 |
| |
Treating
Prostate Cancer After Lupron Fails
March 26, 2007
Frequently men come to my clinic after having failed treatment
with Lupron or similar drugs, like Eligard, Zoladex, and Trelstar.
These drugs aren’t perfect and they don’t suppress
testosterone in every man. The first step in treating a man who’s
failed Lupron treatment is to measure their testosterone and
dihydrotestosterone blood levels. You would be surprised how
often we find that there’s enough of either testosterone
or dihydrotestosterone to fully explain why the treatment has
failed. I find it very puzzling that most urologists don’t
measure testosterone in their patients and that nearly all fail
to measure dihydrotestosterone. If the goal of treatment is to
lower androgen levels, it seems obvious to me that you would
want to measure androgen levels to make sure the drugs are working.
When you go on a diet, you measure your weight. When you depress
the gas pedal on your car, you look at the speedometer. So, when
you are trying to treat cancer by suppressing testosterone, you
check to see that the drugs are doing what they should. This
is not rocket science. If Lupron doesn’t do the job, often
switching to one of the competing products will get the job done.
Surgical castration is another option. The final option is to
prevent the remaining testosterone from binding to the androgen
receptor.
In the previous section, we discussed how a prostate cancer that
progresses after Lupron is still dependent on testosterone and
outlined the various mechanisms the cancer cell uses to grow
despite low testosterone levels. It turns out that in nearly
every paper published on this subject, researchers added Casodex
and subsequently showed that it prevented low levels of testosterone
from supporting cancer growth. The concentrations of Casodex
used are similar to those obtained in patients who received 150–250
mg of oral Casodex per day. I can find only one clinical trial
that has tested this. Brown, R.S., et al biopsied the metastatic
cancer masses that continued to grow despite medical or surgical
castration and tested for androgen receptor content. In those
patients where the cancer appeared to be making an abnormally
large amount of androgen receptor, Casodex caused a response
in 80% of the patients.
Since I opened my clinic—the American Institute for Diseases
of the Prostate—in 2002, I’ve made it a practice
to measure dihydrotestosterone levels in each patient we see.
And I have to tell you that medical castration, while effective
at reducing testosterone from the normal range of 300-800 ng/dL
to below 30 ng/dL, often leaves dihydrotestosterone levels within
the normal range (30-80 ng/dL). And dihydrotestosterone is ten
times more powerful than testosterone at stimulating prostate
growth, so a dihydrotestosterone of 30 ng/dL is potentially as
powerful as a testosterone of 300. Dihydrotestosterone formation
can be blocked in most patients with either Proscar or Avodart,
with Avodart being more consistently effective. I’ve found
this can aid in inducing remission in patients who’ve failed
Lupron. Luckily, Proscar and Avodart don’t cause any additional
side effects in men on hormonal therapy. But again, we have to
measure dihydrotestosterone levels to see if Proscar or Avodart
are in fact suppressing dihydrotestosterone.
|
|
|
|
