Giant cell arteritis during risankizumab therapy: a possible paradoxical reaction to IL-23 inhibition

Risankizumab is a selective interleukin (IL)-23p19 inhibitor used for psoriasis. Although IL-23 is implicated in giant cell arteritis (GCA), biologic therapy can occasionally be associated with paradoxical immune-mediated events. We report a 67-year-old woman who developed GCA during long-term risankizumab therapy for psoriasis vulgaris. She presented with progressive night sweats and fatigue, with marked systemic inflammation. Contrast-enhanced computed tomography and gadolinium-enhanced magnetic resonance imaging demonstrated large-vessel inflammation involving the aorta and its major branches. Temporal artery biopsy showed intimal hyperplasia, fragmentation of the internal elastic lamina, and mild inflammatory cell infiltration. She fulfilled the 2022 ACR/EULAR classification criteria for GCA and was treated with high-dose prednisolone, followed by methotrexate. Her symptoms and inflammatory markers improved rapidly, and risankizumab was continued because of excellent psoriasis control. Pretreatment serum cytokine analysis showed low IL-17 levels, whereas IFN-γ, IL-6, and TNF-α were comparable to or higher than those in other patients with GCA. This case highlights that GCA can develop during selective IL-23 blockade and may involve Th1-skewed inflammation or a paradoxical immune reaction.