Secukinumab, an interleukin-17A (IL-17A) inhibitor, is a biologic agent widely used for autoimmune conditions such as psoriasis, psoriatic arthritis, and hidradenitis suppurativa. While effective for these disorders, IL-17A inhibition has been increasingly associated with paradoxical gastrointestinal inflammation, including the development or exacerbation of inflammatory bowel disease (IBD).

We describe a 43-year-old woman with hidradenitis suppurativa who developed new-onset ulcerative colitis after approximately eight months of treatment with secukinumab. She presented with bloody diarrhea and abdominal pain. Laboratory evaluation revealed elevated inflammatory markers, including an erythrocyte sedimentation rate of 42 mm/hr, a C-reactive protein level of 18 mg/L, and fecal calprotectin of 306 µg/g. Colonoscopy demonstrated Mayo 2 inflammation confined to the rectosigmoid colon, and biopsy confirmed moderate active chronic colitis with cryptitis and crypt architectural distortion. Secukinumab was discontinued, and the patient was treated with prednisone 40 mg daily, resulting in rapid and complete resolution of symptoms.

This case highlights a paradoxical immune-mediated complication of IL-17A inhibition. Although secukinumab is highly effective for dermatologic and rheumatologic diseases, clinicians should be aware of its potential to induce or unmask IBD. Early recognition of gastrointestinal symptoms and prompt discontinuation of the agent are essential to prevent disease progression.