This subject is coming over and over into surface, so I decided to start a specific thread as I got bored in writing the same things over and over again:
Post RP patients with a rising PSA are discouraged to take a PSMA PET/CT imaging before deciding on sRT, on the grounds that it will detect "nothing" at their low PSA value, usually in the range of 0.1 to 0.2.
First important comment is that the pre-test PSA value is not the only and _certainly_ not the best metric for this. PSADT is more important, but the clumsy way by which PSADT is usually derived leads us to better leave it out of this discussion. A brief explanation to this is that PSADT is the mathematical/numerical first derivative of PSA. Elementary knowledge of math and their application to measurements, indicates that the accuracy of the first derivative of any variable is an order of magnitude inferior compared to that of the variable itself. Taking 20% as a ballpark for the PSA measurement accuracy, the thus derived PSADT mounts up to 200%. There are ways to do better for the former and consequently the latter, but this is not our current subject.
Now lets have a look at Table 4 of the paper entitled:
"Use of gallium-68 prostate-specific membrane antigen positron-emission tomography for detecting lymph node metastases in primary and recurrent prostate cancer and location of recurrence after radical prostatectomy: an overview of the current literature" (2019)
ncbi.nlm.nih.gov/pmc/articl...
Three studies for the PSA range of 0.01 to 0.20 (cumulatively 121 cases) are recorded. Out of them 59 cases (48.8%) led to a positive detection. The second comment here is that the radio tracer used in all three studies was 68Ga while today there are its 18F counterparts that are considered of being more sensitive in the lower PSA scale. Also, since 2 years ago there are digital PET scanners that are equipped with more sensitive detectors. Consequently, this 48.8%, considered as "nothing" by the naysayers, is a conservative figure by today's standards.
But the most important part of this discussion comes from the break-down of the location of the detected lesions:
Recurrence fossa only: 17 cases -> 14%
Pelvic lymph nodes +/- fossa: 22 cases -> 18%
Distant metastases +/- fossa: 20 cases -> 16.5%
Now, if we make the assumption that a similar break down characterizes all the lesions that due to their low concentration (not size < 5 mm - another grossly silly statement) that evaded detection, it is clear to see why sRT has a ~65% roof in success score. The remaining ~35% failed because the cancer was distant or distant as well to the irradiated field.
Lastly, there is the ultimately silly argument: Why take the test if it is not going to change your treatment plan. Because, there is a myriad of studies concluding that after a positive PSMA detection 1/3 to 1/2 of all irradiation plans were modified slightly or heavily to the limit of excluding this 16.5% (distant metastases) as bringing nothing but late toxicities.
The only difficult thing about it is to find a competent RO among the sea of incompetence that wants to rule.
~6 months ago I asked my MO for a PSMA scan. She said that my PSA was too low (zero) and that the insurance companies would deny it unless my PSA was over 0.3. I replied, "0.3? I can do that". She didn't really understand what I meant (my wife was with me and she looked at me and laughed - she knew that I wasn't joking).
I might readdress this. I'm doing BAT+ and on the high T phase, my PSA goes well above 0.3. So far it has been undetectable a month into the low T phase. I can easily get her proof of PSA > 0.3 (last phase I went as high as 0.71).
If you really want a PSMA test and need your PSA to be >0.3 to get one, maybe a few applications of Androgel will get you there?
First, edit your last paragraph to read PSA instead of T.
Second, in my case I highly doubt it. My currently endogenous tT is ~2000.
I will pay out of pocket and be done with it.
That is really high. What type of T are you using?
I use Androgel and propionate, and soon I'm going to try oral undecanoate. Recently I tested Androgel efficacy so I applied 300 mg and had my tT measured 4 hours afterward to get the approximate max. It was 4971 ng/dl, fT was 181 ng/dl and bioT was 4481 ng/dl.
My PSA when I got the T up to 1800 measured 0.2-0.3 with corresponding lower levels of fT and bT (SHBG and albumin haven't changed much). I had my PSA measured at the same time as the 4971 T test and it was 0.71. I hope that it was due to androgen stimulated PSA increases NIH estimates the PSA increase from T can be 7x or higher. The graph below is from the patient's guide to BAT by Denmeade. Cancer can be regressing yet PSA increases. My MO discussed that with me. Even my urologist at Mayo hinted at it years ago.
That said, I wouldn't advise doing SPT unless you really like that particular QoL and are willing to take risks to get it. If you want to go the insurance route you might need to find a more sympathetic MO. My MO told me that even with undetectable PSAs she would authorize the test for me. But she told me that my insurance would not pay and that there was "nothing to find" in my case. Still, it would be nice to get a baseline so I might ask her again. And now I have the required insurance company proof.
Thanks for letting me know about my grammatical error. I wrote that at 3 AM my time so I'm surprised that it was in English and was somewhat legible.
Thanks for the graph, I will study it to see if there is something compatible with my personal case as, in the past before starting Bicalutamide, I had tried the correlation of PSA to tT, even that of the rate of rise of PSA to tT with R^2 coefficients disappointingly low.
I use two labs. The first specifies the method for tT measurement as: Electrochemiluminescence / ECLIA. After starting Bicalutamide, reported values are more volatile, spanning from 2250 to 3090.
The other lab, doesn't specify the method used but reports lower and more tightly spaced values (1650-1700) for the same period.
My regards to your MO. She got a seat in my non-silly doctors list. Kudos to her!
That's right. I forgot that you were on Caso. That will cause your serum tT to go high. Do you have fT and bioT measurements from pre and post-Casodex? We could maybe see something from the individual levels (activity).
The graph is in this doc:
1. Bipolar androgen therapy (BAT): A patient’s guide - Denmeade - - The Prostate - Wiley Online Library
onlinelibrary.wiley.com/doi...
Even if r-squared was better it's a moving target. Be hard to get a good correlation without hundreds of data points and maybe that wouldn't be good enough. My self stats are problematic but I think that they are infinitely better than nothing. And many times they are better than what we get in trials. People have various responses. Even the experts know this and sometimes scratch their heads and look for clues. Yet people frequently fall into the trap of thinking that everyone is average and acts the same. Wrong. Why did I respond so well to high testosterone for 2 years? Why did my PSA never bounce high after I started?
Here you are, if you can spot anything useful.
Do you have that in excel? Do you mind sending me a copy? (PM me if you want)
PM me your email and thy receive.
Russ, you have got mail.