LOW NADIR TESTOSTERONE AS PROGNOSTIC FACTOR IN PROSTATE CANCER

In an analysis from the PR-7 trial reported in the Journal of Clinical Oncology, Klotz et al found that in men with prostate cancer with biochemical failure after radiotherapy with or without surgery, a nadir serum testosterone level ≤ 0.7 nmol/L during the first year of continuous androgen-deprivation therapy was predictive of improved cause-specific survival and prolonged time to hormone resistance.

In the PR-7 trial, 1,386 patients were randomly assigned to continuous androgen-deprivation therapy (n = 696) or intermittent androgen-deprivation therapy (n = 690). Of 626 men in the continuous androgen-deprivation therapy group eligible for the current analysis, 226 developed castration-resistant prostate cancer, with a median time to diagnosis of 10.0 years; the 5-year event-free rate was 69%.

Effect of Nadir Testosterone Value

Nadir testosterone of ≤ 0.7, > 0.7 to < 1.7, and ≥ 1.7 nmol/L was achieved in 78%, 21%, and 1% of patients. Cause-specific survival was significantly greater (P = .015) in patients with first-year nadir testosterone levels ≤ 0.7 nmol/L; hazard ratios [HRs] of dying from prostate cancer were 2.08 (95% confidence interval [CI] = 1.28–3.38) in those with levels > 0.7 to < 1.7 nmol/L and 2.93 (95% CI = 0.70–12.30) in those with levels ≥ 1.7 nmol/L. Patients with the lowest testosterone nadir also had a significantly prolonged time to hormone resistance (P = .02); hazard ratios were 1.62 (95% CI = 1.20–2.18) in those with nadirs of > 0.7 to < 1.7 nmol/L and 1.90 (95% CI = 0.77–4.70) in those with nadirs ≥ 1.7 nmol/L.

The investigators concluded: “Low nadir serum testosterone (ie, < 0.7 nmol/L) within the first year of androgen-deprivation therapy correlates with improved [cause-specific survival] and duration of response to androgen deprivation in men being treated for biochemical failure undergoing [continuous androgen deprivation].”

Laurence Klotz, MD, FRCSC, of the University of Toronto, is the corresponding author of the Journal of Clinical Oncology article.

The study was supported by the Canadian Cancer Society Research Institute, National Cancer Institute, and National Institutes of Health Royal Marsden Institute for Cancer Research Biomedical Research Centre. For full disclosures of the study authors, visit jco.ascopubs.org.