Abstract
INTRODUCTION: Secukinumab, an interleukin (IL)-17 antagonist used in the management of rheumatological diseases, has been associated with new onset and exacerbation of pre-existing inflammatory bowel disease (IBD). There are very few reports of cases of new-onset severe IBD after initiating secukinumab therapy, and we describe one such case. CASE DESCRIPTION/METHODS: A 44-year-old male with a history of psoriasis, recently initiated on secukinumab with first dose 1 month prior, presented with bloody diarrhea and abdominal pain. Admission workup was notable for elevated inflammatory markers, negative workup for infectious causes of diarrhea and CT abdomen showing colitis. Colonoscopy revealed severe inflammation and ulcerations in the left colon and inflammation with erosions in terminal ileum. Biopsies revealed findings consistent with Crohn's disease. Secukinumab was discontinued and he was started on budesonide and mesalamine. Diarrhea and abdominal pain significantly improved prior to discharge. On a clinic visit 2 weeks later, he had complete resolution of symptoms, and was then initiated on ustekinumab for control of both his Crohn's disease and psoriasis. DISCUSSION: The pathogenesis of IBD is thought to involve complex interactions between genetic, environmental or microbial factors and dysregulated immune responses. IL-17 was thought to contribute to IBD pathogenesis based on increased expression of IL-17 in the mucosa and serum in IBD patients. However, trials of IL-17 antagonists in patients with IBD were not successful. Exacerbation of IBD or new-onset IBD in patients on secukinumab has been increasingly described in case reports, and has been reported to be around 1%. In one case report of new IBD, the patient had a positive family history. On the other hand, other reviews have reported no increased incidence of IBD in patients treated with secukinumab compared to known rates of IBD in patients with ankylosing spondylitis, psoriasis, and psoriatic arthritis. It appears that the overall incidence of IBD in patients using secukinumab is rare. Prior to initiating this drug, evaluating patients for IBD or the susceptibility to IBD should be considered including any GI symptoms and personal or family history of IBD. In the emergence of new GI symptoms, the possibility of drug-induced IBD should be considered. Biologic drugs targeting other pathways like ustekinumab (IL12/23) or infliximab and adalimumab (TNF-alpha) may be a safer choice in patients with co-existing IBD and rheumatological conditions.
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