EP521 - Secukinumab-Induced Inflammatory Bowel Disease: A Case Report Highlighting a Rare but Alarming Cause of Medically Refractory Ulcerative Colitis

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Purpose/Background: Secukinumab, a monoclonal antibody that blocks interleukin (IL)-17, has become a mainstay in the treatment of several autoimmune disorders, namely psoriatic arthritis (PsA). Medical providers must be aware of the rare but serious complication of induced inflammatory bowel disease (IBD) with this medication.

Methods/Interventions: This is a 48-year-old male with a past medical history of PsA. Treatment was changed from adalimumab to secukinumab (IL-17 inhibitor) four months prior to presentation. He presented to our Emergency Department with abdominal pain and bloody diarrhea and was noted to be hypotensive, tachycardic, and diaphoretic. Leukocytosis to 15K/µL, c reactive protein of 16mg/dL, erythrocyte sedimentation rate of 42mm/hr, and lactate of 4.9mmol/L were noted. CT scan showed diffuse colonic wall thickening with pericolonic stranding. Colonoscopy revealed severe, congested, erythematous, eroded, friable, and deeply cratered ulcerated mucosa. Rectal biopsies demonstrated active chronic proctitis. He denied recent travel and fecal ova, parasites, and major enteric pathogens were negative. He had no personal or family history of IBD. Intravenous steroids and infliximab were initiated, but his symptoms worsened over the next three days so he underwent a total abdominal colectomy (TAC) with end ileostomy (EI).

Results/Outcomes: Postoperatively, he was initially nil per os with a nasogastric tube and parenteral nutrition, followed by slow advancement to a low residue diet. He required drain placement by interventional radiology for an intraabdominal abscess. He was discharged on postoperative day 18. His drain has since been removed, and he has been started on golimumab, a tumor necrosis factor-alpha (TNF-α) inhibitor, for his PsA.

Conclusion/Discussion: Secukinumab has become a mainstay in the treatment of autoimmune conditions such as PsA, plaque psoriasis, and ankylosing spondylitis. It is a human monoclonal antibody that selectively binds to the proinflammatory cytokine IL-17A and renders it ineffective. The exact role of IL-17, and therefore IL-17 inhibitors, in IBD is unclear, with the understanding that development of IBD is multifactorial involving a combination of genetic predisposition, abnormal immune responses to intestinal microorganisms, and environmental exposure. Some animal studies have implicated its involvement in neutrophil aggregation, effector T-cell production, intestinal permeability, expression of gut antimicrobial peptides, and immunity against yeast. While there is a known increased risk of developing IBD in patients with PsA, observational studies have shown even higher degrees of IBD in patients on secukinumab. Some cases have revealed IBD resolution with secukinumab cessation. In this case, the patient’s disease severity led to TAC with EI, highlighting the importance of considering a patient’s personal and family history of IBD prior to starting IL-17 inhibitors, and the high index of suspicion needed by the colon and rectal surgeon to guide management.