Rising PSA
khilde...@casselsbrock.com
follow-up radiation about 5 years ago. Since that time his PSA has
been rising steadily and in less than a year has doubled, from .22 to .
44. I realize that number isn't very high but he seems inclined to do
nothing and I wonder if he needs to be looking at hormone therapy
soon. His PSA on diagnosis was 13 and his gleason was 8 (3+5).
Cancer had spread to the seminal vesicles and the margins were
"focally involved" (I've never been able to find out what that means).
Any opinions?
Thanks,
Karen in Toronto
Dave P
Looks like it is rising - but only trained professionals would know.
You should definetly encourage him to see his Doctor to stay on top of
it while the psa is still low.
Some believe it is best to start hormone therapy at low psa levels
others wait until it rises to 1.0 - 5.0 or more.
I would be one to choose it early and keep the psa at low or
undectable levels. Our hope is that a cure or treatment other than
hormone therapy is around the corner.
I know its difficult since he has been through the surgery then
radiation but the goal is to survive and live a long life. So you have
to do whatever it takes to win the battle. If that's taking hormones
then you have to do it.
Stay positive
Dave P
John Loomis
It is not easy and your husband has been through a lot.
Help him out the best you can, and do see the oncologist.
John Loomis
<khilde...@casselsbrock.com> wrote in message
news:1172672855.2...@a75g2000cwd.googlegroups.com...
dave perry
I had a "well-focused" 2mm tumor at the edge of the sample. It meant
"up to the edge but no evidence it crossed over." Still, technically
a positive margin but not as bad as slicing right through it and
leaving a chunk behind. No matter though since your husband's cancer
is still with him so he at the very least has to consult with an
expert (an oncologist - urologists are surgeons) and do a lot of
research to decide the best treatment course. Good luck.
Dave Perry
I.P. Freely
> Looks like it is rising - but only trained professionals would know.
>
> You should definetly encourage him to see his Doctor to stay on top of
> it while the psa is still low.
>
> Some believe it is best to start hormone therapy at low psa levels
> others wait until it rises to 1.0 - 5.0 or more.
Still others, including big guns such as Walsh and Scholz, suggest we
consider holding off ADT (hormone therapy) until recurrence is at least
clinical (it shows up on a scan) and maybe even becomes symptomatic,
because of ADT's therapeutic ratio -- the ratio of benefit to side
effects. ADT is a *very* personal decision when the only indication of
PC is PSA or even a spot on a bone scan. I believe the ADT timing
decision requires as much or more research and introspection than the
first treatment choice, because its expected benefits are less and its
side effects are arguably harsher for many patients.
> you have to do whatever it takes to win the battle. If that's taking hormones
> then you have to do it.
Agreed, but first we must define our own definition of "win", because
one man's victory is another's defeat, depending on . . . ta daaaa . . .
the benefits defined by statistics and the side effects as indicated by
statistics and ultimately encountered by that individual. We don't
"have" to do *anything* other than the research and introspection,
because in many cases that leads to a personally valid choice of
watchful waiting.
This got discussed here at great length throughout '05, beginning in
about Dec '04, usually with the "words" HT or ADT in the topic. If you
don't know how to Google the archives up, ask; it's easy and very
productive.
I.P.
Heather
I think you might have *delurked* once before......I recognize your
*company* because I worked in that field for 20 years.
I assume that your husband was either at Princess Margaret or
Sunnybrook. Perhaps get a referral back to one of the medical
oncologists there?? Mine goes to Sunnybrook......brother-in-law to PMH.
Definitely get him to go to a doctor and get an opinion which may
persuade him to at least keep an eye on it. He is too young to *do
nothing*!!!!
Heather in Brampton
<khilde...@casselsbrock.com> wrote in message
news:1172672855.2...@a75g2000cwd.googlegroups.com...
Steve Kramer
Gleason 8 is not good, especially with a 5 in there. Seminal Vesicle
Involvement (SVI) is also not good. However, a spread from zero (I assume)
to only 0.44 over a span of 8 years is a good indicator for a relatively
long life -- relative to the rest of who have cancer of course.
That said, it is time to consider hormone therapy.
--
PSA 16 10/17/2000 @ 46
Biopsy 11/01/2000 G7 (3+4), T2c
RRP 12/15/2000 G7 (3+4), T3cN0M0 Neg margins
PSA .1 .1 .1 .27 .37 .75
EBRT 05-07/2002 @ 47
PSA .34 .22 .15 .21 .32
Lupron 07/03 (1 mo) 8/03 (4 mo), 12/03, 4/04, 09/04, 01/05, 5/05, 10/05,
2/06, 6/06
PSA .07 .05 .06 .09 .08 .132 .145
Casodex added daily 07/06
PSA <0.04, <0.05
Non Illegitimi Carborundum
Steve Kramer
Obviously not.
--
PSA 16 10/17/2000 @ 46
Biopsy 11/01/2000 G7 (3+4), T2c
RRP 12/15/2000 G7 (3+4), T3cN0M0 Neg margins
PSA .1 .1 .1 .27 .37 .75
EBRT 05-07/2002 @ 47
PSA .34 .22 .15 .21 .32
Lupron 07/03 (1 mo) 8/03 (4 mo), 12/03, 4/04, 09/04, 01/05, 5/05, 10/05,
2/06, 6/06
PSA .07 .05 .06 .09 .08 .132 .145
Casodex added daily 07/06
PSA <0.04, <0.05
Non Illegitimi Carborundum
<khilde...@casselsbrock.com> wrote in message
news:1172672855.2...@a75g2000cwd.googlegroups.com...
Steve Jordan
> Hello from a lurker - my husband, 48, has had a prostatectomy and
> follow-up radiation about 5 years ago. Since that time his PSA has
> been rising steadily and in less than a year has doubled, from .22 to .
> 44. I realize that number isn't very high but he seems inclined to do
> nothing and I wonder if he needs to be looking at hormone therapy
> soon.
According to the Prostate Cancer Research Institute (PCRI), a PSA
doubling time equal to or less than ten years may be a sign of prostate
cancer (PCa).
Here is PCRI's definition:
"PSA doubling time (PSADT): the calculation of the time it takes for the
PSA value to double based on at least three values separated by at least
three months each; before diagnosis, a PSADT of less than 10 years may
be an indication of the presence of PC."
Careful reading discloses that the criterion is based upon a series of
tests, not just one. IMO, one should never act based upon only one test
result.
> His PSA on diagnosis was 13 and his gleason was 8 (3+5).
> Cancer had spread to the seminal vesicles and the margins were
> "focally involved" (I've never been able to find out what that means).
I suspect that "focally involved" is a euphemism for "positive margins."
The uro should be prepared to define his terms.
> Any opinions?
If a series of tests confirms a serial rise in PSA, here are mine:
1. This may or may not be a sign of recurrence (as if the PCa was ever
gone!) or treatment failure. The suspicion exists, and should be
investigated.
2. There is a number of tests available to develop clinical information
that could tell one the status. They include prostatic acid phosphatase
(PAP), chromogranin-A (CGA), carcino-embryonic antigen (a non-specific
cancer test), and neuron-specific enolase (NSE). These tests are
well-covered on the PCRI website at:
http://prostate-cancer.org/index.html
3. Another life-saving source of information is _A Primer on Prostate
Cancer_ 2nd ed., subtitled "The Empowered Patient's Guide" by medical
oncologist and PCa specialist Stephen B. Strum, MD and PCa warrior Donna
Pogliano. It is available via the PCRI website and at many other
PCa-related sites, as well as any bookstore.
4. This is no time to rely upon a urologist. However competent a surgeon
he might be, he is no more than a surgeon. This case, unless he is one
of the rare uro-birds who is also qualified as a cancer specialist, is
well beyond his capabilities.
What may be happening is the early stages of systemic (not necessarily
metastatic at this time) PCa. If such be the case, the best possible
recourse is to consult a medical oncologist who specialises in tx of PCa
-- or who consults with one of the masters in the field.
Good luck!
Regards,
Steve J
"There is NOWHERE in oncology where waiting for the tumor cell
population to increase (and to mutate) is in the better interests of the
patient. The use of early ADT3 as advocated by our group (Scholz, Lam &
myself) & also by Leibowitz & Tucker & also per the experiences of Myers &
Tisman, all attest to the rational, logical endocrinologic approach to PC
management. Surprisingly, only a few others in academic medicine have ever
gone that route. Dr. Oefelin in Cleveland is one of these. In my experience
it is the early use of therapy before the tumor burden increases
substantially that allows for long term responses. I realize I am battling
the academic world which only sees results in peer-reviewed literature as
having the sole take on the truth. This is just not the case...."
--Stephen B. Strum, MD
Alex
"I.P. Freely" <fuhghed...@noway.nohow> wrote in message
news:WQiFh.234$S21...@newsfe05.lga...
This and the other advice you've received here is all on the mark. If your
doctor says ADT is not warranted, you might wask him or her for an opinion
on taking Proscar or Avodart. Both are relatively low-risk prescription
drugs (originally intended to treat hair loss) which reduce the production
of testosterone and DHT, shrink prostate cells and, according to my
oncologist, actually slow the growth of prostate cancer cells. This latter
belief is not universally accepted in the medical community, but it's pretty
well founded. Proscar has fewer side effects, Avodart has a slightly higher
incidence of them (mainly tenderness or swelling of the breast tissue in a
few percent of men taking it.)
Again, this is NOT instead of ADT, etc. It's sort of "ADT-lite."
Alex
ron
> "I.P. Freely" <fuhgheddabou...@noway.nohow> wrote in message
>
> - Show quoted text -
Alex...Proscar or Avodart don't reduce T production, they just reduce
the conversion of T to DHT...Best wishes and good health, ron
Ed Friedman
> This and the other advice you've received here is all on the mark. If your
> doctor says ADT is not warranted, you might wask him or her for an opinion
> on taking Proscar or Avodart. Both are relatively low-risk prescription
> drugs (originally intended to treat hair loss) which reduce the production
> of testosterone and DHT, shrink prostate cells and, according to my
> oncologist, actually slow the growth of prostate cancer cells. This latter
> belief is not universally accepted in the medical community, but it's pretty
> well founded. Proscar has fewer side effects, Avodart has a slightly higher
> incidence of them (mainly tenderness or swelling of the breast tissue in a
> few percent of men taking it.)
>
> Again, this is NOT instead of ADT, etc. It's sort of "ADT-lite."
>
> Alex
Alex,
Actually, Proscar raises T levels by ~10% (see Table 4 of the paper at:
http://theoncologist.alphamedpress.org/cgi/content/full/6/2/177).
However, raising T while lowering DHT is actually a good thing, as
animal studies have shown. Basically, intermittent ADT followed by high
T/low DHT was shown in to be ~5 times more effective than continual ADT
(http://www3.interscience.wiley.com/cgi-bin/abstract/112221624/ABSTRACT).
I understand that this goes against the myths that most doctors hold,
but it is consistent with my model (http://www.tbiomed.com/content/2/1/10).
I'm afraid my paper is a little hard to follow, but hopefully my next
one will clarify things for everyone.
Ed Friedman
Steve Jordan
> Actually, Proscar raises T levels by ~10% (see Table 4 of the paper at:
> http://theoncologist.alphamedpress.org/cgi/content/full/6/2/177).
I have reviewed Ed's citation, and am unable to discern therein evidence
in support of Ed's statement. The table shows that some pts who had been
off tx for 12 months or more had T levels 29 (ng/dL, presumably) higher
than baseline. But there is no reason set forth for that. IOW, there is
no evidence presented that the increase in T is *caused by* Proscar.
What am I missing?
Regards,
Steve J
ron
Steve...There are other studies that support increased T levels when
its conversion to DHT is blocked. Several pseudohermaphroditic
population clusters around the world lack the gene needed to create
the enzymes used in the 5AR pathways. The men in these groups have
high T and very low DHT levels. So its not the finasteride or
dutasteride that "causes" the increased T level, but rather they
remove or block a pathway that metabolizes T. Removal of this pathway
for consumption of T (conversion to DHT) results in an increase in T
levels somewhat higher than normal...Best wishes and good health, ron
Ed Friedman
> Steve...There are other studies that support increased T levels when
> its conversion to DHT is blocked. Several pseudohermaphroditic
> population clusters around the world lack the gene needed to create
> the enzymes used in the 5AR pathways. The men in these groups have
> high T and very low DHT levels. So its not the finasteride or
> dutasteride that "causes" the increased T level, but rather they
> remove or block a pathway that metabolizes T. Removal of this pathway
> for consumption of T (conversion to DHT) results in an increase in T
> levels somewhat higher than normal...Best wishes and good health, ron
>
Ron,
You are quite correct. E.g., the following is from the web site:
http://www.dutasteride.com/articles/dutasteride-finasteride.html
"Dutasteride and finasteride both increase median circulating
testosterone concentration. Increase of 10-20% from baseline values have
been noted, however concentrations remained within normal physiologic
limits."
Dutasteride is the chemical name for Avodart and finasteride is the
chemical name for Proscar.
Ed Friedman
Steve Jordan
(snip quote of Ron, which is upthread)
I am pleased to see clarification.
My issue was that Ed's thesis was not supported by the reference he used.
Regards,
Steve J