INTRODUCTION
Psoriatic arthritis (PsA) is a debilitating inflammatory arthropathy and a major long-term complication of psoriasis, affecting up to 30% of patients.1 Although the mechanistic link between cutaneous psoriasis and PsA is not fully elucidated, both conditions are mediated by dysregulated immune signaling, prominently involving the IL-23/IL-17 axis and downstream proinflammatory cytokines.2 Emerging evidence suggests that systemic therapies for psoriasis may differentially influence the subsequent development of PsA, underscoring the clinical importance of treatment selection in patients at risk.3-5
Psoriasis is a chronic immune-mediated inflammatory disease driven by adaptive immune pathways, particularly those involving IL-23 and IL-17.2,6 IL-23 signaling activates the tyrosine kinases JAK2 and TYK2, leading to STAT3 phosphorylation and induction of the transcription factor RORγt, which promotes Th17 cell differentiation and IL-17 cytokine production.7-10 IL-17 and IL-23 inhibitors have become cornerstone therapies for moderate-to-severe psoriasis, while JAK inhibitors represent an additional systemic option.1,11 Notably, JAK inhibitors are also widely used in inflammatory joint diseases, raising the possibility that they may confer benefit in preventing or delaying PsA, albeit with potentially less robust cutaneous efficacy.12 In current clinical practice, JAK inhibitors are typically reserved after inadequate response or intolerance to conventional disease-modifying antirheumatic drugs.13
Determining how different systemic therapies influence the risk of developing PsA is essential for optimizing psoriasis management. While prior studies have examined to a degree the comparative efficacy of IL-17 and IL-23 inhibitors, the relative impact on PsA risk remains poorly characterized.1,11,14 To address this knowledge gap, we conducted a retrospective 5-year outcomes study evaluating incident PsA among patients
Psoriasis is a chronic immune-mediated inflammatory disease driven by adaptive immune pathways, particularly those involving IL-23 and IL-17.2,6 IL-23 signaling activates the tyrosine kinases JAK2 and TYK2, leading to STAT3 phosphorylation and induction of the transcription factor RORγt, which promotes Th17 cell differentiation and IL-17 cytokine production.7-10 IL-17 and IL-23 inhibitors have become cornerstone therapies for moderate-to-severe psoriasis, while JAK inhibitors represent an additional systemic option.1,11 Notably, JAK inhibitors are also widely used in inflammatory joint diseases, raising the possibility that they may confer benefit in preventing or delaying PsA, albeit with potentially less robust cutaneous efficacy.12 In current clinical practice, JAK inhibitors are typically reserved after inadequate response or intolerance to conventional disease-modifying antirheumatic drugs.13
Determining how different systemic therapies influence the risk of developing PsA is essential for optimizing psoriasis management. While prior studies have examined to a degree the comparative efficacy of IL-17 and IL-23 inhibitors, the relative impact on PsA risk remains poorly characterized.1,11,14 To address this knowledge gap, we conducted a retrospective 5-year outcomes study evaluating incident PsA among patients
