S3972 A Rare Incidence of Etanercept Induced Inflammatory Bowel Disease

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Introduction: Etanercept (ETA), a dimeric fusion protein combining tumor necrosis factor (TNF)p75 and the Fc region of IgG1, blocks both TNF-a and TNF-B receptors diminishing the inflammatory response in the body. TNF-a blockers provide a benefit in rheumatoid arthritis (RA) by reducing the cytokine-mediated synovial inflammation. However, common gastrointestinal side effects are proposed due to autoimmunity from disruption of cytokine balance in the gut, or the induction of the formation of antinuclear antibodies and other autoantibodies. Case Description/Methods: A 72-year-old woman with a past medical history of type II diabetes mellitus, 6-year history of rheumatoid arthritis being treated with ETA 50mg injection weekly and a 5-year history of irritable bowel syndrome- diarrhea subtype treated with Ibguard. She denies recent antibiotic use, vomiting or abdominal pain. She presented to the gastroenterology clinic for a surveillance colonoscopy with prior history of polyps. No family history of inflammatory bowel disease, colon cancer or malignancy was noted. Physical exam showed a nodule on the left lateral epicondyle. Labs showed: Albumin: 3.1 g/dL, Total bilirubin: 0.5mg/dL, Alkaline Phosphatase: 362 U/L, aspartate aminotransferase: 61U/L, alanine aminotransferase: 38 U/L. antinuclear antibodies positive; 1:40; Cytoplasmic, reticular/ AMA pattern. Negative SSA / SSB antibodies. Erythrocyte sedimentation rate: 50 mm/h, C-reactive protein: 22.9 mg/L. Colonoscopy showed diffuse moderate inflammation characterized by edema, erythema, friability and loss of vascularity in the entire colon with greater severity on the left side. Biopsies visualized mild nonspecific active chronic colitis in the entire colon, sparing the terminal ileum and cecum with few ulcers present at the hepatic flexure. Immunohistochemical stains of ulcer biopsies indicated positive ae1/3, sma, vimentin, S-100 and cd68 (Figure 1). No granuloma, dysplasia or viral cytopathy seen. ETA was discontinued and Mesalamine (MES) 2.4 grams daily was prescribed. Patient’s diarrhea resolved however, liver enzymes trended upwards prompting discontinuation of mesalamine. Patient did not report diarrhea upon 1 month follow up. Discussion: Patients with RA are commonly prescribed ETA for symptom control. However, the rarity lies in ETA’s action as a provoking agent of ulcerative colitis. Patient’s diarrhea was resolved upon discontinuation of ETA. She continued to be symptom free even upon discontinuation of MES showing clear evidence of Etanercept acting as a trigger.Figure 1.: Immunohistochemical stains of ulcer biopsies indicated positive ae1/3, sma, vimentin, S-100 and cd68. Negative Adenovirus, cytomegalovirus, herpes simplex virus-1 and BSV-2. No granuloma, dysplasia or viral cytopathy seen.

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