Testosterone and PSA Dynamics in Benign Prostatic Hyperplasia and Prostate Cancer: Evidence from Patients at Lagos University Teaching Hospital, Nigeria

Introduction: Prostatic diseases, including prostate cancer (CAP) and benign prostatic hyperplasia (BPH), are prevalent pathologies in ageing men. While prostate-specific antigen (PSA) is a well-established diagnostic marker, the role of serum testosterone in distinguishing between these conditions remains a subject of debate. This study examines the dynamics of serum testosterone and PSA levels to determine their clinical utility in distinguishing between CAP, BPH, and healthy control subjects within a Nigerian population. Aim: The major goal of this study was to compare the mean serum PSA and testosterone levels among patients with prostate cancer, benign prostatic hyperplasia, and a healthy control group to assess their discriminatory power. Methods: This cross-sectional hospital-based study was conducted at Lagos University Teaching Hospital (LUTH), Idi-Araba, Lagos, Nigeria and included 70 patients with CAP, 68 patients with BPH, and 69 healthy control subjects. Serum levels of total PSA and total testosterone were measured for each participant. Independent-samples t-tests were used to compare mean PSA and testosterone levels across the three groups. A p-value of <0.05 was considered statistically significant. Results: A statistically significant difference in mean PSA levels was observed across all pairwise comparisons: The Control 1.22±0.68 < BPH 15.13±9.49 < CAP 59.42±55.36. The testosterone levels in both the CAP (18.02±8.87 nmol/L) and BPH (16.78±8.36 nmol/L) groups were significantly higher than those in the control group (10.52±8.79 nmol/L) (all p<0.001). Crucially, there was no significant difference in mean testosterone levels between the CAP and BPH groups (p = 0.399). Conclusion: Total PSA remains a robust biomarker for differentiating between prostate cancer, BPH, and healthy subjects. In contrast, total serum testosterone, while elevated in patients with prostatic disease compared to controls, lacks the discriminatory power to distinguish between benign prostatic hyperplasia and prostate cancer. This suggests that total testosterone should not be used as a standalone marker for differentiating these conditions in this population.