My PSA level on Friday was 0.14. So from a recurrence point of view, it is still below the 0.2 threshold for people who had their prostate removed through surgery and it is still MUCH below the 2.0 for people like me who had radiation instead of surgery.
Yet, my oncologist is very insistent that I go back on ADT. She wanted me back on ADT even when my PSA was of 0.09. The problem is that I don't want to go on ADT unless I really need it as it is quite debilitating for me.
So having already gone through the RT + ADT treatment with curative intent, and not presently having PSA level that is considered an indicator of recurrence, why would it make sense to go back on ADT right now since I am supposed to be fine for now (or possibly fine for a long while if, god willing, it does not rise above 2.0) ?
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Mascouche
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But in this case, why say that recurrence begins at 0.2 for surgery and at 2.0 for radiation? Why pretend that a treatment is curative if there is no level of PSA that can be considered safe?
Silly docs parrot "magic" numbers. Please don't allow them to convert you into a silly patient.
In a nutshell, your PSA is still being governed by the ADT that you recently had. It doesn't indicate anything more but that you are still hormone sensitive. PSA after ADT should be considered always side-by-side with Testosterone. After T comes back to your pre-ADT value, a time series of monthly PSAs will determine your PSADT. This will be the only true indication of your current status. Anything else is meaningless.
Thanks for the info Justfor_. Just looked at my old tests and pre-ADT my testosterone was between 18 and 20. Since it is now at 11.3, I should expect it to keep rising for some more weeks and the PSA will rise along with it.
I do appreciate your insights and wisdom as waiting until T is back to my pre-ADT levels before looking at my PSA Doubling Time.
I'm in a similar situation. Had 39 fractions of RT and 2 years lupron. Last injection June 2022. First PSA/T test 6 months later =<0.01,and T=0.5nmol/L
the recent 6 month test September PSA = 0.08 while T = 18 nmol/L (normal )
So while my PSA is now detectable I'm putting that down to the increase in Testosterone and still holding out for a cure. Like you my treatment was with "Curative intent". I'm in no hurry to go back on that LUPRON, but if PSA goes above 2.0 I guess I'll have to. I don't understand your Oncologists reasoning. Hopefully wiser heads here will explain it.
I read through your very detailed history. One thing I wonder - have you ever had a PSMA PET scan? For YEARS, normal PET scans showed there were “shadows” and not much more. In 2022, I had a PSMA PET which confirmed I had metastases to numerous bones.
I would suggest getting a PSMA Pet Scan. After seeing those results, you should have a better idea what your future treatment path should be. I agree that your PSA is quite low and wonder why ADT is recommended? It appears you and your MO do not always see eye to eye. Maybe obtain a second opinion and see what that MO suggests? Please keep us updated.
It was in my profile but I had not written the PSMA in front of the Pet Scan in my profile.
But in short, I had a PSMA Pet Scan in April of 2020 which showed some very tiny metastasis outside of the envelope that would be too small to show up on the previous scans. I was told they are in abdomen and pelvic region. Nothing on bones, lungs or otherwise.
When they decided to put me in a curative treatment, they opted to go back use CT Scans to restage me because they said that in Chart (or Stampede, I forget) it was CT Scans that had been used in those trials rather than the more powerful PSMA Pet Scans that might show metastases not otherwise visible under CT Scans and hence it was impossible to determine if the people in the trials might have also shown more metastases had they also used PSMA Pet Scans.
From my I hear, and I could very well be remembering this wrong, but I think that one of the issues with PSMA Pet Scans is that they are so powerful that they may detect metastases that are small enough that they might have been dealt with by the immune system itself unless they grew bigger. We apparently have at all times about 20,000 (or is it 20,000,000 ?) cancerous cells in our bodies but that are being handled by our immune system. The issue comes when the immune system is not taking care of those and lets them grow to become bigger is size/volume.
PSA is just a blood test, not a direct measurement of cancer tumor cell lines etc. A low PSA on ADT does _not_ mean cancer is gone. PSMA PET CT scans are not 100% accurate. See this link for more on that dailynews.ascopubs.org/do/d....
Thanks for the link. The article key points are pretty much was I was saying that my doctor had told me back then:
KP #1: The increased sensitivity of PSMA PET will reclassify patients into higher-stage disease states.
KP #2: PSMA PET has been integrated into the clinical decision before data supporting decision-making based on PET findings have been generated.
KP #3: Until data are available, we recommend disease volume based on conventional imaging be included in decision making.
This part also goes in the direction of false positives due to its power: "As PSMA PET scan use has become more common, we are also encountering an increase in false positive findings. Other malignancies can be detected via PSMA PET, as well as infections and benign processes such as Paget’s disease. We therefore recommend careful evaluation and verification, including potential biopsy, to confirm the diagnosis."
I am hoping I won't ever need it but that approach where you get a break after 36 weeks if your PSA is below 2.0 and remain on break until it reaches 5.0 does not seem as bleak as ADT non-stop for life. Of course it can make for a short vacation if your PSA reaches 5.0 rapidly.
Have you considered Taxotere and/or prophylactic radiation of lymph nodes outside the local area. I realize every case is different, but that combination enabled me to avoid ADT for 7+ years and keep my PSA below 0.20.
p.s. Personally I wouldn't get too hung up on who is "right" or "wrong" and instead focus on looking at the pros and cons of all alternatives. Adding another oncologist who has 1000+ prostate cancer patients might help investigate all your choices.
Thank you for your suggestion Ron. For the moment, and despite my oncologist wants, there is nothing to be treated since my testosterone has not yet fully come back and my PSA is still within the norm for someone who still has a prostate.
However, the day it becomes clear that the curative treatment failed, hopefully never but we know it is a beast hard to get rid of, then I am fine with discussing Taxotere with my oncologist.
That said, I do not think I could get prophylactic radiation of lymph nodes outside the local area since they already radiated my pelvic lymph nodes at the same time they were radiating my prostate.
I got my Taxotere plus prophylactic radiation of additional lymph nodes (north of the local area running toward the heart) when my PSA doubled from 0.03 to 0.06 and I consulted with Mark Scholz who is one of the best prostate oncologists. It may be a good choice for you if you really want to avoid ADT as long as possible. That 0.20 threshold is a somewhat arbitrary number. Your PSA velocity is more important.
It's your quality of life, not your doctor's, so it's your decision on how aggressive to treat. Virtually every treatment works best the sooner it's given.
Did you have surgery prior to that? I ask because you mentioned that your PSA doubled from 0.03. If you had surgery then being above 0.02 is likely that you have metastases somewhere. But if you did not have surgery, that 0.03 seems very low for someone who still has a prostate and is not on ADT.
On my first recurrence of detectable PSA, I waited until it reached 0.20. I wish I had not waited that long even though the location radiation gave me 7.5 years of undetectable PSA.
On my second recurrence of detectable PSA, I decided it was time for a more aggressive response - so I didn't wait until 0.20 (which of course would have given the cancer more time to spread and morph).
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