Metabolic parameters, insulin resistance surrogates, and Peyronie's disease: a cross-sectional analysis of disease presence and curvature severity.

METHODS: This retrospective, cross-sectional study included 317 adult men, comprising 123 patients diagnosed with PD and 192 control subjects without clinical evidence of PD. Demographic data, body mass index (BMI), comorbidities, and fasting laboratory parameters (glucose, total cholesterol, LDL, HDL, and triglycerides) were collected. TG/HDL ratio and TyG index were calculated using established formulas. Between-group comparisons were performed using Mann-Whitney U and chi-square or Fisher's exact tests, with false discovery rate correction for multiple comparisons. Multivariable binary logistic regression analysis was conducted to identify independent predictors of PD presence. Within the PD cohort, associations between penile curvature degree and metabolic parameters were evaluated using Spearman's correlation analysis. RESULTS: Patients with PD had a significantly lower median BMI compared to controls (25.0 vs. 27.3 kg/m², p < 0.001). LDL-cholesterol and total cholesterol levels were lower in the PD group on univariable analysis; however, these differences did not remain significant after correction for multiple testing. No significant differences were observed between groups for fasting glucose, triglycerides, HDL, TG/HDL ratio, or TyG index. In multivariable analysis, BMI emerged as the only independent predictor of PD presence (OR 0.83 per kg/m² increase, 95% CI 0.76-0.90; p < 0.001). No metabolic parameter, including insulin resistance surrogates, was independently associated with PD. Among PD patients, penile curvature degree showed no significant correlation with BMI, lipid profile components, TG/HDL ratio, or TyG index. CONCLUSIONS: In this cohort, BMI - but not lipid profile components or insulin resistance surrogate markers - was independently associated with the presence of Peyronie's disease, while metabolic factors were not related to curvature severity. These findings suggest that systemic metabolic dysregulation may play a limited role in PD development and phenotypic expression, highlighting the importance of local tissue-specific mechanisms in disease pathogenesis.