S3007 What Lies Beneath: A Curious Case of Eosinophilic Gastroenteritis

Abstract

INTRODUCTION: The serosal form of eosinophilic gastroenteritis (EG) is the least common but typically the most responsive to corticosteroids. The diagnosis can be elusive, as there are no standard diagnostic criteria for this form of EG, and endoscopic mucosal biopsies may frequently fail to reveal tissue eosinophilic infiltrates. This case demonstrates that the diagnosis of serosal eosinophilic gastroenteritis requires a high index of suspicion that incorporates clinical presentation, laboratory data, radiologic findings, and response to corticosteroids. CASE DESCRIPTION/METHODS: A 50-year-old Caucasian male with a history of ADHD and GERD presented with progressive abdominal distention and pain radiating to the back. Vital signs were notable for a temperature of 100.5o F. Physical exam was notable for decreased breath sounds at the lung bases, mild distention of the abdomen and mild diffuse abdominal tenderness. Laboratory studies were all normal including WBC count except for absolute eosinophil count >5,000. CT imaging revealed a right > left sided pleural effusion, small bilateral pulmonary nodules, hilar and mediastinal lymphadenopathy, long-segment small bowel thickening, ascites, and distal esophageal thickening. Paracentesis revealed eosinophilic ascites. Evaluation for parasitic, nematodal, neoplastic, allergic, and hematologic etiologies for eosinophilia was unrevealing including flow cytometry. Subsequent bone marrow evaluation excluded an eosinophilic myeloproliferative disorder. Endoscopy and biopsies from the esophagus to jejunum were normal except for Barrett’s esophagus. Prednisone was initiated for presumed serosal EG with a complete clinical response within one week and complete normalization of eosinophilia. Over the course of several years, prednisone tapering was inevitably followed by symptomatic recurrence of ascites and systemic eosinophilia. He has remained in complete remission 6 years from initial presentation on low dose prednisone maintenance. DISCUSSION: Eosinophilic ascites (EA) is a rare presentation of EG and is due to serosal involvement. Peripheral eosinophilia may or may not be present. Exclusion of other etiologies of EA is important before initiating therapy. Serosal EG may have a relapsing course (as in our patient) in 25% of patients who then require chronic low dose prednisone or immunomodulator therapy. Laparoscopic full-thickness gastric or small bowel biopsies may be necessary to make the diagnosis in cases without a prompt corticosteroid response.