ArticleFrontiers in endocrinology2025
Cross-sectional and longitudinal associations between pan-immune-inflammation value and serum uric acid.
Article in Frontiers in endocrinology, 2025. 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
Background: Elevated serum uric acid (SUA) correlates with inflammation, but the pan-immune inflammation value (PIV)-a novel integrated inflammatory marker-has not been explored in relation to SUA. We investigated cross-sectional and longitudinal PIV-SUA associations. Methods: We analyzed 5,766 participants aged ≥60 years from a 2018 cardiovascular examination cohort with 2022 follow-up. The PIV was calculated as neutrophil number × platelet number × monocyte number/lymphocyte number, with cell counts expressed as ×1000 cells/μL. Hyperuricemia was defined as SUA concentrations ≥ 420 μmol/L (7 mg/dL) in males and ≥ 360 μmol/L (6 mg/dL) in females. Cross-sectional associations were assessed via multivariate linear/logistic regression; longitudinal associations via Cox regression. Results: At baseline, hyperuricemia prevalence was 22.4% among 5,766 participants (mean age 68.5 years). Restricted cubic spline showed a nonlinear PIV-SUA relationship. In fully adjusted models, each 1-SD PIV increase associated with higher SUA (β ± SE: 3.7 ± 1.1; P<0.0001). PIV quartiles (vs. lowest) showed β values: Q2 = 7.5, Q3 = 6.7, Q4 = 12.5 (P trend<0.001). Logistical regression revealed each 1-SD PIV increase linked to higher hyperuricemia risk (OR = 1.12, 95%CI 1.05-1.29; P = 0.0003). PIV quartiles (vs. lowest) had ORs: Q2 = 1.27, Q3 = 1.23, Q4 = 1.54 (P trend<0.001). Over 4-year follow-up, Cox regression indicated a J-curve relationship between PIV and SUA/hyperuricemia, with the lowest risk at PIV quartile 2. Conclusions: PIV showed a nonlinear relationship with serum uric acid and hyperuricemia in cross-sectional analyses, while exhibiting a J-curve relationship in longitudinal studies. These suggest dynamic interactions between inflammatory markers and uric acid metabolism, dependent on inflammation duration.
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