IL-6 as an integrative biomarker of residual inflammation and visceral adiposity in psoriasis: a VAI threshold-dependent model.

Psoriasis patients had significantly higher serum IL-6 levels compared to healthy controls.

• Serum IL-6 was 38.1 pg/mL [35.5-41.3] in psoriasis patients versus 21.4 pg/mL [19.5-33.4] in controls (p<0.001).
• The study included 80 patients with well-controlled skin disease and 20 matched healthy controls.
• IL-6 was measured by ELISA.
• The study design was cross-sectional.

A distinct VAI threshold of 1.3 was identified, above which IL-6 levels rose steeply in a non-linear pattern.

• IL-6 levels rose steeply between VAI 1.3 and VAI 2.2, after which they plateaued.
• Visceral adiposity was estimated using the Visceral Adiposity Index (VAI).
• The threshold-dependent dynamic was described as a 'clinically meaningful inflection point.'
• The non-linear amplification of IL-6 occurred specifically once visceral adiposity exceeded the critical VAI threshold of 1.3.

Patients with VAI ≥1.3 had markedly higher IL-6 and pro-inflammatory cytokines than those below this cutoff.

• The VAI cutoff of 1.3 distinguished two groups with distinct inflammatory profiles.
• Pro-inflammatory cytokines were elevated in the higher VAI group alongside IL-6.
• This finding supports the VAI threshold as a meaningful stratification tool for inflammatory burden in psoriasis.

Random forest regression identified IFN-γ, IL-1β, IL-12p70, and IL-17 as dominant predictors of IL-6 levels.

• Random forest regression was used to identify predictors of IL-6 among measured variables.
• HbA1c, FIB-4, and treatment contributed minimally to IL-6 prediction.
• These findings indicate that IL-6 elevation in psoriasis primarily reflects cytokine-driven residual inflammation rather than metabolic or treatment factors.

Psoriasis patients in this study were characterized by well-controlled skin disease yet displayed residual inflammation and visceral adiposity.

• The study specifically enrolled patients with 'well-controlled skin disease,' suggesting inflammatory elevation was not driven by active cutaneous disease.
• Residual inflammation and visceral obesity were identified as two factors that 'synergistically increase cardiometabolic risk' in psoriasis.
• The cross-sectional study included 80 psoriasis patients and 20 matched healthy controls.