Related Experiment Video
Updated: Jan 11, 2026
An R-Based Landscape Validation of a Competing Risk Model
Published on: September 16, 2022
Inflammatory index-based nomogram for risk stratification of erectile dysfunction: a cross-sectional study with
Zhaokun Shi1, Yixin Zhang1, Shanjin Ma2
1Department of Urology, Xijing Hospital, Air Force Medical University, Xi'an, China.
Background:
Erectile dysfunction (ED) diagnosis primarily relies on subjective assessments (e.g., international index of erectile function-5), lacking objective biomarkers tied to its inflammatory pathophysiology. This study had three core objectives: (I) to analyze the associations between neutrophil-lymphocyte ratio (NLR) and lymphocyte-monocyte ratio (LMR) with ED; (II) to construct and validate a Least Absolute Shrinkage and Selection Operator (LASSO) regression-derived nomogram for ED risk prediction; (III) to clarify causal relationships between immune phenotypes, inflammatory cytokines, and ED via bidirectional Mendelian randomization (MR).
Methods:
Using National Health and Nutrition Examination Survey (NHANES) data (2001-2004; n=3,082), we analyzed NLR and LMR associations with ED, constructed a LASSO regression-derived nomogram, validated it internally [receiver operating characteristic (ROC) analysis] and externally in a Chinese cohort (n=9,161), and performed bidirectional MR on Genome-Wide Association Study (GWAS) data (731 immunophenotypes/91 cytokines).
Results:
Elevated NLR increased ED risk [odds ratio (OR) =1.15, 95% confidence interval (CI): 1.06-1.24, P=0.001], whereas higher LMR was protective (OR =0.93, 95% CI: 0.87-0.99, P=0.03). The 8-predictor nomogram (NLR/LMR included) achieved superior discrimination in NHANES [area under the curve (AUC) 0.8553 vs. 0.6101 for NLR alone] and the Chinese validation cohorts (AUC 0.7648). MR identified 25 ED-associated immunophenotypes, with C-C motif chemokine 23 (CCL23) elevating risk (β=0.13, P=0.03) and interleukin-8 (IL-8) conferring protection (β=-0.19, P=0.02), indicating divergent inflammatory mechanisms.
Conclusions:
This study pioneers an inflammation-driven ED nomogram for objective risk stratification, validated across dual cohorts. It also reveals cytokine-specific inflammatory pathways in ED pathogenesis, laying a foundation for personalized ED screening and targeted therapeutic development.
