Year : 2010 | Volume
: 26 | Issue : 1 | Page : 152--153
Intermittent androgen deprivation for locally advanced and metastatic prostate cancer: Where is the evidence?
TJ Nirmal, S Kumar
Department of Urology, Christian Medical College, Vellore, India
T J Nirmal
Department of Urology, Christian Medical College, Vellore
|How to cite this article:|
Nirmal T J, Kumar S. Intermittent androgen deprivation for locally advanced and metastatic prostate cancer: Where is the evidence?.Indian J Urol 2010;26:152-153
|How to cite this URL:|
Nirmal T J, Kumar S. Intermittent androgen deprivation for locally advanced and metastatic prostate cancer: Where is the evidence?. Indian J Urol [serial online] 2010 [cited 2020 Oct 22 ];26:152-153
Available from: https://www.indianjurol.com/text.asp?2010/26/1/152/60470
This multicenter, phase III, randomized study compares intermittent hormonal therapy (IHT) with continuous therapy for the treatment of advanced prostate cancer.  Men below 80 years of age, with histologically confirmed prostate cancer of stage T3 and above, with or without metastasis; and a prostate specific antigen (PSA) level ≥4 to  It helps to palliate, delay or prevent the onset of symptoms related to the disease and its complications but does not improve overall survival.  Majority of the patients on continuous therapy become vulnerable to its various side effects and ultimately progress to hormone resistant prostate cancer (HRPC) in two to three years.  The concept of IHT for prostate cancer and its beneficial effect on QoL was first clinically described by Klotz et al., in 1986. IHT in murine models (lymph node cancer of the prostate [LNCaP] and Shionogi carcinoma significantly delayed the onset of HRPC  and heralded the beginning of various clinical trials. Over the years, >20 phase two trials which have included >2000 patients have evaluated the feasibility, efficacy, and safety of IHT.  It is apparent that IHT has a beneficial effect on QoL and has additional advantages in terms of reduced health care costs. However, the two essential questions to be answered are:
Does IHT delay the onset of hormone resistance?Can IHT improve overall survival?IHT seems to fall short of expectations in the randomized phase III study by Calais da silva et al. It is known that patients with bulky disease, bone metastasis and PSA levels >100 ng/ ml have a poor response to IHT.  Hence, majority of the patients included in this study had asymptomatic, non-metastatic T3 disease and a Gleason score of ≤7. A later amendment restricted entry to PSA  or take antiandrogens to avoid side-effects of castration.
The highlight of the SEUG trial is the fact that it used a three- month induction period without any demonstrable impact on survival unlike previous trials advocating six to nine months.  At three months of induction, 81% of the patients were able to achieve a PSA nadir of  relative to continuous therapy but is still not comparable to the cost effectiveness of orchiectomy.
Results of the SEUG trial only fuel the debate as to whether the "average improvement in QoL" offered by IHT stands up to the "average improvement in quantity of life" promised by the conventional continuous therapy.
To conclude, the SEUG trial doesn't give us sufficient evidence to recommend its routine clinical use and we must await the results of other phase III trials to define a patient population most likely to benefit from IHT.
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