Emma Hitt, PhD

May 22, 2012

May 22, 2012 (Atlanta, Georgia) — Testosterone replacement therapy is safe in men with hypogonadism after radical prostatectomy for prostate cancer bearing high-risk characteristics, according to findings from a retrospective review.

Alexander W. Pastuszak, MD, PhD, from the Scott Department of Urology at the Baylor College of Medicine in Houston, Texas, and colleagues presented the findings in a moderated poster session here at the American Urological Association 2012 Annual Scientific Meeting.

"Testosterone replacement therapy in the setting of prostate cancer, particularly prostate cancer bearing high-risk characteristics, is controversial," Dr. Pastuszak and colleagues note. There is "concern that exogenous testosterone can stimulate prostate cancer recurrence or progression."

In this retrospective review, conducted from 2003 to 2011, Dr. Pastuszak and colleagues compared 103 men with hypogonadism after radical prostatectomy for prostate cancer with 50 nonhypogonadal men after radical prostatectomy. Of the patients, 77 had prostate cancer with no high-risk characteristics and 26 had prostate cancer with high-risk characteristics.

Serum testosterone, free testosterone, prostate-specific antigen (PSA), hemoglobin, and hematocrit were assessed at the initiation of testosterone replacement therapy and every 3 to 6 months thereafter for 36 or more months.

Over a median follow-up of 27.5 months, significant increases in median testosterone and free testosterone were observed in the 2 groups. Mean increases in hemoglobin were 1.46 g/dL in the high-risk group and 0.79 g/dL in the nonhigh-risk group, but they were not significant for any of the subgroups.

A significant increase in median PSA was noted only in the nonhigh-risk group (from 0.004 to 0.009 ng/mL; P ≤ .001), not in the high-risk group.

The median PSA velocity was 0.002 ng/mL per year (95% CI, –0.037 to 0.041) for the high-risk group and 0.001 ng/mL per year (95% CI, 0.0005 to 0.001) for the nonhigh-risk group. The researchers observed 4 PSA recurrences (4%) in the group receiving testosterone replacement therapy and 8 (16%) in the control group.

Biopsy and final pathologic Gleason scores were evaluated, as were surgical margins. The final pathologic diagnosis resulted in 25% of patients being upgraded and 13% of patients being downgraded in the group receiving testosterone replacement therapy.

"Testosterone replacement therapy remains a viable treatment alternative in men with a history of prostate cancer who have undergone prostatectomy," Dr. Pastuszak and colleagues conclude, "even those with prostate cancer bearing high-risk characteristics. Recurrence rates in our series were below those published in other series of comparably matched men not treated with testosterone replacement therapy."

A statistically but not clinically significant rise in PSA in the nonhigh-risk subgroup only was observed," Dr. Pastuszak said," and there were more prostate cancer recurrences in the control group than the testosterone replacement therapy group," he added.

"This is a retrospective study. We need prospective clinical trials with longer follow-up because prostate cancer is such a slow-growing malignancy," Dr. Pastuszak told Medscape Medical News. "Ultimately, there are questions remaining about the impact of testosterone on prostate cancer in humans; we need to understand that relationship at the molecular level."

In another presentation at the session by the same researchers, testosterone replacement therapy in patients with prostate cancer after radiation therapy was associated with a rise in serum total testosterone levels and an improvement in hypogonadal symptoms without evidence of prostate cancer recurrence or progression.

"I am seeing more and more people who are on testosterone replacement therapy getting diagnosed with prostate cancer, and they do not stop their testosterone replacement therapy," said Irwin Goldstein, MD, from Alvarado Hospital in San Diego, California. "This represents a fascinating group for study."

The study was not commercially funded. Dr. Pastuszak and Dr. Goldstein have disclosed no relevant financial relationships.

American Urological Association (AUA) 2012 Annual Scientific Meeting: Abstract 1488. Presented May 22, 2012.


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