diagnosed April 2018 PSA 30 Gleason 9. On PET/CT PSMA found some uptake in several pelvic lymph nodes as well an inoperable prostate( out of the capsule)
Started Lucrin + Zityga on May 2018.
Did 25 sessions of whole pelvic IMRT on December 2018.
PSA readings during this time:
06/18 : 2.44
08/18 : 0.12 1.15ng/DL
12/18: 0.07 1.15ng/DL
3/19 : 0.04 1.15ng/DL
06/19: undetectable 1.15ng/DL
09/19:undetectable 1.15ng/DL
01/20:undetectable 1.15ng/DL
last Lucrin shot : April 2018
Stopped Zytiga: 06/20
05/20:undetectable 1.15ng/DL
09/20:undetectable 1.15ng/DL
01/21: 0.3 440 ng/DL
Due to the jump in PSA ,my MO ordered PET/CT PSMA which found a single uptake in rib 9 which could not be correlated to the CT findings and radiologist suggested doing an MRI.
What are the chances that the rib uptake is kind of false positive? is that possible ?
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dorke
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A single bone met is frequently a false positive. If there is no CT correlate just ditch this finding. Get another PSMA PET/CT at a PSA value of 2.0 ng/ml and check again.
"Our results indicate that the vast majority of these lesions have low‐intensity uptake and are benign. Intervention to confirm this is not usually required. "
Yes, there are false positives. They usually have a SUV of 4 or less. The MRI can help to make a final diagnosis.
If the SUV max uptake is mild and your alkaline phosphatase is a normal level, it could be a false positive. What was your alka phos reading? To me that is the most important number for a possible bone met. But...i’m not a brain
Yes ..You are a Brain..Anomalous.. Because you understand the importance of checking Bone Alkaline Phosphatase . BALP is a sensitive marker and will be up if there is bone met showing osteoblastic repair. If in normal range,.. then nothing to worry.
Alkaline phosphatase will not always be elevated especially with low burden bone metastasis. I had over a dozen bone mets early in my disease with normal alk phos. It is elevated now but that took nearly 4 years and loss of control of my disease. Labs are NEVER 100% sensitive or specific and alk phos is a terrible screening lab (ie low sensitivity).
See? I told you I wasn’t a brain. Despite tests of all kinds showing otherwise, PCA can appear and the tests seem to be a lagging indicator. Which is depressing
I've had 10 PsMa Ga68 PT-CT scans and one FDG PET scan and not one false positive. What I have learnt is that after first mets begin to appear in scans, more and more will follow as they grow big enough to be seen by scans. I also had Gleason 9, 2010, not operable, and had EBRT over 35 days and ADT. Psa went from 8 at aborted RP to 0.08 in 18 months. Then I quit ADT at 24 months, and within 6 months Psa was back to 8. I went back to ADT in mid 2013, and first mets were seen when Psa was 5 and ADT failed in mid 2016. All I can do is chase after the big mets, but maybe I have countless tiny mets for which nothing may work in future.
I had Cosadex, salvation IMRT, Zytiga, chemo, LU177, 7 6 doses, now will start Ra223 soon, but after that, Hoo Noze.
I Don’t get it. T is produced by the testes and adrenal glands. It’s not produced by prostate cancer. But T is a catalyst for prostate cancer which is why ADT is used to reduce T. Estradiol has the same effect as Lupron and its ilk except that it has less side effects . That’s why I switched.
The reason why ADT fails is that Pca mutates to be able to make its own supply of Testosterone in form of dy-hydro-testosterone, 20 times more powerful than T made by testicles or adrenal glands. When Cosadex, Xtandi, or Zytiga is added to ADT these interfere with adrenal gland T production and also interfere with T production in Pca, or they block any T getting to Pca. But then Pca mutates just little bit more and defeats all attempts to stop Pca from growing. A friend of mine who died last year got 3 months slow down of Pca from ADT, then ADT failed, and when Cosadex was added, it speeded up the rise of his Psa. He lived less than 3 years after diagnosis. I probably had Pca begin in about 2004, but Psa was <5 before I got examined with biopsy, and then they found in-operable Gleason 9, in 2009, so diagnosis was 5 years TOO LATE, and I am probably fighting the spread of Pca ever since before diagnosis. the first mets became visible with a first PsMa scan in 2016 when ADT failed. Nobody ever mentioned Estroidial to me.
The side effects of chemical castration by Eligard, Lucrin ADT for me were very mild, and although I did have hot flushes for awhile, I kept working OK and I kept cycling, and my mind remained sane ever since I began ADT in 2010.
My athletic ability now at 73 on a bicycle is as good or better than most other men 60 and over, and who have a full amount of T.
I prove that T is not necessary for a good QOL.
But I am now due to get Ra223. Doc giving this treatment must be away on holidays as he has not yet booked me in after my oncologist referred me.
I don't want a feminizing chemical to give me man-tits. I am still on ADT although I believe after it stopped working in 2016, adrenal gland T production continued, thus use of Cosadex and then Zytiga, and maybe by now my testicles are permanently ruined, and would not ever again make T, so I just don't see any reason to take any Estradiol. But its possible that nothing is stopping the small amount of T made by adrenal glands, but its very highly likely Pca is growing quite well by making its own T, or growing without needing any T at all. I have never read anywhere that says Pca that has gone to bones and does not respond to any form of ADT would now stop growing if Estradiol was used.
If there was something that worked reliably to stop Pca growing after ADT fails, we would all know about it and it would be part of mainstream therapy.
Yes, I thought it was a female hormone, but I have not heard of anyone here taking it recently here for suppression of Pca growth.
I did here of one man who was able yo get some bone marrow that was cloned up from a sample taken from Germaine Greer, the famous feminist. All went well, and he is now in remission, but ppl don't like him any more because he's had a terrible side effect of becoming a very grumpy old woman.
Get a copy of the PSMA scan on disc and take it or have it sent to the RO that did your pelvic RT. He can give you detailed opinion and check SUV max. The MRI of the rib area would be good to sort it out. Since your PSA jumped up you need to know if it is cancer outside the pelvis. Repeat PSA to confirm rate of rise will also be important information in planning how to proceed. You have had really good results so far so best of luck going forward.
Not sure about the references to "false positives"... Anecdotal? Please provide some substantial data to corelate the assessment. I've not read or seen any study indicating anything in that regard. The biggest issue with the "data" would be relavent to the person reviewing the scan, that is where the issue might occur (human error).
The G68-PSMA-PET scan uses an agent that attaches to a secretion that is present "only" with cancerous prostate cells. Therefore... It's not intuitive to think there could be a "false" positive. To be sure, there are known spots whereas the ligand will accumulate, such as the kidneys and salivary glands, etc. And disregarding those as uptake not associated with the presence of PCa cells requires a trained and proficient technician. Again... This is why it's very important to have such tests, especially when there's questionable conclusions made, viewed by a 2nd opinion, and one not associated with the treatment possibility.
G68-PSMA-PET scan is the most sensitive at this time for detecting the smallest lesions at the lowest PSA. But there still limits, size = >2mm and >.5ng or .8ng even better! Above +1.2ng or higher it all evens out with other scans if I recall correctly. For some advanced patients, I would be more worried about false negative, rather than positive! PSMA resistance is a real hoot! And there are some PCa variants that do not show the PSMA well... You can ask me about that sometime
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