My first meeting with a medical oncologist is a week from Tuesday, on 19 March, so I’ve been putting together a series of questions to ask.
I’d like to leave the meeting with an understanding of whether there’s value in delaying the start of hormone therapy so my PSA can get high enough for a PSMA PET scan to locate the cancer so we know exactly what we’re dealing with, or if it’s better to start hormone therapy sooner rather than later.
I’d also like to understand whether they would want to start with just ADT or with a combination therapy of ADT and antiandrogen therapy and how to manage the side effects from both options.
I’m sure I’ll post an update after the meeting.
On an unrelated general health note, I’ve been pretty faithful about getting in a daily walk this year. I started out with short walks and now I’m up to 6 km / 3.7 miles per day. So far this year, I’ve logged about 240 km / 149 miles. Not bad for this old geezer who was always picked last for the team in school PE classes.
Stay tuned for more.
Dan's Journey through Prostate Cancer 
Hi Dan, you probably know this particular PCRI video.
This Dr Kwon video is interesting and perhaps applicable to your dilemma.https://www.youtube.com/watch?v=81iAzYV39Gw
You can skip to about 12 minutes in when he goes over the need for PET scanning. The bit he doesn’t cover is the rate of detection of prostate cancer versus the PSA. As you know at very low levels of PSA the rate of detection can be low too as you have found from your own experience. Allowing the PSA to rise to 1 to 2 ng/ml increases the sensitivity to around 90%. This is covered in another PCRI video by Dr Mark Sholz. As Dr Kwon argues if you don’t know where the hot spots are, your treatment is sub-optimal. So this forces the patient down the route of systemic treatments such as ADT and chemo and larger field radiotherapiy because the patient and doctor don’t know what they are dealing with. In this video is an interesting example of two patients with a PSA of 36 but with very different prostate cancer situations. If the source of your PSA rise is a single lymph node then a zap of radiotherapy to that particular lymph node becomes a possibility. ADT treatments of Lupron and or one of the newer ones like Xtandi are needed when the cancer is too spread or large etc. Anyway best of luck with your research and resolving your dilemma.
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Thanks, Charles! You’re right. I actually had posted that video on my blog on 13 December 2021 and had forgotten about it. It was good to watch it again.
Believe me, I’m in no rush to start any systemic treatments if we don’t know what’s going on yet.
Thanks again!
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High five for logging those miles, Dan.
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Thanks, Frank!
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Dan,
Just a thought – it “may” be that your PC is growing much slower than you think. I watched your slow PSA rise over the years and then your PSA spike before the decision to start SRT – and just want you to know that a PSA spike is sometimes not indicative of a real trend. I have communicated with Dr. Schulz about PSA spikes and he mentioned that they are not uncommon and often a pattern of PSA rise reverts to what has been historically more normal for an individual. Given that – optimistically…I hope that you find that after your ADT stoppage and you reach the end of the “reactivation” phase (period when PSA climbs rapidly with testosterone coming back)…your PSA continues its historical slow rise.
Please note that from a fairly recent UCI Med. Center article on PSA & DT kinetics it was postulated that up to one third of BCR could be low risk (PSADT greater than 12 months…with other criteria) and may be able to be safely followed with active observation versus treatment (obviously – observation now includes PSMA PET/CTs at appropriate intervals for possible targeting). “If” I understand it – their theory is that some PC cells escape the prostate prior to surgery and typically land in the pelvis (lymph nodes, nerves, etc.) causing a slow PSA rise…and unlike other cancers – a subset of cells seemingly lose the ability to further metastasize & progress…sincerely hope you might be in that group of patients.
Max
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Hi Max,
Thanks so much for taking the time to post such useful information. It will be interesting to discuss with the MO next week.
I know that many guys would love to have a PSA at my levels, so I am aware that it may be too early to know what’s really going on. And given my long run-up (6 years) to biochemical recurrence, I’m in no rush to start ADT quite yet, so the UCI Med. Center study is good to know. (Although my PSADT is 6.2 months using my last 5 readings.)
It would be interesting to know the timing of a “reactivation” spike in relation to the end of the effectiveness of the ADT dose. My six-month dose of Eligard was given on 3 May 2022 and should have “worn off” around 3 November 2022. (I know it’s not like turning off a light switch; the ADT may linger for a while longer.) So does that reactivation phase happen three months after the dose wears off? Six months? A year? All things to ask the MO.
In my case, the PSA hit 0.13 and 0.11 in March and May 2023, four and six months after the dose should have worn off. It hit 0.21 a year after it should have worn off and 0.33 thirteen months after it wore off.
The thing that rattled my RO and making him think something else was going on was the fact that the PSA had climbed to slightly higher than it was before we started SRT (0.37 v. 0.36).
We’ll see what the MO says next week but, at this point, I’m inclined to do my next PSA test in the second half of April (3 months from my last one), and see where it lands. You could be right. The rate of increase between my last two readings slowed compared to my previous two readings, so this may confirm that slowing. Or not. I think that waiting the full three months between PSA tests has value, too, in that we’ll get a better picture of what’s happening over time.
Sorry. I’ve rambled on. But thanks again for your insights, as they have given me food for thought for next week.
Dan
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