Testosterone after Prostate Cancer

Ultima Vez Modificado: 26 de agosto del 2007

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Question

Dear OncoLink "Ask The Experts,"

I was diagnosed with prostate cancer about 18 months ago and had radiation treatment. My PSA has dropped, and all seems to be going well. But my libido, erectile function, and general energy level are not what I'd like them to be. I'm 74 and in good health. My testosterone level is at the low end of the normal range. I wonder if testosterone therapy would help, or would it be too risky? I have heard opinions on both sides of this question and wonder what you think .

Answer

Richard Whittington, MD, Associate Professor of Radiation Oncology at the University of Pennsylvania School of Medicine, responds:

Since testosterone will stimulate the growth of any residual prostate cancer, it is permanently contraindicated after treatment for prostate cancer. There were studies in the past that gave prostate cancer patients testosterone to stimulate the tumor growth, and then later gave them anti-cancer treatment, figuring that proliferating tumor cells would be more sensitive to therapy. Unfortunately, not only did the treatment not work, but the growth rate of the tumor did not slow down in some patients after the testosterone was stopped. In the trials of testosterone administration followed by P-32 for known bone metastases, the survival in the testosterone pretreated group was significantly worse than in the non-pretreated group. If there is truly no tumor left in your body after treatment, then theoretically, taking testosterone should not have any effect, one way or the other. Ultimately, however, no one can say for sure that you will remain prostate cancer-free forever, and so using testosterone carries a great potential risk in anyone with a history of prostate cancer.


News
Alternative DHT Synthesis Pathway Key in Prostate Cancer

Aug 2, 2011 - Dihydrotestosterone synthesis from adrenal precursor steroids in castration-resistant prostate cancer bypasses testosterone synthesis, and occurs through an alternative pathway involving conversion of Δ4-androstenedione to 5α-androstanedione by 5α-reductase isoenzyme-1, according to an experimental study published online July 27 in the Proceedings of the National Academy of Sciences.



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