Abstract

Inflammatory bowel disease (IBD) and psoriasis are chronic inflammatory immune-mediated diseases. The interleukin-23- (IL23-) T helper (Th)17 pathway has been implicated in their pathogenesis, with multiple biologic therapies targeting this pathway. IL-17, the main proinflammatory cytokine produced by (TH)17, has been targeted by antibodies and IL-17 receptor blockers with favorable outcomes in treating psoriasis and psoriatic arthritis. However, their role in IBD is unpredictable as studies reported worsening of IBD with agents targeting IL-17 and rare case reports with new-onset IBD. We present a case of Crohn's-like severe terminal ileitis and worsening diverticulitis complicated by intestinal perforation requiring total parenteral nutrition shortly after being started on secukinumab.

Highlights

  • Secukinumab, a fully human monoclonal antibody that selectively neutralizes IL-17A, has been shown to have significant efficacy in the treatment of moderate-to-severe psoriasis and psoriatic arthritis [1]

  • Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, is characterized by chronic relapsing intestinal inflammation. Both environmental and genetic factors play a role in the pathogenesis of IBD. e interleukin-23- (IL23-) T helper ( )17 pathway regulated by multiple genes, including IL12B and IL23R, has been associated with both IBD, psoriasis, and psoriatic arthritis [5,6,7,8]

  • IL23 promotes the differentiation and expansion of the effector 17, which subsequently secretes IL-17, a proinflammatory cytokine that has been implicated in multiple autoimmune diseases [9, 10]

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Summary

Introduction

Secukinumab, a fully human monoclonal antibody that selectively neutralizes IL-17A, has been shown to have significant efficacy in the treatment of moderate-to-severe psoriasis and psoriatic arthritis [1]. IBD and psoriasis are both chronic immune-mediated diseases that share overlapping genetic profiles [2]. Prior studies show benefits and increased rate of adverse events in IL-17A inhibition in Crohn’s disease [3]. Exacerbation of IBD or new-onset IBD has been reported in rare case reports. Psoriasis with concomitant psoriatic arthritis is associated with an increased risk of Crohn’s disease [4], which poses the question of whether the emergence of IBD in psoriasis patients treated with IL-17A antibodies is related to IL-17A inhibition or merely their increased risk of developing IBD

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