He was diagnosed in summer 2022 with stage 4, Gleason 4+4, PSA of 122 and many osteoblastic bone metastases throughout the whole skeleton (very high volume) He did the triplet therapy, which lowered his PSA to 0.4 (January 2023). Scans afterwards stated that the metastases are still there, but a little bit decreased in activeness.
Since then, he still gets his 3month Lupron shot, Xgeva and daily Zytiga (2x500mg and 5mg Prednison). The PSA declined further in 2023 every time it got measured and is now around ~0.03. During the summer he had no pain and one could forget that he has this terminal illness. In the last few months the pain, especially in the pelvic and the lower back, reoccured, more during the night, but also during the daytime here and there. A new MRI of the pelvic indicated that all metastases are still there and have become more sclerotic compared with the scans of 2022 (which regarding osteoblastic metastases I think isn't a good thing?). In the last session his doctor adviced him to increase the Predinsolon to 10mg because now he is mCRPC. He accepted this during the meeting, but afterwards didn't really unterstand why he was seen as castration resistant now despite the ever decreasing PSA. Could the doctor classify him as castration resistant just because of the result of the MRI? It's a bit until the next meeting with the doctor, so maybe someone here has some advice or a similar experience?
Thanks in advance for reading
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kennycool
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If the metastases grow, they are resistant against hormone therapy. You are usually determined castration resistant when the PSA value goes up in spite the hormone therapy. But it can also be based on imaging showing that the cancer grows. Increasing the dose of Predinsolon will not fight the cancer, just avoid side effects from Zytiga.
Don't worry about whether it is hormone sensitive or castration resistant. It is on a continuum, and not an either/or kind of thing. The only thing worth worrying about is whether the current therapy is helping, and whether a change in therapies is warranted.
There is a benefit in being deemed castration resistant because more therapies become available.
Thank you very much for the response, the continuum explanation is very helpful.
I will checkout the link you posted!
It's kind of strange, his PSA has fallen so much and declined every time, nevertheless on every CT/MRI/Bone scan he had since the diagnosis, stated the same: Diffuse osteoblastic / sclerotic bone metastases throughout the bones. No lesions in the bones disappeared, but the prostate has decreased in size.
My PSA dropped to below 0.1 and stayed there but the bone and node mets never shrunk. Then tumours started appearing in my liver and I was deemed CRPC. So you can progress to CRPC via scans alone even though the PSA stays very low - it depends on the specific type of PCa you have.
That's unfortunate for you mate, but nevertheless thank you for your input, I wish you the best. Sounds quite similar to my dad, I hope he is still far away from soft tissue mets.
How did they find the liver mets? Through scans or did some blood count indicate it?
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Statin and COX2 inhibitor for MCRPC?
Genetics tests: Genetics tests-what suggested for G9 mCRPC with low PSA, failed Zytiga
PSA on ADT but post EBRT
Stable PSA, deep fall testosterone lab results. 
PSA rising - follow-up, now falling again
