Interesting new study (off-topic for most of us) [1].
"We retrospectively analyzed RARP patients whose pathological stage is T2a to T3b without lymph node or distant metastasis from 2007 to 2017. All patients received a daily dose of 0.5 mg of dutasteride {Avodart} when post-RARP {Robot-Assisted Radical Prostatectomy} PSA levels were increasing but had not achieved biochemical recurrence."
"None of the patients received radiotherapy (RT) or androgen-deprivation therapy (ADT) before taking dutasteride."
"Twenty-three out of 35 included patients (65.7%) did not require further RT/ADT." "The cut-off value of the PSA level to avoid further RT/ADT was 0.195 ng/ml."
"If dutasteride was provided before the PSA value increased to 0.195 ng/ml after RARP, it would reduce the probability of acquirement of RT/ADT."
Front Oncol. 2019 Aug 2;9:691. doi: 10.3389/fonc.2019.00691. eCollection 2019.
Early Dutasteride Monotherapy in Patients With Elevated Serum Prostate-Specific Antigen Levels Following Robot-Assisted Radical Prostatectomy.
Lu CH1, Ou YC1, Huang LH1, Weng WC1, Chang YK2, Chen HL2, Hsu CY1, Tung MC1.
Author information
1
Division of Urology, Department of Surgery, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan.
2
Department of Medical Research, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan.
Abstract
Background: To evaluate the efficacy of early dutasteride administration in patients with a detectable prostate-specific antigen (PSA) levels after robot-assisted radical prostatectomy (RARP). Methods: We retrospectively analyzed RARP patients whose pathological stage is T2a to T3b without lymph node or distant metastasis from 2007 to 2017. All patients received a daily dose of 0.5 mg of dutasteride when post-RARP PSA levels were increasing but had not achieved biochemical recurrence. PSA levels were monitored every 3 months after dutasteride administration. None of the patients received radiotherapy (RT) or androgen-deprivation therapy (ADT) before taking dutasteride. All follow-ups were begun from RARP to January 2019 or to the date of RT/ADT. Results: Thirty-five patients were included in this analysis. The median followed up was 53.6 months. Twenty-two patients (62.9%) showed a PSA response in which the PSA decreased more than 10% at the first follow-up after dutasteride administration. The Pathological stage > T2 (p = 0.012) and positive surgical margin (p = 0.046) were prognostic factors for a PSA response. Twenty-three out of 35 included patients (65.7%) did not require further RT/ADT. The significant risk factor was the PSA level (p = 0.011) at the beginning of dutasteride treatment. The cut-off value of the PSA level to avoid further RT/ADT was 0.195 ng/ml. Conclusions: Early dutasteride administration showed a significant decline in the PSA levels of patients with pathology stage >T2 and positive surgical margin in our retrospective hypothesis-generating study. If dutasteride was provided before the PSA value increased to 0.195 ng/ml after RARP, it would reduce the probability of acquirement of RT/ADT.
KEYWORDS:
biochemical recurrence (BCR); dutasteride; prostate cancer; prostate specific antigen; robotic assistance for radical prostatectomy
"Conclusions: Early dutasteride administration showed a significant decline in the PSA levels of patients with pathology stage >T2 and positive surgical margin in our retrospective hypothesis-generating study. If dutasteride was provided before the PSA value increased to 0.195 ng/ml after RARP, it would reduce the probability of acquirement of RT/ADT."
How does this square with well known phenomenon that PSA readings when on Avodart to Proscar are roughly 50 % of actual clinical results when when compared to PSA reading prior to usage of these drugs?
I do not find reference to this in study abstract.
In the U.S. it is considered 'normal' for the aging male to have BPH. BPH increases PSA levels. The drugs you mention are FDA-approved to treat BPH & thereby reduce PSA.
When I was diagnosed, the PSA cutoff for biopsy was 4.0. I did not have BPH & my PSA was only 0.8. For men with BPH successfully controled by these drugs, 4.0 would not be a good threshhold. For untreated BPH cases, 4.0 might have been a good cutoff, although BPH 'noise' can vary quite a bit.
In the study, there wouldn't be any benign cells remaining after RARP. Therefore, no BPH noise.
In these cases, PSA is taken to be attributable to cancer cells. If the men with very low PSA saw no increase while on Avodart, this would be due to a real effect of Avodart on the cancer. No PSA adjustment required.
Hi everyone, brand new here. Hello and sorry to be here with you all but obviously good information and nothing to lose by educating and supporting each other.
I heard about this trial two weeks ago and it applies to me pretty closely. I had RARP in April 2019 and am gleason 9 stage 3b with sv invasion on one side. The surgeon did nerve sparing on one side and there was no lymph nodes affected yet. He said it went well but gave me the you never know type answer. By end of October my PSA was .02 and bythe start of February .17. He has now referred me to a RO which I don't yet have an appointment scheduled. Not long after that I saw this trial and immediately contacted him and asked to go on Avodart. At first he said it doesn't apply to me and it wouldn't help because that drug was only for BPH and because I had no prostate it wouldn't do anything. I referred him to the actual trial and when he had read it he relented and wrote me a 3 months prescription. So now I will find out if it helps me at my next psa appointment at the end of May, and in the meantime will see a RO to go through the initial consultation for that. The only thing I'm concerned about is that I'm afraid whether the Avodart masks with a lower PSA but somehow cancer is growing somewhere. I read a post on another website that had happened to another person and now he has mets and stage 4.
The problem with responding to old posts is that most men have moved on. I began the thread & so I was notified when you posted.
Glad to have you in the group. Suggest that you introduce yourself to the others via a completely new post.
I had surgery 16 years ago. I have spinal mets. I have been using Avodart for years.
Masking of PCa only occurs when Avodart has been used for BPH. It beings the PSA down for the BPH cells.
For PCa cells, the inhibition of DHT may reduce PSA - more likely it will lengthen PSA doubling time, if it does anything at all. That isn't masking, though.
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