Abstract

Abstract Background Secukinumab is a monoclonal antibody targeting interleukin-17A and is commonly used for managing autoimmune diseases such as, psoriasis, psoriatic arthritis, and ankylosing spondylitis. Prior studies have suggested that anti-IL17 therapy may worsen symptoms in patients with pre-existing inflammatory bowel disease (IBD). However, it remains unclear if secukinumab is associated with new-onset IBD or in provoking a flare of previously quiescent IBD. Aims We evaluated patients referred to our IBD clinic who developed intestinal inflammation after starting secukinumab for the management of autoimmune diseases. Methods We performed a retrospective, observational study at a single tertiary care center between 2017 and 2020. Patients referred to our IBD clinic who developed intestinal inflammation after starting secukinumab were included. We excluded patients with an established pre-existing diagnosis of IBD and patients who had positive stool testing for infectious organisms. Patient demographics, disease characteristics, distribution of intestinal inflammation and clinical outcomes were assessed. The pathology slides were reinterpreted by a single pathologist with a specialty in gastroenterology to determine the histologic characteristics of the inflammation. Results A total of 8 patients developed gastrointestinal symptoms after starting secukinumab: 4 (50%) males with a median age of 42.5 (IQR: 35–50 years old). Secukinumab was initiated for psoriasis in 3 (37.5%) patients, psoriatic arthritis in 2 (25%) patients, ankylosing spondylitis in 2 (25%) patients and juvenile idiopathic arthritis in 1 (12.5%) patient. The median time of onset for gastrointestinal symptoms after starting secukinumab was 7 months (IQR: 4–15 months). Of the patients who underwent testing for inflammatory biomarkers, the median CRP was 25.5 (IQR 25.4–34.2). Endoscopic disease distribution involved the colon in 5 (62.5%) patients and the ileum and colon in 3 (37.5%) patients. In this series of patients, the histologic characteristics demonstrated three patterns of colitis: IBD-like (ulcerative colitis or Crohn’s disease) in 6 (75%) patients based on mucosal granulomas and/or chronic inflammatory changes, MMF-like histology in 1 (12.5%) patient, characterized by an abundance of intraepithelial eosinophils in the lamina propria and numerous crypt apoptotic bodies, and finally active colitis in 1 (12.5%) patient characterized by an absence of chronic mucosal injury or granulomas. The treatment for these patients was cessation of secukinumab and initiating alternative therapies with close clinical monitoring. Conclusions In this small case series, Secukinumab was temporally associated with the development of gastrointestinal inflammation. Further larger studies are required to confirm this association and to determine if IL-17 contributes to the pathogenesis of IBD. Funding Agencies None

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