I'm confused about something, and I'm hoping someone can clarify.
In an interview I saw with UCLA's Michael Steinberg re: PSMA imaging, he says that there's a 50-50 chance of finding something at PSA 0.2, and if you wait until you're at 0.35, you're risking missing a chance of preventing metastatic disease. If you find something and radiate it, with Gleason 8+ (mine is G4+5=9), it should be done with 12 - 18 months' ADT. Is this correct?
My local people are telling me that treatment isn't mandatory until my PSA is in whole numbers, as high as 4 or 5. I suppose they both can be correct. I.e., in the absence of a positive scan, it's OK to wait much longer. Correct?
Has anyone come across anything recently that further validates tE2 as ADT?
Thanks very much.
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The purpose of the PSMA scan is NOT to detect mets to be treated (although if they are detected, you can try to treat them, but there is no data that that will improve survival).
Your situation is that you have failed prostatectomy. The new PSMA PET scans are good at ruling OUT distant metastases. That means that salvage radiation should be done UNLESS distant metastases are discovered. The exception is if metastases are found in pelvic lymph nodes (stage N1). Then, there is still a chance that with salvage whole pelvic radiation and 2-3 years of ADT, the cancer can be cured.
But you should NEVER wait for PSA to rise just so you can detect metastases. If you wait, you WILL detect metastases and it will be too late to cure you.
OK, thanks. My PSA has risen from 0.1 to 0.2 over a period of three years. G4+5=9. PSA at dx 11. IMRT after RP with positive margins. What would be recommend for me, and when?
So, you have a very slow PSADT. All you can do is monitor it closely. If it speeds up, you can have a PSMA PET scan. If in pelvic LNs, you can irradiate the entire area.
Hi TA - My husband is in a similar situation (RP, ADT, UCSF Androgen Annihilation Trial) with currently rising PSA (2 month doubling time). At this point we understand the goal is not curative, but long term management. Dr. Agarwahl recommended waiting until PSA was .5 for a PSMA scan. His PSA has reached .5 and he’s scheduled for the scan Monday at UCSF. We thought 1 purpose was to see if something is visible to be targeted. Although we’ve read a lot, we both find ourselves confused and with even more unanswered questions. Any clarification would be much appreciated. Perhaps this question should be posted as a separate thread? Thanks for any help and guidance.
The value of targeting of distant mets has not been established, but why not if it is safe? Important to include lifelong systemic therapy too if there are metastases.
Because there are thousands of metastases you can’t see. Pissing in the ocean doesn’t get the ocean any wetter. Picking a mushroom doesn’t slow down the fungus plant.
I understand that there are thousands invisible metastases, but they're not (currently) threatening the patient's life, correct? It is for this reason that I would think the repetitive process of scan/radiation would extend OS.
Obviously, it's not curative.
To go back to your mushroom analogy, of course it would be far better to kill the fungus, but given that that's impossible, if you don't want big ugly mushrooms on your lawn, you CAN pick the visible ones every few days.
Metastases threaten patient's life when they invade bone marrow, bones and organs. We KNOW the best way to slow down their growth and spread is with systemic therapy. There is no data yet to reinforce your belief that radiation of metastases has any oncological benefit. I'm not saying there is no benefit; in fact, I'm saying why not treat them if safe? But the greatest documented benefit is from systemic treatment. Systemic treatment is known to shrink metastases and delay progression.
Well, here's a question for you. My MO says: a) scan at PSA 0.2, and b) IADT for life when PSADT<10 months (regardless of actual PSA value). Are you saying if the scan shows ANYTHING, I should be on (I)ADT for the rest of my life regardless of my PSA/PSADT?
Now, if your metastases are detectable on a PET scan/CT but not a bone scan/CT, iADT monotherapy may be all you need for now. But given all the above, what do you feel comfortable doing?
What the people at City of Hope say is to get a PSMA scan if PSA increases markedly/rapidly from here (0.2). Re: treatment if mets detected, radiate and try to quantify the increased OS from IADT begun immediately vs. some time in the future.
I've seen papers that report zero difference from immediate commencement of ADT vs. waiting for clinical progression.
When required, go with tE2, and see how I feel.
This is trickier for me than most people because my 18-month experience with Eligard was essentially torture. I really wanted to die, and it was a horrific experience for my wife and kids watching me suffer.
I don't understand what you mean by "Re: treatment if mets detected, radiate and try to quantify the increased OS from IADT begun immediately vs. some time in the future." Increased survival is only vs a control group - not from an individual.
"I've seen papers that report zero difference from immediate commencement of ADT vs. waiting for clinical progression." But if you have metastases, you already have clinical progression. You don't re-stage just because you zapped it.
You can talk to your MO about something experimental like Zytiga or Xtandi monotherapy.
Re: ADT, I have reason to believe that tE2 will be far more tolerable.
I'm also on antidepressants now, where I wasn't while I was on Eligard. That alone may make a difference.
Worst case, one more thing that's improved in the interim is Relugolix. Knowing that I can take a break and feel good again in a matter of weeks is a huge relief.
I did 5 months of estrogen patch ADT. No mental issues. I've done 5 1-2 month ADT sessions since then. Most of them were with Lupron but one with Firmagon and one without drugs (my endogenous T was zero at the time). During each of the short ADT sessions, I used a low-dose estrogen patch (0.05 mg/day). No mental issues.
One time I tried not using the estrogen patch. Within 2 weeks I was in a bad place mentally and my wife almost moved out. I learned my lesson. It is possible that it was a coincidence but the mental state that I was in was like no other in my lifetime and cleared within hours of replacing hormones (I replaced testosterone with Androgel but I don't have reason to believe that estrogen wouldn't have kicked me out of the mental pit).
Before I started the 5-month estrogen patch ADT four out of four doctors that I talked to said that it would not work. Two of them went so far as to tell me that the estrogen would not cause my T to go down. One finally admitted that he really didn't know. One of them said that my T would go down but that they didn't think it would go low enough. I thought otherwise but at least one MO that I talked to said that it would do something. She's been my MO ever since. ... my T was undetectable for 5 months and my PSA was <0.01.
It never ceases to amaze me that specialists in MO will give their opinions on a subject, in this case parenteral high-dose estradiol as ADT, when they have no idea what they're talking about. All they need to do is read the latest study.
I agree. I'd respect them much more if they admitted ignorance. We all have it and it's not a sin. Whether we choose to admit it or not is another story. If someone can't admit when they are wrong they are less of a person in my eyes.
So the doctor who admitted ignorance after I pressed him is my urologist to this day. The doctor who actually knew a little bit but told me that she didn't "think" that estrogen patches would lower T enough is my MO to this day.
If you want to be a BS artist as a real estate salesperson or a grocery store manager, I don't have a huge problem with that. In medicine, where people's lives are at stake, however, it's unacceptable.
It never occurred to me to be skeptical of a doctor's advice until PCa came into my life. The urologist who did my RP left me with positive margins, which happens, but he also dislodged one of my ureters, leaving me with a nephrostomy for four months, thus delaying IMRT to my G4+5=9 tumor, and resulted in permanent 100% ED or no sexual feeling in my penis, ending my sex life and turning my wife into my roommate.
I was even OK with this until I was one of four people in a nine-man support group who had had their lives ruined by the same surgeon.
I tried to get his license to practice medicine removed, but the top hospital administrator sensed that I was trying to sue, and shut me down.
As I told her, "I'm here only to protect other innocent men. I had a problem that was weighing on my conscience. Now it's weighing on yours. Good bye."
If the PSA is 0.2 after a prostatectomy, if nothing is shown in the PSMA PET/CT you should discus whole pelvis radiation. ADT may be considered it but it may not be necessary if the PSA is less than 0.5.
If the scan shows distant metastases you should discus ADT for life plus abiraterone or other new anti androgen or ADT for life plus chemo or a combination of ADT for life plus chemo and abiraterone..
If there are distant metastases you could go outside the SOC and do ADT and Lu 177 PSMA therapy, in Europe or India, if financially possible. If it works stop ADT and see what happens. It is unknown if this approach will offer a survival advantage over the SOC. There are not data I know showing this approach is better or worse than the SOC mentioned above.
I was trying to avoid radiation if possible. A post-RP surgery Gallium68 PSMA saw affected nodes that were missed during surgery. Option was radiation or a second surgery…I chose surgery as the urologist/surgeon was optimistic about the outcome. Well, it didn’t work and my PSA began to rise a few months later. Second G68 scan at .5 PSA showed two tiny lymph mets and a met on my iliac spine (hip bone). Now I’m on ADT (Lupron/Zytiga/prednisone) and have had great results. PSA has been undetectable now for nearly a year.
My understanding is initially after RP and PSA rising That you've eliminated the source of new PC "mothership" with the RP.
The cells that already escaped will land and anchor, they stay there where ever there is.
They then have to grow substantially before they can become a spreader to additional spots and this is not achieved until a high PSA much higher than is needed for a effective scan.
Estradiol has been found to reduce cardiac and bone problems compared to standard ADT , but does cause breast enlargement. I’ve found it to be a lot easier to endure than standard ADT and easier to stay on “ permanently “.
I have oligometastatic Pca. I’ve used SBRT to kill three bone mets over the last four years . But it’s clear that high risk Pca ( I’m 4+5) requires systemic treatment. It’s my belief that with oligomets , SBRT confers an advantage and it’s been proven that guys with oligomets survive longer which makes intuitive sense. Lower volume = longer survival.
I believe I’m a case in point. In 2013 at age 69 after psa reached 6.6 a biopsy showed Gleason 4+5=9 but low volume. I had RP later that year which failed in that psa never reached zero . RP disclosed that I was stage T3b with SVI, ECE and positive margin at site of ECE, but negative lymph nodes. When Psa increased to .3 in 2014 I had SRT to prostate bed . A year later in 2015 I had a MRI which found two suspicious iliac lymph nodes. So I had whole pelvic IMRT.
I was on intermittent ADT. Whenever I stopped it, psa quickly increased . In 2017 an axumin scan at psa of 1.2 found a femur met which I hit with SBRT . In 2018 a Ga68 PSMA scan at psa of 1.9 found one met on scapula and one on a rib. Again I hit them with SBRT and went on estradiol patches in early 2019 realizing I needed full time systemic therapy. My psa stayed at nil then gradually increased to .2 then .5 and the latest was .6 this October. T stays at 3.0.
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