I'd be interested to know why Steve is undergoing ADT from a surgeon rather
than a med onc.

I have previously written extensively (FWIW) on the subject of Lupron (and
other LHRH agonists) dosages at lengthy intervals and the insurers'
(especially Medicare's) stubborn insistence upon intervals that are clearly
at odds with the intervals recommended by the manufacturers and by
knowledgeable med oncs. What it can come down to is injections that are as
much as *ten days late* with possibly-dangerous effects. This is why I
insist that my injection intervals be 28 days as recommended. Medicare pays
without a whimper. I can see no reason for the lengthier intervals other
than some perceived convenience. Not a good enough reason, IMO, considering
the risk.

According to the 2005 Second Edition of _A Primer on Prostate Cancer_ the
latest study on the subject of IADT (2000) the criteria for resort to that
mode of therapy was, while on ADT2 or ADT3,  maintenance for one year of
undetectable PSAs. UDPSA is defined as any value less than 0.05 ng/mL.

Based upon that, I suggest caution. It does not appear that Steve quite
meets the criterion of UDPSA.

What effect on it all the fact that he is evidently on only ADT1 might have
I dunno. I'm also on ADT1, so this can apply to me, too. FWIW, I had
planned to suspend ADT at the one-year point (about now) until I read
"Implication of cell kinetic changes during the progression of human
prostatic cancer." This is a Johns Hopkins paper dated 1995. PMID is
9816006. For me, the most important sentence was, "The transition of late
stage high-grade prostatic intraepithelial
neoplastic cells into localized prostatic cancer cells involves no further
increase in proliferation but a decrease in death resulting in net
continuous growth of localized prostatic cancers with a mean doubling time
of >/=475 days." Consequently, I decided to continue on ADT at least to the
18-month point. I want to overlap the doubling time.

There is an excellent article on the subject of IADT at
http://www.prostate-cancer.org/education/andeprv/Strum_IADT.html
and use of the Search function will find many articles on this subject as
well as ADS (Androgen Deprivation Syndrome).

AIUI, it was Strum, Scholz, McDermott et al. who first proposed IADT as a
mode of tx *for a select group of pts,* mainly those who clearly had
hormone-dependent PCa.

Regards,

Steve J

"We must tailor the treatment to the nature of the disease. We must listen
to the biology."
-- Stephen B. Strum, MD

Steve Kramer wrote...snip...

Steve...I've included the abstracts below from two papers that argue
opposite sides of the CHB / IADT question.  From what I've read, IADT
seems to have more followers.  Or perhaps I should say IADT and / or
switching from one HT to another in an attempt to prevent the androgen
receptor from mutating sooner rather than later seems to have captured
peoples interest...Best wishes and good health, Ron

Small study warning posted!

Clin Prostate Cancer. 2002 Dec;1(3):163-71.  Related Articles, Links

Intermittent versus continuous total androgen blockade in the treatment
of patients with advanced hormone-naive prostate cancer: results of a
prospective randomized multicenter trial.

de Leval J, Boca P, Yousef E, Nicolas H, Jeukenne M, Seidel L,
Bouffioux C, Coppens L, Bonnet P, Andrianne R, Wlatregny D.

Department of Urology, University Hospital, University of Liege,
Belgium.

The aim of this study was to compare the efficacy of total intermittent
androgen deprivation (IAD) versus total continuous androgen deprivation
(CAD) for treating patients with advanced prostate cancer in a phase
III randomized trial. A total of 68 evaluable patients with
hormone-naive advanced or relapsing prostate cancer were randomized to
receive combined androgen blockade according to a continuous (n = 33)
or intermittent (n = 35) regimen. Therapeutic monitoring was assessed
by use of serum prostate-specific antigen (PSA) measurements. Patients
in the CAD and IAD groups were equally stratified for age, biopsy
Gleason score, and baseline serum PSA levels. The outcome variable was
time to androgen-independence of the tumor, which was defined as
increasing serum PSA levels despite androgen blockade. Mean follow-up
was 30.8 months. The 35 IAD-treated patients completed 91 cycles, and
19 of them (54.3%) completed > or = 3 cycles. Median cycle length and
percentage of time off therapy were 9.0 months and 59.5, respectively.
The estimated 3-year progression rate was significantly lower in the
IAD group (7.0% +/- 4.8%) than in the CAD group (38.9% +/- 11.2%, P =
0.0052). Our data suggest that IAD treatment may maintain the
androgen-dependent state of advanced human prostate cancer, as assessed
by PSA measurements, at least as long as CAD treatment. Further studies
with longer follow-up times and larger patient cohorts are needed to
determine the comparative impacts of CAD and IAD on survival

Urology. 2002 Jul;60(1):115-9

Can combined androgen blockade provide long-term control or possible
cure of localized prostate cancer?

Labrie F, Candas B, Gomez JL, Cusan L.

Prostate Cancer Clinical Research Unit, Department of Medicine, Laval
University Medical Center (CHUL) and Laval University, Quebec City,
Quebec, Canada.

OBJECTIVES: To investigate the possibility that more complete blockade
of androgens or combined androgen blockade (CAB) could lead to even
longer term control of localized prostate cancer. A series of recent
studies have shown important benefits on survival using medical or
surgical castration in localized or locally advanced prostate cancer.
METHODS: The effect of CAB on long-term control or possible cure of
prostate cancer was evaluated by the absence of biochemical failure or
prostate-specific antigen (PSA) rise for at least 5 years after
cessation of continuous treatment. A total of 57 patients with
localized or locally advanced disease received CAB for periods ranging
from 1 to 11 years. Twenty patients with Stage B2/T2 prostate cancer
who were treated for a median duration of 7.2 years (range 2.8 to 11.7)
with CAB stopped treatment and were followed up for a median of 4.9
years. Eleven patients with Stage B2/T2 also received CAB but for only
1 year. Twenty-six patients with Stage C/T3 treated with continuous CAB
for a median of 9.9 years (range 3.8 to 11.3) with undetectable PSA
levels stopped treatment and were followed up for a median of 5.6
years. The median follow-up since diagnosis was 14.6 years for patients
with Stage B2/T2 and 16.4 years for patients with Stage C/T3 disease.
RESULTS: With a minimum of 5 years of follow-up after cessation of
long-term CAB, two PSA rises occurred among 20 patients with Stage
T2-T3 cancer who stopped treatment after continuous CAB for more than
6.5 years, for a nonfailure rate of 90%. For the 11 patients who had
received CAB for 3.5 to 6.5 years, the nonfailure rate was only 36%.
The serum PSA increased within 1 year in all 11 patients with Stage
B2/T2 treated with CAB for only 1 year, thus indicating that active
cancer remained present after short-term androgen blockade despite
undetectable PSA levels. In all patients who had biochemical failure
after stopping CAB, the serum PSA level rapidly decreased again to
undetectable levels when CAB was restarted and remained at such low
levels afterward. Of these patients, only 1 patient had died of
prostate cancer at last follow-up.
CONCLUSIONS: The present data suggest that long-term and continuous CAB
offers the possibility of long-term control or possible cure of
localized prostate cancer.

Steve,

Wishing you the same psa reading or lower.

Hope you can get off the hormones for a while.

My prayers are with you.

Keep fighting and don't quit

Dave P

My main info on IADT was from Strum's study, which Steve Jordan has
already cited.

I read the two abstracts posted by Ron, and noted the following sentence
in the second one: "In all patients who had biochemical failure
after stopping CAB, the serum PSA level rapidly decreased again to
undetectable levels when CAB was restarted and remained at such low
levels afterward."

It sounds to me like the authors, who are advocating continuous ADT,
have said that if you take time off and come back, the ADT starts working
again.

As we so often see with this disease, our knowledge is incomplete
and every decision we make is based only on probabilities and partial
evidence.  Expert advice is important, but it's hard to find an expert.
Strum says on his page cited by Steve Jordan, that an understanding
of endocrinology is essential in managing ADT, but I wonder how many
urologists and even medical oncologists really understand it.

My inexpert reading of the summary data is that IADT _appears_ to
do more good than harm.  But if it's true, as I've just said, that a typical
urologist doesn't fully understand the problems, then it's easy to imagine
how much less I understand.

I have several bits of advice:

1. Try to find an expert medical oncologist.  One who, when you mention
the name "Steven Strum" immediately knows who you are talking about
and what Strum said.

2. If you do decide to go on IADT, get frequent PSA and testosterone
tests.  I think Strum said he tested his patients every single month.  The
testosterone test seems essential to me in order to understand when
you really are done with the ADT, and will also show you something
about the relationship between rising PSA and rising T.  The med onc
may want other tests too.

3. Make a plan with the oncologist.  For example, you might plan that
you will go off the ADT, get tested each month, and get back on if
and when the PSA reaches some level X.  You can always modify
the plan if need be, but having a plan will at least give you a strategy
for dealing with any changes in PSA that occur from month to month
and the emotional rollercoaster may not be quite as steep.

Best of luck with it.  We're all rooting for you, our chief record keeper
and cheer leader!

    Alan