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Life sciences · Journal article
Diagnostics · August 18, 2026
Early or partial results. Treat as a signal, not a conclusion.
This single-center case–control study found serum asprosin levels were nominally lower in HS patients than controls (p = 0.028), but this difference was not independent of BMI and other confounders in adjusted analyses. Asprosin showed poor discrimination (AUC 0.364) and no association with disease severity, failing to support its role as a biomarker in HS.
Single-center, case–control study. 44 patients with hidradenitis suppurativa and 44 age- and sex-matched healthy controls; single center; no additional eligibility criteria stated.. Intervention: Measurement of serum asprosin levels.. Compared with: Healthy controls matched for age and sex.. n = 88. Single center; specific geographic location not stated..
Unadjusted serum asprosin: 30.07 ± 28.15 ng/mL in HS vs. 40.94 ± 33.11 ng/mL in controls (p = 0.028) HS status not independently associated with asprorin after adjustment for BMI, smoking, metabolic syndrome, age, and sex BMI showed consistent negative association with serum asprosin across all three adjustment models
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The loss of significance after adjustment and poor discriminatory performance suggest asprosin is not useful as a diagnostic or disease severity biomarker for HS. Clinicians should not rely on this biomarker for patient assessment or monitoring.
Single-center case–control study with modest sample size and a biomarker endpoint that lost statistical significance after adjustment for confounders, offering early exploratory evidence but not sufficient to establish clinical utility.
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The loss of significance after adjustment and poor discriminatory performance suggest asprosin is not useful as a diagnostic or disease severity biomarker for HS. Clinicians should not rely on this biomarker for patient assessment or monitoring.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
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.
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