KIU Publications

Emerging evidence indicates that the prostate, liver, and immune system are linked through common molecular and cellular pathways that influence disease development beyond organ-specific boundaries. Traditionally, benign prostatic hyperplasia (BPH) has been viewed as an isolated urological condition of aging males, while hepatotoxicity is considered a consequence of toxic exposures and metabolic stress. However, systemic inflammation, immune dysregulation, metabolic alterations, and redox imbalance contribute to both prostate enlargement and liver injury. Shared mechanisms include chronic low-grade inflammation, cytokine networks, oxidative stress, influence of metabolic syndrome, gut–liver–prostate interactions, and roles of innate and adaptive immunity. Understanding the prostate–liver–immune axis provides a unified framework to explain overlapping risk factors and comorbidities, with implications for early diagnosis, integrated therapeutic strategies, and biomarker discovery. Addressing systemic inflammatory drivers rather than isolated organ pathology may improve outcomes in patients with co-existing BPH and liver dysfunction.