Introduction
As of 2018, prostate cancer (PCa) was the second leading cause of cancer
and the sixth common cause of cancer-related death in men [1].
Almost 20% of patients have locally advanced or metastatic disease at
the time of first diagnosis [2]. The primary goal in the treatment
of metastatic disease is to keep the serum androgen level below the
castration level of 50 ng/dL [3]. Medical castration with
antiandrogen- or gonadotropin-releasing hormone (GnRH) agonists and
surgical castration with bilateral orchiectomy are cornerstones of
metastatic disease management [4]. However, lowering the serum
testosterone below castration level may increase the risks of
osteoporosis, anemia, gynecomastia, erectile dysfunction, and systemic
disorders including diabetes and cardiovascular events [5,6].
Androgen deprivation affects cognitive functions in a majority of men
over 65 years of age, whereas atherosclerotic or degenerative changes
are more common. Although there are some relevant reports in the current
literature [7], further comprehensive, prospective studies are
needed to examine the effect of ADT on cognitive function. McGinty et
al. conducted one of the largest and the most up-to-date systematic
reviews, evaluating 14 studies (417 patients) and 7 cognitive domains
and concluded that cognitive functions other than visuomotor ability
remain largely unchanged [8]. Furthermore, Sun et al. conducted a
meta-analysis of androgen deprivation therapy and concluded that it does
not cause cognitive impairment [9]. However, due to the small number
of prospective studies, the debate is still open regarding the impact of
ADT on cognitive changes. Furthermore, greater age, advanced stage of
primary disease, and presence of accompanying comorbidities may worsen
underlying cognitive disorders in patients under long-term ADT.
The present study aimed to evaluate changes in cognitive functions and
depressive symptoms in men who received ADT for metastatic prostate
cancer using GnRH analogues.