Well, this is kind of interesting. Anti-androgen monotherapy, stopping cells from using testosterone (AA), (e.g. Casodex daily tablets) vs. immediate chemical castration (stopping production of testosterone).
This is simply a moot point in the USA, no one would consider anti-androgen monotherapy like this. But this study explores exactly that, with somewhat surprisingly positive results. Here's a link to the study (from today's "Uroalert
s" email), offered for general information. Draw your own conclusions. Based on the study's limitations, it may be sufficiently positive to perhaps generate a randomized trial some day. Surprisingly it rather favors AA.
It's an interesting idea. If embarking on primary hormone therapy, do AA first. Wait to embark on T-suppression until the AA isn't holding anymore. The side-effects of no-T are considered broader and more problematic than those of AA. This would effectively delay the need for testosterone suppression therapies.Anti-androgen monotherapy versus gonadotropin-releasing hormone agonists in men with advanced, non-metastatic prostate cancer: a register-based, observational study
From the study:Using a hypothetical trial in a real-world setting, our results indicate that in men with high-risk PCa with no distant metastasis, PCa-specific mortality is similar for those treated with AA and those treated with GnRH agonists. However, all-cause mortality was lower for men taking AA compared with men on GnRH agonists. Starting on AA instead of GnRH agonists may result in less exposure to GnRH agonists and hence potentially less risk of adverse events.
This is a retrospective study, an "observational" study. They've tried to eliminate bias as much as possible, but that's an inherent risk in any such study. Randomized Controlled Trials (RCT) are the best, but are quite expensive, lengthy, and sometimes don't yield actual results. The study's authors state:...our study provides sound evidence for a non-randomised study, but cannot be considered comparable to a well-performed RCT. Consequently, our results are deemed to be hypothesis-generating.
55@Dx on 4/16/13. PSA 5.2, G9(5+4), PNI+, cT3a by MRI.
IGRT - 44 sessions (79.2 Gy, 50.4 Gy pelvic)
ADT2 - Lupron+Casodex (5/13-3/16)
8/13-5/16 <0.1 (ADT2)
5/16-3/17 recovering from ADT2
3/17-7/18 ~ 0.6 - 0.8 (no TX)
10/18 = 1.0My Story