It has been established that women who undergo hysterectomy, even in cases where the ovaries are preserved, frequently experience premature ovarian insufficiency syndrome, which can lead to various endocrine and metabolic disorders. A comparable inquiry emerges in the context of radical prostatectomy (RP) in males: whether the extraction of the prostate gland itself influences testicular function and the emergence of polymetabolic disorders in the absence of androgen deprivation therapy (ADT).

Radical prostatectomy has been recognized as an effective treatment for localized prostate cancer (PCa), providing high survival rates for patients diagnosed with this disease. The primary focus of specialists in this field has historically centered on the surgical consequences of RP, such as erectile dysfunction and stress urinary incontinence. However, mounting evidence suggests that prostate removal itself can also result in a transient decrease in testosterone levels, manifesting as biochemical or manifest hypogonadism, along with moderate metabolic disturbances, though not to the same extent as observed with adjuvant hormone therapy. In some cases, patients already in the preoperative period may have risk factors for metabolic syndrome, osteopenia, and other perioperative complications, which makes it difficult to objectively assess the direct effect of RP. A more profound comprehension of the pathophysiologic mechanisms underlying these changes appears to be a pivotal element in facilitating timely diagnosis, prevention, and treatment of potential endocrine-metabolic complications associated with RP.