Pro-Inflammatory Synergy Between IL-17, IL-1 and Hyperuricemia in Psoriatic Arthritis: Clinical Implications of a...

Background: Hyperuricemia is a prevalent comorbidity in psoriatic arthritis (PsA), yet its influence on the IL-1α/IL-17 cytokine balance remains unexplored. We aimed to characterize serum IL-1α and IL-17 profiles in PsA stratified by hyperuricemia status and to compare these with patients with hyperuricemia without psoriatic disease (HU). Methods: This cross-sectional study included 34 consecutively recruited PsA patients (19 hyperuricemic, 15 normouricemic) and 30 HU controls. Serum IL-1α and IL-17 were measured by ELISA. The PsA cohort was stratified by hyperuricemia status, cutaneous psoriasis, disease pattern, obesity grade, hypertension, sex, and enthesitis. Between-group comparisons used Mann-Whitney U and Kruskal-Wallis tests with Bonferroni-corrected post hoc analyses. Bivariate associations were assessed using Spearman's rank correlation. Results: Within the PsA cohort, hyperuricemic patients had significantly lower IL-17 than normouricemic patients (31.1 ± 15.7 vs. 49.5 ± 25.3 pg/mL; p = 0.01), while IL-1α did not differ significantly (37.3 ± 11.7 vs. 34.0 ± 8.19 pg/mL; p = 0.24). No correlation was observed between IL-1α and IL-17 (ρ = -0.05), indicating independent immunological axes. In the three-group comparison, IL-17 differed significantly across PsA-normouricemic, HU, and PsA-hyperuricemic subgroups (p = 0.022), whereas IL-1α was comparable across all three groups (p = 0.584). None of the traditional clinical classifications-disease pattern, cutaneous psoriasis, or sex-were significantly associated with either cytokine. Conclusions: Hyperuricemia was associated with significantly lower circulating IL-17 in PsA without a corresponding change in IL-1α levels, and this association appeared more pronounced within the inflammatory context of psoriatic disease than in hyperuricemia alone. These exploratory findings suggest that metabolic factors may play a role in defining the immunological profile of PsA and warrant prospective validation in larger cohorts. Owing to the cross-sectional design, this study does not allow inference of causal relationships between hyperuricemia and cytokine alterations.