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Dutasteride slows doubling time, slows disease progression after recurrence of prostate cancer.


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Jim Marshall (not a doctor) said ...

The men in this study had rising PSA after a primary treatment of:

  • surgery;
  • surgery then radiotherapy; or
  • just radiotherapy.

When their PSA began to climb:

  • half were put on Avodart (dutasteride), one 0.5 mg tablet per day
  • half were given a tablet that looked the same, but had no active ingredient (placebo, "sugar pill").

After 2 years:

The men on Avodart (dutasteride) had:

  • a longer time until their PSA doubled; and
  • a longer time until they showed clinical progression (presumably seen on scans, or reported pain, etc)

Both of these were statistically significant.

We do not know whether this will lead to longer survival, but with clinical progression delayed by Avodart (dutasteride), it looks hopeful at this stage.

... end Jim

Eur Urol. 2012 Nov 12. pii: S0302-2838(12)01337-1. doi: 10.1016/j.eururo.2012.11.006. [Epub ahead of print]

Dutasteride Treatment Over 2 Years Delays Prostate-specific Antigen Progression in Patients with Biochemical Failure After Radical Therapy for Prostate Cancer: Results from the Randomised, Placebo-controlled Avodart After Radical Therapy for Prostate Cancer Study (ARTS).

Schröder F, Bangma C, Angulo JC, Alcaraz A, Colombel M, McNicholas T, Tammela TL, Nandy I, Castro R.


Erasmus Medical Centre, Rotterdam, The Netherlands. Electronic address: secr.schroder@erasmusmc.nl.



Rising prostate-specific antigen (PSA) levels after radical therapy are indicative of recurrent or residual prostate cancer (PCa). This biochemical recurrence typically predates clinically detectable metastatic disease by several years. Management of patients with biochemical recurrence is controversial.


To assess the effect of dutasteride on progression of PCa in patients with biochemical failure after radical therapy.


Randomised, double-blind, placebo-controlled trial in 294 men from 64 centres across 9 European countries.


The 5a-reductase inhibitor, dutasteride.


The primary end point was time to PSA doubling from start of randomised treatment, analysed by log-rank test stratified by previous therapy and investigative-site cluster. Secondary end points included time to disease progression and the proportion of subjects with disease progression.


Of the 294 subjects randomised (147 in each treatment group), 187 (64%) completed 24 mo of treatment and 107 discontinued treatment prematurely (71 [48%] of the placebo group, 36 [24%] of the dutasteride group). Dutasteride significantly delayed the time to PSA doubling compared with placebo after 24 mo of treatment (p<0.001); the relative risk (RR) reduction was 66.1% (95% confidence interval [CI], 50.35-76.90) for the overall study period. Dutasteride also significantly delayed disease progression (which included PSA- and non-PSA-related outcomes) compared with placebo (p<0.001); the overall RR reduction in favour of dutasteride was 59% (95% CI, 32.53-75.09). The incidence of adverse events (AEs), serious AEs, and AEs leading to study withdrawal were similar between the treatment groups. A limitation was that investigators were not blinded to PSA levels during the study.


Dutasteride delayed the biochemical progression of PCa in patients with biochemical failure after radical therapy for clinically localised disease. The safety and tolerability of dutasteride were generally consistent with previous experience.


ClinicalTrials.gov, NCT00558363.

Copyright © 2012. Published by Elsevier B.V.

PMID: 23176897

This extract can be found on http://PubMed.com, and is in the public domain.

On PubMed.com there will be a link to the full paper (often $30, sometimes free).

Any highlighting (except the title) is not by the author, but by Jim Marshall.

Jim is not a doctor.

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  • 10 months later...

There seems to be a school of thought (Snuffy Myers) that measuring your dihydrotestosterone will give you a better indication of the necessary dose rate of dutasteride. My oncologist does not think measuring will be of any help. The usual rate recommended by my oncologists is one per day (0.5mg).  

However, I think Myers has a valid point. Some of his patients are taking 1-4 per day. See his latest blog.

Any thoughts?

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I asked my doctor about a dihydrotestosterone test about three months ago and he did not think it was necessary. I only needed the testosterone test was his view.

I do not agree with him of course.

Mind you I am only having the testosterone test, along with many other blood test, because I requested them to be preformed. 

I have been on continuous Eligard for two and a half years and I would like to be sure the dihydrotestosterone levels are low. I have no idea if all testing laboratories do the blood test for dihydrotestosterone.  

Maybe I should be on Avodart as well. I had a radical four and a half years ago.

I am sorry John I can not answer your question.

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