ArticleClinical rheumatology2026
Phenotype-treatment dissociation in psoriatic and nonpsoriatic peripheral spondyloarthritis: a propensity score-matched analysis with novel treatment intensity metrics.
Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo 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.
methodsWe 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.
resultsAt 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.
conclusionPsoriasis 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.
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