Impact of leuprolide and goserelin on androgen suppression and adverse events in patients with prostate cancer.

Androgen deprivation therapy (ADT) is widely employed in the management of advanced prostate cancer, with luteinizing hormone-releasing hormone (LHRH) agonists such as leuprolide and goserelin being common options. However, pharmacological and metabolic differences between these agents may affect the efficacy of hormonal suppression and adverse event profiles. This study compared the effects of leuprolide (22.5 and 45 mg) and goserelin (10.8 mg) on prostate-specific antigen (PSA) and testosterone reduction, as well as their metabolic and cardiovascular impacts and the influence of genetic variants on therapeutic response. A prospective, randomized, controlled study was conducted with 174 patients diagnosed with prostate cancer and treated with ADT for 12 months. Serum PSA and testosterone levels, lipid and glycemic profiles, and adverse events were monitored. Genetic analyses were performed to identify mutations in the TP53, BRCA1, BRCA2, and ATM genes. All treatment groups exhibited significant reductions in PSA and testosterone levels. Leuprolide 22.5 mg achieved the most pronounced PSA reduction, whereas goserelin 10.8 mg demonstrated greater variability in testosterone during the early months of therapy. Hot flashes were the most frequent adverse event, reported in 90% of patients treated with leuprolide 22.5 mg, while cardiovascular events were more prevalent in the goserelin 10.8 mg group. The TP53 gene was the most frequently altered (20.4%), followed by BRCA2 (7.4%) and ATM (6.5%), though these mutations did not significantly affect treatment response. ADT effectively achieves hormonal suppression in prostate cancer; however, differences between LHRH agonists influence clinical and metabolic outcomes. Leuprolide 22.5 mg showed superior PSA reduction but higher rates of vasomotor symptoms and weight gain, while goserelin 10.8 mg was associated with hormonal instability and cardiovascular risk. Genetic findings suggest that BRCA2 variants may affect lipid metabolism, reinforcing the need for personalized ADT strategies integrating metabolic and genetic profiles.