It has been postulated that, beside androgens, estrogens may also play
an important role in the pathogenesis of BPH. By aromatase inhibitors
the formation of estrogens out of androgens can be inhibited selectiv
ely and the effect of estrogen deprivation on BPH can be investigated
for the first time. Within a phase II-study, men with a symptomatic BP
H were treated with the aromatase inhibitor MADD (1-methyl-androsta-1,
4-diene-3,17-dione) (200 mg p.o. t.i.d.). After 3 months of treatment
4 patients with unchanged symptoms had an open prostatectomy and these
BPH specimens were investigated histologically as well as immunohisto
chemically. Results were compared to data obtained in the histologic s
ections of 11 men with untreated BPH. After MADD-treatment, androgen-r
eceptor concentration was lowered slightly in epithelial cells and ext
ensively in stromal cells. In addition, it appeared that estrogen rece
ptors were reduced after estrogen deprivation. On the other hand, in t
hose MADD pretreated prostates the proliferation rate was higher in ep
ithelium (0.200 % vs. 0.121 %) and slightly lower in stroma (0.095 vs.
0. 120 %) compared to untreated BPH. By morphometric assessment, howe
ver, no difference was seen between both patient groups. In conclusion
, the aromatase inhibitor-induced estrogen deprivation seems to have a
n inhibitory influence on prostatic stroma and it may well be that BPH
is affected via a suppression of androgen receptors. Whether or not t
hese observed changes may cause an improvement of symptoms in BPH pati
ents remains unclear, especially as the morphometric analysis did not
reveal any differences between MADD-treated and untreated prostates.