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Evaluation of the Relationship Between the Pan-Immune-Inflammation Score and the Systemic Immune-Inflammation Index
Safiye Kübra Çetindağ Karatlı1,2, Ebru Uğraş1,2, Erhan Şimşek1,2
1Department of Family Medicine, Ankara Yıldırım Beyazıt University, Ankara 06760, Türkiye.
Abstract:
Background: Inflammation is believed to play a significant role in the pathophysiology of hypertension (HT). The aim of this study was to evaluate the relationship between the systemic immune-inflammation index (SII) and the pan-immune-inflammation value (PIV) and HT in adults. Methods: A total of 1060 adult individuals who presented between 1 December 2025 and 1 February 2026, were included. Participants were grouped according to the presence of HT. SII and PIV were calculated. Univariate and multivariate logistic regression analyses were performed to identify factors independently associated with HT. Due to the high correlation between SII and PIV, they were evaluated in separate models. Discriminatory performance was examined using ROC analysis, and correlations were assessed using the Spearman test. Results: HT was present in 18.1% of participants. In the HT group, SII and PIVs were significantly higher (p < 0.001 for both). In univariate analysis, older age (p < 0.001), male gender (p = 0.030), presence of comorbidities (p < 0.001), high SII (p < 0.001), and high PIV (p < 0.001) were found to be associated with HT. In multivariate analyses, age and comorbidities remained independent predictors in both models (all p < 0.001). In the multivariable models adjusted for available covariates, high SII was significantly associated with HT in the SII model (adjusted OR: 2.035; 95% CI: 1.374-3.010; p < 0.001). Similarly, high PIV was significantly associated with HT in the PIV model (adjusted OR: 5.577; 95% CI: 3.398-9.160; p < 0.001). In the ROC analysis, both indices demonstrated modest predictive ability, with PIV showing slightly higher performance compared to SII (AUC: 0.648 vs. 0.623). A positive correlation was observed between the duration of HT and both SII (r = 0.700; p < 0.001) and PIV (r = 0.847; p < 0.001). Conclusions: The finding that SII and PIV were significantly associated with HT after adjustment for available covariates supports the potential role of systemic inflammation in the pathophysiology of HT. These indices, which can be easily calculated from routine laboratory parameters and do not require additional costs, may potentially assist in risk assessment in clinical practice.
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