The normal development and function of the prostate, as well as its patholo
gical growth, are governed by a lifelong dependency on endogenous androgens
,the majority of which are of testicular origin. In contrast to other andro
gen-sensitive tissues, androgenic effects in the prostate are only exerted
by the intracellular metabolite dihydrotestosterone.
Conflicting evidence exists regarding changes of the intracellular prostati
c androgen receptors in benign prostatic hyperplasia and prostatic carcinom
a. Equally conflicting is the clinical evidence concerning androgen metabol
ism in patients with manifest or metastatic prostate cancer. So far, there
is no clear evidence for an increased risk of prostatic neoplasia with test
osterone substitution in absolute or partial androgen deficiency. However,
in view of the high prevalence of latent prostate cancer, caution is advisa
ble.