Inflammatory Bowel Disease Unmasked by Interleukin-17 Inhibitor for Psoriasis

Background: Psoriasis and inflammatory bowel disease (IBD) have shared characteristics including risk factors, susceptibility, mechanisms, and comorbidities. Psoriasis and IBD may occur independently or concurrently on a spectrum of severity for each disease. Both can be managed using biologic medications. Interleukin (IL)-17 inhibitors are used primarily to treat psoriasis. However, this mechanism is known to exacerbate, or at times induce, IBD. Previous studies suggest switching therapy to alternative biologics can effectively treat both. We present a case of new onset Crohn’s Disease (CD) with previously diagnosed psoriasis on IL-17 inhibitor who responded to a therapeutic change to IL-23 inhibitor. Methods: A 61-year-old male with 6 year history of plaque psoriasis presented to the Emergency Department for 3 months of abdominal pain significantly worsened prior to presentation with obstipation. Psoriasis was previously in remission with IL-17 inhibitor Secukinumab 300 mg subcutaneous (SQ) every four weeks for one year with the last dose three weeks prior to presentation. Previous treatments included Brodalumab and Ixekizumab due to insurance coverage, not treatment failure. Colonoscopy for colorectal cancer screening four years prior was without inflammation, no random biopsies obtained. Computed Tomography (CT) of the abdomen and pelvis showed small bowel obstruction secondary to terminal ileitis. Nasogastric (NG) tube placed for decompression. Inflammatory markers were elevated with C-Reactive Protein (CRP) 7.0 (range 0.0-1.0 mg/dL), Erythrocyte Sedimentation Rate (ESR) 59 (range 0-20 mm/hr), and fecal calprotectin (FC) 581 (range 0-120 mcg/g). After resolution of obstruction with NG decompression, colonoscopy showed ulcerations in the terminal ileum and inflammation at the ileocecal valve. Histology demonstrated terminal ileitis and active colitis consistent with CD. Intravenous (IV) Methylprednisolone 20 mg every 8 hours was given for 48 hours, which improved symptoms followed by oral Prednisone 40 mg tapered by 5 mg over 8 weeks. Magnetic Resonance Enterography (MRE) showed long segment stricture and inflammation of distal terminal ileum. Results: Secukinumab was discontinued. Patient seen four weeks after discharge and started on IV Risankizumab 360 mg standard induction infusion followed by maintenance SQ dose every 8 weeks. After completing induction, clinical remission was achieved with resolution of abdominal pain. Follow up FC 91 and CRP 0.49 with continued remission of psoriasis. Conclusions: IBD often occurs with psoriasis in a variety of presentations with the progression occurring at discrete periods of time. CD may be induced by IL-17 inhibitors or at minimum provide inadequate treatment for luminal inflammation. No current guidance in the timeline of switch in therapy although in prior studies showed a median time to remission after IL-17 inhibitor discontinuation with switch in therapy was 4 weeks. In patients without luminal disease, proactive use of fecal calprotectin may act as a predictive marker prior to onset of luminal symptoms and guide decision making for optimal biologic treatment. In cases of inflammatory bowel and dermatologic disease, therapy with Risankizumab provides appropriate therapeutic coverage for both aspects of inflammation.