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Rev Urol. 2008 Winter; 10(1): 83.
PMCID: PMC2312346
Testosterone Therapy in Men With Localized Prostate Cancer
Jacob Rajfer, MD
Department of Urology, University of California at Los Angeles, Los Angeles, CA
One of the major clinical dilemmas facing urologists who see patients with prostate cancer is what to do with them after they become hypogonadal, either biochemically or symptomatically. It is known that as men age, the incidence of hypogonadism increases at the same time that the incidence of prostate cancer increases. Ever since Huggins and Hodges showed the link between testosterone and prostate cancer more than 6 decades ago,1 it is considered verboten to treat anyone who has a diagnosis of prostate cancer with exogenous testosterone, regardless of whether or not they are hypogonadal. Indeed, all forms of testosterone carry such a warning label, and there have been very few reports attesting to the fact that treatment of men who have localized prostate cancer with exogenous testosterone causes a flare of the cancer. This is in contradistinction to men who have metastatic disease where the treatment with LHRH agonists can cause such a flare, which is presumed to be due to the transient elevation of the serum testosterone right after initiation of LHRH agonist treatment.
Testosterone Replacement for Hypogonadism After Treatment of Early Prostate Cancer With Brachytherapy
Sarosdy MF.
Cancer. 2007;109:536–541 [PubMed].
Recent reports have trickled out to show that men who have undergone radical prostatectomy for localized prostate cancer and have an unmeasurable PSA can be safely treated with exogenous testosterone as long as the PSAs are carefully monitored.2 The assumption here is that there is no remaining prostate cancer following the radical prostatectomy and, therefore, this type of treatment is safe in these patients. In fact, it would be unheard of to treat such post-radical prostatectomy men who have measurable PSAs with exogenous testosterone because of the belief that exogenous testosterone would stimulate the cells that are producing the measurable PSA in those patients.
This latter notion is now being challenged by the recent report of Sarosdy, who treated 31 men who underwent brachytherapy with or without external beam radiation therapy with exogenous androgens despite there being a measurable PSA in many of these patients. In these patients, there was no evidence of metastatic disease, and the prostate cancer was assumed to be 100% localized to the prostate.
What Sarosdy found was that none of these patients demonstrated any stimulation of the PSA, even though 1 patient had a PSA of 1.0 while on therapy. This observation is remarkable and puts our entire mindset about testosterone therapy and prostate cancer on hold. At the same time it gives some ammunition to those patients who are so severely impacted by their hypogonadism that they demand relief from those debilitating hypogonadal symptoms. The findings in this landmark paper will obviously need to be reproduced by others and, if confirmed, will add to the growing controversy of the questionable import of testosterone in “causing” prostate cancer.
References
1. Huggins C, Hodges CV. The effects of castration, of estrogen and androgen injection on serum phosphatases in metastatic carcinoma of the prostate. Cancer Res. 1941;1:293–297.
2. Kaufman JM, Graydon RJ. Androgen replacement after curative radical prostatectomy for prostate cancer in hypogonadal men. J Urol. 2004;172:920–922. [PubMed]

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