Re: BPH story of a PCa patient

Hi Ron,
I agree that the correlation of PSA with prostate volume is not
necessarily accurate and there are important reasons for that lack of
correlation. These are related to the way and zone location where the
PSA leaks into the bloodstream.

The use of 5-AR inhibitors has been mostly ignored to treat or prevent
PCa even when the med lit supports its use. These 5-AR inhibitors
promote apoptosis, a reduction of blood flow to the gland and
antiangiogenic activity causing a reduction of microvessel density.
Treated glands demonstrate reduced cell proliferation and in time a
reduction in gland volume.

In patients with known PCa (along with known BPH) there is no reason to
double PSA when treating with a 5-AR. Why? Because the morphological
and histological changes are real and the PSA level measured is
representative of such changes. DHT is the most potent androgen and its
inhibition cause cell death, reduced cell proliferation and other
physical changes that reduce PSA production. 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. This patient had a positive PCa
diagnosis and is managing his cancer with the least objectionable form
of androgen suppression.

Below, some references. Best regards,

RalphV

1: Sutton MT, Yingling M, Vyas A, Atiemo H, Borkowski A, Jacobs SC,
Kyprianou
N.
Finasteride targets prostate vascularity by inducing apoptosis and
inhibiting
cell adhesion of benign and malignant prostate cells.
Prostate. 2006 May 1; [Epub ahead of print]
PMID: 16652387 [PubMed - as supplied by publisher]

2: Rittmaster RS, Norman RW, Thomas LN, Rowden G.
Evidence for atrophy and apoptosis in the prostates of men given
finasteride.
J Clin Endocrinol Metab. 1996 Feb;81(2):814-9.
PMID: 8636309 [PubMed - indexed for MEDLINE]

3: Maria McCrohan A, Morrissey C, O'keane C, Mulligan N, Watson C,
Smith J,
Fitzpatrick JM, Watson RW.
Effects of the dual 5 alpha-reductase inhibitor dutasteride on
apoptosis in
primary cultures of prostate cancer epithelial cells and cell lines.
Cancer. 2006 Jun 15;106(12):2743-52.
PMID: 16703599 [PubMed - in process]

4: Andriole GL, Humphrey P, Ray P, Gleave ME, Trachtenberg J, Thomas
LN, Lazier
CB, Rittmaster RS.
Effect of the dual 5alpha-reductase inhibitor dutasteride on markers
of tumor
regression in prostate cancer.
J Urol. 2004 Sep;172(3):915-9.
PMID: 15310997 [PubMed - indexed for MEDLINE]

ron wrote:
Hi Ralph...I thought that when Leonard said, "It is interesting that
your PSA has dropped significantly"; he meant this in the sense that we
track PSA as a monitor of prostate and tumor volume, and that in this
sense there was a significant change. Often we operate under the
assumption that PSA level correlates with prostate size and tumor size,
and usually that's a fair assumption for tracking purposes. However,
sometimes when certain drugs are administered (for example avodart,
some LHRH agonists, etc.) the PSA level can change significantly
without a corresponding change in prostate / tumor volume. In the case
of avodart it is known that it will reduce the pre-avodart PSA level by
about 50%; but the prostate and tumor volume haven't decreased 50%.
The avodart has probably reduced the PSA level by affecting some
protein, enzyme, etc involved in PSA expression so that the same cells
are now simply expressing less PSA. The net result is that the PSA has
dropped "significantly" but for PSA tracking purposes (again, the way I
thought Leonard was using the term), the PSA remains, for all intents
and purposes, unchanged...Ron

.

Relevant Pages

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