritin 3 ng/mL. EGD revealed LA Grade A esophagitis, duodenitis, and a non-bleeding cratered antral ulcer, measuring 20 mm (Figure 1). Pathology revealed chronic gastritis without H. pylori. Pantoprazole 40 mg BID and sucralfate 1 g QID were initiated, but she continued to have symptoms and new onset hematemesis. Repeat EGD showed persistent 20 mm ulcer after 2 months of medical therapy. Biopsies showed marked eos in the esophagus, stomach, and duodenum, with >50 eos/HPF at the ulcer (Figure 2). Biopsies from a colonoscopy done at the time same revealed increased eos at the ileocecal valve. A workup for eosinophilia was negative for autoimmune or parasitic etiologies, gastrin level was normal, but serum IgE level was 1862 IU/mL. She was treated with prednisone and repeat EGD 2 months later revealed resolution of mucosal eosinophilia and decrease in ulcer size to 10 mm. DISCUSSION: Our patient was found to have diffuse eosinophilic infiltration throughout the GI tract as well as significant peripheral eosinophilia. While the ulcer may have been initially caused by NSAID use, it was refractory to treatment due to eosinophilic inflammation. Only after initiation of corticosteroids, did it begin to heal. The primary management for EG is elimination diet and avoidance of triggers. Systemic corticosteroids are effective in controlling symptoms if dietary modification is unsuccessful. There is limited evidence for the use of other medications including antihistamine, leukotriene, or IgE antagonists. In patients with ulcers refractory to conventional therapies, EG should be considered.