Psoriasis is a chronic systemic inflammatory disease affecting 2–3% of the population and is associated with increased cardiovascular risk. Despite the therapeutic revolution brought by biologics, which allow effective disease control in the vast majority of patients, it remains unclear whether treatment also reduces cardiovascular risk.
In this cross-sectional study, we included 80 young adults with well-controlled psoriasis (aged 30–45 years), without comorbidities, receiving five different types of therapy (topical treatment, methotrexate, adalimumab, secukinumab, guselkumab). These groups were compared with each other and with a control group of healthy individuals regarding residual systemic inflammation, endothelial function and arterial stiffness, metabolic disturbances, and hemostatic abnormalities.
Compared with controls, psoriasis patients had elevated levels of inflammatory cytokines (tumor necrosis factor (TNF), interferon-γ (IFN-γ), interleukin (IL)-1β, IL-6, IL-12p70, IL-17), while IL-23 levels did not differ. Endothelial function, arterial stiffness, and metabolic parameters were comparable between patients and controls, whereas hemostatic disturbance, reflected by an increased overall hemostatic potential (OHP), was observed in all patients but absent in controls. IL-6 and OHP were strongly associated with obesity. A Visceral Adiposity Index (VAI) threshold of 1.3 was identified, above which IL-6 levels rose markedly, indicating the pathological (inflammatory) activity of visceral adiposity. We also detected associations between depressive symptoms (assessed using the Hospital Anxiety and Depression Scale (HADS)) and inflammatory and metabolic markers (IL-6, IL-23, waist circumference, Fibrosis-4 index (FIB-4), Homeostatic Model Assessment for Insulin Resistance (HOMA-IR)).
Our findings demonstrate that residual cytokine-mediated inflammation persists in young psoriasis patients despite effective treatment. This inflammation already contributes to subtle hemostatic disturbances, particularly in the presence of obesity. The sequence—persistent inflammatory cytokines followed by hemostatic alterations—likely represents the earliest stage of atherogenesis in young but otherwise well-controlled psoriasis patients. With a subsequent rise in IL-23, which remained normal in our cohort, endothelial dysfunction, increased arterial stiffness, and insulin resistance may begin to emerge—a novel observation. Clinically, it is important to note that standard laboratory markers commonly used in daily practice (e.g., C-reactive protein, leukocyte count, D-dimer) fail to detect these subtle early changes, although their recognition would be crucial for timely therapeutic intervention.
Therefore, additional markers capable of identifying subclinical alterations are needed in young psoriasis patients. Based on our results, OHP, VAI, and IL-6 may serve this purpose. Monitoring these markers could help identify patients at increased cardiovascular risk and allow timely intensification of therapy to reduce long-term complications.
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