Vunakizumab-induced severe ulcerative colitis during treatment of psoriatic arthritis: a case report and literature review.

BACKGROUND: Interleukin-17A (IL-17A) inhibitors are effective therapies for psoriasis (PsO) and psoriatic arthritis (PsA), yet they may induce or exacerbate inflammatory bowel disease (IBD). Vunakizumab is a novel humanized anti-IL-17A monoclonal antibody approved in China in 2024; post-marketing real-world data on its gastrointestinal safety profile remain limited. CASE PRESENTATION: We report a 54-year-old male PsA patient who developed acute severe ulcerative colitis (UC) approximately one week after the third injection of vunakizumab, representing the first reported case of vunakizumab-associated IBD in the literature. The patient exhibited marked hepatic enzyme elevation (alanine aminotransferase [ALT] 213 U/L, aspartate aminotransferase [AST] 189 U/L), representing one of the most significant liver injuries reported in this context. The Naranjo Adverse Drug Reaction Probability Scale score was 7 ("probable"). Vunakizumab was immediately discontinued; intravenous methylprednisolone 60 mg/day was administered to induce remission. Following acute-phase control, the patient was switched to guselkumab (an anti-IL-23p19 monoclonal antibody) for maintenance therapy, achieving dual remission of intestinal and articular manifestations. CONCLUSION: Vunakizumab can induce severe UC. As a newly approved IL-17A inhibitor in China, early post-marketing safety surveillance should remain vigilant for IBD risk. The underlying mechanism may involve disruption of the intestinal epithelial barrier and compensatory upregulation of IL-23 following IL-17A blockade. The early treatment period (within the first 3 months) represents a high-risk window. Upon diagnosis, immediate drug withdrawal, corticosteroid-induced remission, and prioritized conversion to an IL-23 inhibitor (such as guselkumab) may be considered as a potential option to achieve dual control of intestinal, skin, and joint disease.