Serum Asprosin Levels in Patients with Hidradenitis Suppurativa: A Case–Control Study

Background: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease involving complex interactions between inflammatory and metabolic pathways. Asprosin is a glucogenic adipokine involved in glucose homeostasis, which has been investigated in relation to obesity, insulin resistance, and inflammatory processes. This study aimed to evaluate serum asprosin levels in patients with HS and to investigate their associations with disease severity and selected metabolic and inflammatory characteristics. Methods: This single-center, case–control study included 44 patients with HS and 44 age- and sex-matched healthy controls. Sociodemographic, clinical, anthropometric, metabolic, and inflammatory parameters were recorded. Serum asprosin levels were measured using an enzyme-linked immunosorbent assay, while disease severity was assessed using Hurley staging and the International Hidradenitis Suppurativa Severity Score System (IHS4). Multivariable regression analyses were performed using log-transformed asprosin concentrations to evaluate the independent association between HS status and serum asprosin after adjustment for relevant metabolic and lifestyle-related factors. Results: Serum asprosin levels were significantly lower in patients with HS than in healthy controls in the unadjusted analysis (30.07 ± 28.15 vs. 40.94 ± 33.11 ng/mL, respectively; p = 0.028). However, HS status was not independently associated with serum asprosin levels after adjustment for BMI, smoking status, metabolic syndrome, age, and sex or after adjustment for BMI, smoking status, fasting glucose, triglycerides, and HDL cholesterol. Additionally, BMI showed a consistent negative association with serum asprosin levels across all three models. Serum asprosin was not significantly associated with Hurley stage, IHS4 score, or metabolic syndrome, and ROC analysis demonstrated poor discriminatory performance of serum asprosin, with an area under the curve of 0.364, a sensitivity of 43.2%, and a specificity of 38.6%. Conclusions: Serum asprosin levels were lower in patients with HS than in healthy controls in the unadjusted analysis; however, this difference was not independently associated with HS after adjustment for relevant confounding factors. The absence of associations with disease severity and the poor discriminatory performance in ROC analysis do not support serum asprosin as a diagnostic or disease severity biomarker for HS. Thus, further prospective and mechanistic studies are required to clarify the biological significance of altered asprosin levels in HS.