S3495 What Do These Eosinophils Mean? Treatment Naive Systemic Lupus Erythematosus Presenting With Eosinophilic Ascites, Eosinophilic Pleural Fluid, and Enteritis of Unclear Etiology

Introduction: Eosinophilic ascites (EA), lupus enteritis (LE), and eosinophilic enteritis (EE) are rare systemic lupus erythematosus (SLE) complications. When they do occur, overlapping diagnostic criteria causes problems in distinguishing between a SLE-related etiology or EE. For example, intestinal eosinophil infiltration associated with EE is also consistently found in disseminated SLE autopsy case reports. Although both conditions are treated with steroids, therapies after treatment failure are different. We present a rare case of a SLE patient with this diagnostic dilemma with suboptimal response to SLE therapies, questioning whether an EE treatment algorithm may be more appropriate. Case Description/Methods: An afebrile 55 year old female with untreated SLE presented with constipation and a mildly tender distended abdomen. Imaging described moderate ascites, continuous small bowel thickening, ileus, and bilateral pulmonary infiltrates with pleural effusions. Significant results included a white blood cell count of 3.8 without eosinophils, erythrocyte sedimentation rate 5, C-reactive protein < 1, positive ANA (1:160), positive double stranded DNA, and low C3/C4 complement. Paracentesis yielded an exudative eosinophilic (71%) ascitic fluid with a low serum-ascites albumin gradient of 0.9 g/dL, high protein of 3.9 g/dL, and no evidence of malignancy or infection. She also had exudative eosinophilic pleural fluid. Endoscopy revealed mild cecal ischemia, mild gastritis, and a normal terminal ileum without eosinophils. Rheumatology diagnosed her with SLE serositis with peritoneal and pleural involvement complicated by LE, but they were unable to rule out EE. She responded to intravenous steroids but deteriorated when she was switched to oral prednisone. She then failed a regimen of hydroxychloroquine and oral prednisone. During her most recent hospitalization, the patient was transitioned to a regimen of hydroxychloroquine, mycophenolate mofetil, and oral prednisone. Discussion: It is unclear whether our patient’s sub-optimal therapy response is due to SLE or EE, with our case illustrating the difficulties in determining a diagnosis. Determining a diagnosis influences treatment and the patient's clinical course. In EE, treatment includes dietary therapy, antihistamines, leukotriene antagonists, and mast-cell stabilizers. However, our patient’s symptoms are attributed to serositis, leading to a focus on escalating her SLE immunosuppressive therapy rather than re-examine the diagnosis.