PO:05:069 | Risankizumab efficacy in peripheral and axial involvement: monocentric experience
Abstract
Risankizumab, an anti–IL-23 monoclonal antibody, is approved for the treatment of peripheral psoriatic arthritis (PsA), and increasing evidence suggests its potential efficacy in patients with concurrent axial involvement. This study presents a preliminary monocentric real-world experience on the use of risankizumab in PsA, with clinical follow-up over six months of treatment. 34 patients with PsA treated with risankizumab at our center were included in this study. Of these, 18 had peripheral involvement only, while 16 presented both peripheral and axial involvement. Clinical assessments included DAPSA for peripheral disease, ASDAS-CRP and modified BASDAI (mBASDAI) for axial involvement. Patients were further stratified by treatment line (naïve to fourth-line) and therapy regimen (monotherapy vs. combination with methotrexate). The aim was to evaluate the evolution of clinical parameters over the course of treatment. Moreover, MRI was used to assess sacroiliac joint inflammation in patients with axial involvement. At baseline (T0), all patients underwent clinical evaluation using DAPSA, ASDAS-CRP, and mBASDAI scores, with regular follow-up assessments over six months (T6). Among the 16 patients with both peripheral and axial involvement, there was a marked improvement in ASDAS-CRP and mBASDAI scores, indicating a beneficial effect of risankizumab in reducing both axial and peripheral symptoms, as shown in the graphs. Regarding treatment lines, 8.8% of patients were treatment-naïve, while 58.8% received risankizumab as second-line, 20.6% as third-line, and 8.8% as fourth-line therapy. Risankizumab was administered in combination with methotrexate (MTX) in 70% of cases, and as monotherapy in 30%, demonstrating efficacy across both treatment regimens, including in patients with prior biologic exposure. As a representative case, MRI images from a 50-year-old female with axial PsA are included, showing marked improvement after six months of risankizumab. Our findings are consistent with current literature supporting the efficacy of risankizumab in peripheral PsA, while also offering new insights into its potential benefits for patients with concurrent axial involvement. This therapeutic effect may be attributed to the distinct pathophysiology of axial PsA (axPsA) compared to ankylosing spondylitis (AS). According to McGonagle et al., axPsA is primarily driven by ligament-centered inflammation, in contrast to the deep bone inflammation of AS. This anatomical and immunological distinction provides a mechanistic rationale for the observed clinical efficacy of IL-23 inhibitors in axPsA—despite their failure in AS—by targeting soft tissue immune responses more responsive to IL-23 modulation. Our center’s experience confirms the efficacy of risankizumab not only in peripheral PsA but also in patients with axial PsA (axPsA), showed in clinical and clinimetric indices improvement. These findings contribute valuable real-world data to the growing body of evidence supporting the therapeutic potential of risankizumab in PsA, including cases with axial involvement. 

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