Fibroblast Growth Factor 23 and Placental Growth Factor in Patients with Psoriasis and their Relation to Disease Severity

Abstract

Purpose. Psoriasis is an immune-mediated skin disease characterised by accentuated keratinocyte proliferation, hyperkeratinisation, leukocyte and T-lymphocyte chemotaxis, and neoangiogenesis. Chronic inflammation, imbalance between pro-and anti-inflammatory cytokines, and many angiogenic mediators has been implicated in the disease etiopathogenesis. The aim of this study was to investigate whether psoriasis is related to fibroblast growth factor 23 (FGF23) and placental growth factor (PLGF)-mediators related to insulin resistance (IR), metabolic syndrome, and atherosclerosis. Materials and Methods. Forty five patients with plaque type psoriasis and forty five healthy controls were included in the study. Serum FGF23 and PLGF concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Results. Mean homeostasis model assessment (HOMA-IR) values and serum levels of insulin, FGF23 and PLGF, in patients with psoriasis were found to be higher than those of in healthy controls (p= 0.001, p= 0.001, p= 0.001 and p= 0.003 respectively). Psoriasis area and severity index (PASI) score correlated significantly with PLGF levels (p= 0.039). There was a significant positive correlation between FGF23 and PLGF (p< 0.001). CRP was significantly correlated with BMI (p= 0.019), glucose (p= 0.017), TC (p= 0.043), TG (p= 0.003), and VLDL-C (p= 0.004) in patients with psoriasis. Conclusion. Increased serum FGF23 and PLGF levels and the presence of positive correlation between PLGF and PASI score probably reflects the inflammatory state and IR seen in psoriasis. Above mentioned correlations provide rationale for possible application of serum FGF23 and especially of PLGF measurements as biomarkers of disease severity, which could be useful for management of treatment efficacy.