Risankizumab e Upadacitinib nel Trattamento dell'Artrite Psoriasica: Meccanismi Diversi, Obiettivo Comune

Psoriatic arthritis (PsA) is a chronic inflammatory disease with a complex clinical phenotype. Its main clinical manifestations are peripheral arthritis, spondylitis, enthesitis, and dactylitis that over time lead to axial and peripheral joint deformities. In addition, different extra-musculoskeletal manifestations (i.e. psoriasis, inflammatory bowel disease and uveitis) and co-morbidities (e.g. metabolic syndrome and cardiovascular disease) are often present. The etiopathogenesis of PsA is not entirely clear, although it is believed to result from a complex interaction of environmental, genetic, and immunological factors, with the dysregulation of the immune system causing a persistent inflammatory response, tissue damage, and pathological bone remodeling. The identification of the key inflammatory mediators of PsA has led to the development of specific inhibitors of interleukin 23 and Janus kinases, including risankizumab (anti-interleukin 23 antibody) and upadacitinib (Janus Kinase inhibitor). Herein, we report the results of the clinical trials that led to the approval of risankizumab and upadacitinib in PsA and their safety profile. In addition, four clinical cases are discussed emphasizing the importance of finding the correct balance among symptom control, treatment efficacy, and possible side effects in the management of the patient with PsA. The different clinical cases involve PsA patients with very heterogeneous articular and extra-musculoskeletal manifestations treated with risankizumab and upadacitinib. While the therapeutic choice was mainly dictated by the need to control the most debilitating symptomatology for the patient, in all the cases the treatment with of risankizumab or upadacitinib has led to the improvement in the extramusculoskeletal manifestations of the disease as well