2112 Delayed Onset of Inflammatory Bowel Disease During Treatment With Secukinumab

Abstract

INTRODUCTION: Secukinumab is an interleukin-17 inhibitor commonly used for treating ankylosing spondylitis (AS). Recent reports described new onset inflammatory bowel disease (IBD) in patients treated with Secukinumab. To our knowledge, this is the first case report to describe a delayed presentation of new onset IBD in a patient 14 months after beginning treatment with Secukinumab. CASE DESCRIPTION/METHODS: A 68 year old male presented with 2-3 bloody bowel movements per day, fever and 20 lbs of unintentional weight loss for six weeks. Past history was significant for AS treated with Secukinumab for 14 months after failing therapy with other biologics (Etanercept, Adalimumab and Infliximab). A screening colonoscopy 3 months prior to presentation revealed no evidence of colitis. Labs were notable for an elevated WBC 13.2 and ESR 74, stool testing was negative for Clostridium difficile. A flexible sigmoidoscopy showed erythematous mucosa beginning in the rectum. Multiple deep ulcerations were noted beginning at 30 cm (Figure 1) and biopsies showed a diffuse pattern of brisk chronic active colitis. Secukinumab was discontinued. Methylprednisolone and mesalamine were begun and resulted in significant improvement in his symptoms. The patient presented again with similar symptoms one month later. Repeat flexible sigmoidoscopy showed partial healing. Biopsies demonstrated chronic active colitis consistent with IBD. A repeat flexible sigmoidoscopy performed 6 later showed complete mucosal healing (Figure 2). DISCUSSION: We present the first case report of delayed onset IBD in a patient with AS treated with Secukinumab. Previously reports demonstrated a rapid onset of presentation, usually either after first infusion or within a few weeks of treatment (JCC, 2018, 1131-1133). Interestingly, our patient had a routine screening colonoscopy 3 months prior to symptom onset which showed no evidence of IBD. The pathogenesis of new onset IBD in patients treated with Secukinumab is not clear. IL-17A is known to be pro-inflammatory in IBD but certain mouse models demonstrated IL-17A to be protective in T cell mediated colitis, and IL-17A-deficient mice developed rapid weight loss and severe colitis (Nat Immunol. 2009;10:603–9). This case suggests that new onset IBD in patients taking Secukinumab may present many months after initiation of therapy. Clinical suspicion should remain in patients with symptoms suggestive of IBD many months after starting, and even tolerating, Secukinumab.