Phenotype-treatment dissociation in psoriatic and nonpsoriatic peripheral spondyloarthritis: a propensity score-matched analysis with novel treatment intensity metrics.

OBJECTIVE: To compare the clinical phenotype, treatment intensity, and outcomes of psoriatic arthritis (PsA) and nonpsoriatic peripheral spondyloarthritis (pSpA) using propensity score-matched real-world data and reproducible quantitative metrics of therapeutic escalation. METHODS: We analyzed a single-center cohort of 204 patients with peripheral SpA. Treatment trajectories were reconstructed line-by-line to derive three metrics: the composite intensity score (maximal escalation), the cumulative treatment burden (total pharmacologic exposure), and the biologic line index (timing of biologic initiation). PsA and pSpA were compared using 1:1 PSM with 12 covariates. RESULTS: At baseline, PsA exhibited a more inflammatory phenotype, with higher frequencies of dactylitis, small-joint involvement, inflammatory back pain, and erosive damage, whereas pSpA displayed a large-joint, lower-limb-predominant pattern. Unmatched biologic exposure was higher in PsA (32.1% vs. 6.1%). After matching, PsA received significantly more intensive therapy: higher cumulative treatment burden (p = 0.002), greater maximal treatment intensity (p = 0.003), and earlier biologic initiation (HR 0.28, log-rank p = 0.003). DAS28-CRP-defined peripheral inflammatory outcomes did not differ between PsA and pSpA (remission 79% vs. 84%, p = 0.773; last-visit DAS28-CRP values were similar). Findings persisted across doubly robust regression and overlap weighting. Among pSpA patients (60% ASAS-positive and 40% ASAS-negative), ASAS subgroups showed similar DAS28-CRP-defined peripheral inflammatory outcomes and treatment patterns. CONCLUSION: Psoriasis shaped phenotype and treatment behavior in peripheral SpA but was not associated with different DAS28-CRP-defined peripheral inflammatory outcomes. Nonpsoriatic pSpA received less intensive treatment escalation despite similar clinical outcomes, highlighting the need to evaluate tailored therapeutic approaches. Key Points • PsA and nonpsoriatic pSpA are phenotypically distinct but can reach similar DAS28-CRP-defined outcomes. • Treatment escalation differed despite comparable peripheral inflammatory control. • ASAS classification status did not separate nonpsoriatic pSpA patients by treatment intensity in this cohort. • Nonpsoriatic pSpA needs evidence tailored to its own clinical pathway.