Inflammatory burden index predicts arteriogenic erectile dysfunction: a mediation analysis involving the TyG index

Inflammation and metabolic dysregulation play important roles in the pathophysiology of erectile dysfunction. The inflammatory burden index (IBI), a composite biomarker integrating C-reactive protein (CRP), neutrophils, and lymphocytes, has emerged as a marker of systemic inflammatory load. However, the association between IBI and arteriogenic erectile dysfunction (AED) remains largely unexplored. To investigate the association between IBI and AED and to examine whether insulin resistance (IR), assessed by the triglyceride-glucose (TyG) index, mediates this relationship.

In this cross-sectional study, men aged 18-65 years were consecutively recruited from the local hospital between April 2023 and November 2025. Erectile function was assessed using the 5-item International Index of Erectile Function (IIEF-5), nocturnal penile tumescence and rigidity monitoring, and penile color Doppler ultrasonography. Multivariable logistic regression models were applied to evaluate the association between IBI and AED. Receiver operating characteristic curves were used to assess the predictive performance of inflammatory markers. Mediation analysis was conducted to explore the potential mediating role of IR using the TyG index.

A total of 211 participants were included (109 AED; 102 controls). Patients with AED exhibited significantly higher inflammatory indices, including CRP, neutrophil-to-lymphocyte ratio (NLR), and IBI. In multivariable analysis, IBI remained independently associated with AED (OR = 1.626, 95% CI, 1.326-1.994, P < .001). Receiver operating characteristic analysis demonstrated that IBI achieved the highest discriminative performance among inflammatory markers (area under the curve [AUC] = 0.736), outperforming CRP and NLR. Mediation analysis revealed a significant indirect effect of TyG (β = -.1885), accounting for 24.08% of the total association between IBI and IIEF-5 scores.

Elevated IBI is independently associated with AED, and IR partially mediates this relationship, suggesting a potential inflammatory-metabolic pathway that may be involved in vascular erectile impairment, although causality cannot be established due to the cross-sectional design.