Akademik Veri Yönetim Sistemi
Archives of Dermatological Research, cilt.318, sa.1, 2026 (SCI-Expanded, Scopus)
Rosacea is a chronic inflammatory skin disorder characterized by persistent facial erythema and episodic inflammatory lesions and is increasingly recognized as a condition with potential systemic inflammatory and metabolic components. Adipokines, including adiponectin and leptin, are key regulators of metabolic homeostasis and immune responses and have been implicated in several chronic inflammatory conditions; however, their role in rosacea remains poorly defined. The present cross-sectional case–control study aimed to investigate serum adiponectin and leptin levels, as well as the adiponectin/leptin ratio, in patients with rosacea compared with healthy individuals. A total of 44 adult patients with clinically diagnosed rosacea and 44 healthy controls with normal body mass index were included. Individuals with metabolic syndrome, diabetes mellitus, cardiovascular disease, or other chronic inflammatory disorders were excluded to minimize potential confounding factors affecting adipokine levels. Fasting serum samples were obtained, and adiponectin and leptin concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Median serum adiponectin levels were significantly lower in patients with rosacea than in healthy controls (4.73 vs. 13.22), whereas median leptin levels were significantly higher in the rosacea group (3.29 vs. 1.46; both p < 0.001). Consequently, the adiponectin/leptin ratio was markedly reduced in patients with rosacea compared with controls (1.67 vs. 6.22; p < 0.001). Correlation analyses revealed no consistent or clinically meaningful associations between serum adipokine levels and clinical parameters. In conclusion, patients with rosacea exhibit a distinct imbalance in circulating adipokine profiles, characterized by decreased adiponectin levels and increased leptin levels. These findings indicate an association between rosacea and altered systemic inflammatory–metabolic markers. However, given the cross-sectional design, these results do not establish causality, and adipokine dysregulation should be interpreted as a correlate rather than a driver of the disease.