# Association Between Inflammatory Cytokines and Systemic Inflammation Indices in Patients With Psoriasis: A Cross‐Sectional Study

## TL;DR

This study explores how blood-based inflammation markers relate to cytokine levels in psoriasis patients, finding that some indices like SIRI are consistently elevated.

## Contribution

The study provides novel insights into the relationship between CBC-derived inflammation indices and cytokine levels in psoriasis patients.

## Key findings

- Psoriasis patients had higher cytokine levels and elevated SIRI compared to controls.
- SIRI and PIV showed the most consistent co-variation with cytokines, though associations were modest.
- Findings suggest the need for larger studies to validate CBC-derived indices as markers of psoriasis inflammation.

## Abstract

Systemic inflammation indices derived from complete blood counts (CBC) are accessible markers of inflammatory burden, but their relationship with circulating cytokines in psoriasis remains unclear. We investigated associations between CBC‐derived indices and serum cytokines in psoriasis.

In this cross‐sectional study, we included 28 patients with psoriasis and 23 healthy controls. Serum IL‐17, IL‐22, IL‐23, IL‐31, IL‐33, IL‐36, TNF‐α, TGF‐β, and IFNγ were quantified by ELISA. CBC‐derived indices were computed (neutrophil‐to‐lymphocyte ratio (NLR), platelet‐to‐lymphocyte ratio (PLR), systemic immune‐inflammation index (SII), systemic inflammation response index (SIRI), and pan‐immune‐inflammation value (PIV). Case–control comparisons used the full sample. Cytokine–index associations were evaluated in psoriasis patients using bivariate correlations and multivariate GLM adjusted for age, smoking, and NAFLD. Multiplicity was controlled using Benjamini–Hochberg false discovery rate (BH‐FDR); prespecified sensitivity analyses used log‐transformed cytokines and Spearman correlations.

Psoriasis patients had higher levels of all cytokines (all p < 0.001) and higher SIRI versus controls (p < 0.001; q = 0.005). PIV showed a nominal case–control difference (p = 0.022) that did not remain significant after BH‐FDR (q = 0.055), while NLR, PLR, and SII did not differ. In adjusted multivariate GLM, TGF‐β showed a global association with the joint set of indices (Pillai's trace = 0.295; p = 0.039) that did not survive BH‐FDR (q = 0.507) and was attenuated with log‐transformation. Nominal univariate effects for TNF‐α on SIRI (F = 4.600; p = 0.039) and PIV (F = 5.660; p = 0.023) did not remain significant after BH‐FDR.

SIRI was consistently elevated in psoriasis, whereas PIV showed a nominal difference versus controls. Across exploratory analyses, SIRI and PIV showed the most consistent directional co‐variation with cytokines, but associations were modest. These findings are hypothesis‐generating and support further validation in larger cohorts to determine whether CBC‐derived indices can serve as scalable adjunct markers of inflammatory activity in psoriasis.