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Updated: Jan 7, 2026

Author Spotlight: Integrated Multi-Omics Analysis for Unveiling Multicellular Immune Signatures in Clinical Heart Attack Cohorts
Published on: September 20, 2024
Cross-sectional and longitudinal associations between pan-immune-inflammation value and serum uric acid
Zi-Long Lu1, Rui Chu2, Ling-Meng Wang1
1Department of Cardiovascular Medicine, Center for Epidemiological Studies and Clinical Trials and Center for Vascular Evaluation, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
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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