Exocrine Pancreatic Function in Erectile Dysfunction: A Prospective Study Based on Fecal Elastase Measurement

Objectives: Exocrine pancreatic function, assessed via fecal pancreatic elastase (FPE), could contribute to the pathophysiology of erectile dysfunction (ED); however, supporting evidence is limited.The present study aimed to prospectively evaluate FPE levels in men and investigate the association between exocrine pancreatic insufficiency (EPI) and erectile function.Methods: This prospective observational study was carried out between June and August 2025 at the urology outpatient clinic of the hospital.Male patients aged between 40 and 65 years presenting with any complaint were enrolled.Erectile function was assessed using the International Index of Erectile Function-5 (IIEF-5).Stool samples were analyzed for FPE by ELISA.Demographic, clinical, and laboratory data were collected.Group comparisons were performed using non-parametric tests, and predictors of erectile function were assessed with multivariate regression.Results: A total of 153 patients were included.Median FPE levels demonstrated nominal variation across erectile function groups (p=0.048,Kruskal-Wallis), yet no statistically significant post-hoc differences after Bonferroni correction.Multivariate regression analysis revealed that diabetes mellitus (=-0.234,p=0.016) and hypertension (=-0.167,p=0.040) were independent negative predictors of erectile function, whereas FPE (=0.184,p=0.017) was a positive predictor.Other variables, including age, BMI, testosterone, and prolactin, did not significantly contribute. Conclusions:To our knowledge, this is one of the first studies to explore the link between exocrine pancreatic function and ED.Findings suggest that preserved pancreatic exocrine function may be beneficial for erectile health, while diabetes and hypertension remain major negative determinants.Exocrine pancreatic function deserves further investigation as a potential diagnostic and therapeutic target in the multifactorial management of ED.