Re: BPH story of a PCa patient

Hi Ron,
The question of Proscar (finasteride) reducing PSA by 50% has confused
many. That included me for a number of years until I did some research
on that matter. Finasteride was developed by Merck to treat BPH. Since
BPH and PCa are two diseases that could cause a PSA elevation and those
prostate conditions can and do coexist in many males, Merck promoted
studies known as The Finasteride Group Study to ensure that men treated
with finasteride for BPH would not be at increased risk of PCa by
having reduced levels of PSA. In other words, Merck wanted to ensure
that a man treated for BPH would have a biopsy triggered if his PSA
exceeded 2.0 ng/ml and had no claim against them for masking their PSA
with Finasteride.

In those studies, men treated with Proscar for prostate enlargement
experienced a blood serum PSA reduction of approximately 50%. There is
ample evidence that this PSA reduction is related to a reduction in
gland volume (maximized by one year of treatment) caused by cell death
and reduced cell proliferation. In other words, the PSA reduction is
not an artifact causing a masking effect on the measuring test, but
simply an effect caused by definitive biological factors induced by the
inhibition of DHT.

JE Damber and coworkers in Sweden showed that finasteride treatment
decreases VEGF expression in the human prostate. Vascular endothelial
growth factor (VEGF) is a potent regulatory factor of angiogenesis in
human prostate tissue. Also Wang and coworkers at New York University
demonstrated that the level of androgen receptor was dramatically
decreased in the cells treated with finasteride.

Merck's action to demonstrate that the use of finasteride in BPH does
not result in an impairment of prostate cancer detection by a 50%
reduction in PSA level has caused much confusion when the product is
used off label in someone diagnosed with PCa. The PSA reduction is real
and caused by the action of Proscar in inhibiting DHT, VEGF expression
and down regulation of the androgen receptor and not by a PSA masking
effect without a direct biological effect on androgen dependent cancer
cells. In other words, in such PCa patients, PSA results are what they
are and need not to be doubled.

Best regards,

RalphV

Sources:

Damber JE et al. Effects of finasteride on vascular endothelial growth
factor. Scand J Urol Nephrol 2002;36(3):182-7


Wang LG et al Down-regulation of prostate-specific antigen expression
by
finasteride through inhibition of complex formation between androgen
receptor and steroid receptor-binding consensus in the promoter of the
PSA gene in LNCaP cells.
Cancer Res 1997 Feb 15;57(4):714-9



ron wrote:
ralphv_in_az@xxxxxxxxx wrote...snip...
The doubling of PSA to avoid missing a diagnosis of PCa when treating a
patient with BPH does not apply in the case under discussion.

Hi Ralph...I thought that anyone taking a 5-AR inhibitor, whether they
have PCa or not, should double their PSA value to get a "true"
(non-medicated) PSA reading. Am I understanding you to say that men
with PCa using 5-AR inhibitors need not do this "doubling"? Are you
saying that, in such cases of men with PCa using finasteride or
dutasteride, the tumor kill and prostate shrinkage due to the 5-AR
inhibitor use is what is causing the PSA to fall to half of the
pre-5-AR inhibitor value?..Ron

.

Relevant Pages

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