Abstract
Introduction
Reductions in testosterone concentration play a significant role in the treatment
of prostate cancer. We studied the role of testosterone as a prognostic marker for
advanced prostate cancer (stage C or higher) treated with primary androgen-deprivation
therapy (ADT).
Patients and Methods
A total of 348 patients were treated using ADT as first-line therapy for prostate
cancer at Chiba University Hospital between 1999 and 2016. Of these, 222 patients
with advanced prostate cancer (stage C or higher) were enrolled onto this study. The
prognostic values of serum testosterone level and other clinical factors were evaluated
in association with prostate-specific antigen (PSA), progression-free survival during
first-line therapy, and overall survival.
Results
Median age was 73 years. PSA at baseline was 86 ng/mL. Gleason scores of ≤ 6, 7, 8,
and ≥ 9 were seen in 2.3%, 19.4%, 21.2%, and 41.9%, respectively. Mean follow-up was
60.5 months. Median testosterone at baseline was 482 ng/dL and nadir testosterone
was 13 ng/dL. No variable associated with testosterone predicted progression-free
survival. With regard to overall survival, multivariate analysis identified nadir
testosterone ≤ 20 ng/dL (hazard ratio = 0.44, P = .026) and testosterone reduction ≥ 480 ng/dL (hazard ratio = 0.35, P = .030) as independent prognostic factors. With regard to progression-free survival,
multivariate analysis identified nadir PSA ≤ 0.1 ng/mL (hazard ratio = 3.07, P < .001), presence of lymph node metastasis (hazard ratio = 1.67, P = .017), and time to nadir PSA (hazard ratio = 0.30, P < .001) as independent prognostic factors.
Conclusion
Our data suggested both nadir testosterone (< 20 ng/dL; P = .026) and testosterone reduction (≥ 480 ng/dL; P = .030) to be key prognostic factors for primary ADT in advanced prostate cancer
in Japanese men.
Keywords
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Article info
Publication history
Published online: August 02, 2017
Accepted:
July 27,
2017
Received in revised form:
July 23,
2017
Received:
May 21,
2017
Footnotes
S.Y. and S.S. contributed equally to this work as first authors.
Identification
Copyright
© 2017 Elsevier Inc. All rights reserved.
