S4869 New Onset Crohn’s Disease Following Secukinumab Therapy for Hidradenitis Suppurativa in a Young Adult Man

Introduction: Secukinumab is a monoclonal antibody that inhibits interleukin-17A (IL-17A). It is approved for treatment in several autoimmune conditions including hidradenitis suppurativa (HS). However, IL-17A inhibition is associated with rare cases of new-onset inflammatory bowel disease (IBD). We present a case of a 20-year-old man whose workup for acute diarrhea and weight loss after initiating secukinumab for HS led to a diagnosis of Crohn’s disease. Case Description/Methods: A 20-year-old man with HS presented to our clinic for acute, non-bloody diarrhea and weight loss. Three months prior to presentation, he was prescribed secukinumab for treatment of HS. His physical exam was unremarkable. Labs revealed elevated liver-associated enzymes, iron deficiency anemia, and an elevated C-reactive protein of 7.5 mg/dL. Esophagogastroduodenoscopy was performed which identified white plaques in the esophagus; biopsies confirmed candidal esophagitis. Colonoscopy was then performed which revealed moderate ileitis in the distal ileum and severe colitis throughout the colon characterized by deep ulcers with loss of vascular pattern and friability. Histological specimens revealed chronic active ileocolitis; biopsies were negative for infectious etiologies, such as cytomegalovirus. Computed tomography enterography was obtained which demonstrated mural enhancement, bowel wall thickening, extensive fat stranding, and strictures within the colon. These findings supported the diagnosis of Crohn’s disease. Secukinumab was discontinued, and the patient was treated with fluconazole and intravenous corticosteroids, which led to symptom resolution. Discussion: IL-17A supports mucosal immunity and innate immunity at barrier surfaces, such as the gastrointestinal tract. Although IL-17A inhibitors are effective in treating many autoimmune diseases, recent data suggests they may trigger underlying IBD. Inhibition of IL-17A disrupts mucosal integrity and alters the intestinal microbiome, thereby exacerbating intestinal inflammation in individuals predisposed to IBD, as in our patient. Additionally, the esophageal candidiasis in our patient further supports the impaired mucosal immunity secondary to IL-17A blockade. Discontinuation of secukinumab and initiation of corticosteroids resulted in symptom resolution, supporting the interplay between impaired IL-17A function and IBD. This case highlights the relationship between IL-17A inhibition and the development of IBD.