Asking For Advice

[podsart]

Asking for Advice – all labs via Labcorp

Diagnosis: 10/2009 G 4+3, RP 1/2010, Active Surveillance [Dr Myers] till Feb 2016 when I started Xtandi; PSA went undetectable and stayed undetectable, as Dr Myers slowly reduced Xtandi dose till reached 3 x week. Dr Drake took over after Dr Myers retired. Became detectable [PSA=.014] on 5/30/22, when started Apalutamide. 12/8/22 PSA went undetectable for 2 years, then detectable 12/3/24 [PSA=.014]. Stopped Apalutamide. Apalutamide also had been interfering with stabilizing my thyroid [hypothyroid] and created a bad rash over my back and chest. Dr Drake said that a PSA of .014 is the first [all labs via Labcorp] PSA step above undetectable. Note: genetic analysis of remaining RP tissue showed PTEN silenced via methylation and a less understood ERBB2 mutation.

Dr Drake then put me on Relugolix monotherapy on 12/5/24, PSA went undetectable for a couple months, becoming detectable on 2-17-25 [PSA=.014, Testosterone=undetectable]. My labs included new thyroid data, showing a huge jump to hyperthyroid levels, which I think was the result of stopping Apalutamide [Dr Drake actually found data to support this]. Also, Vit D, which I check regularly, jumped above hi normal from average normal levels present over the past, Traditionally, I tweak my Vit D supplements to keep at Dr Myers target of about 75.

Dr Drake said that the PSA increase could be influenced by the large change in both the thyroid and Vit D levels. Not sure I believe this. What do others think?

I told him that I thought that each of these treatment failures indicated ongoing Pca mutation adaptions to these treatment pressures. He said that was low probability, for example, if I had a P53 mutation, my PSA trajectory would be different.

I understand that many don’t believe an increase of PSA from <.006 to .014 is meaningful; however, Dr Drake does. I know biological recurrence require 3 increases such as .01 to .02 to .03. Regardless, this change raises the issue of what are the best strategies now.

I know that multiple simultaneous treatments are better than my history of monotherapy.

The dr suggested that the initial strategy is to add Daralutamide [I understand I might not meet the requirements of Daralutamide, currently]. What are Pros and Cons of this first step strategy?

He suggested doing a PSMA scan when my PSA rises to a sufficient level for detection.

The dr suggested my redoing my MRI and Bone scans now. I told him I don’t understand why I should do these scans, which are not as sensitive as PSMA scan, at my current low PSA. Any ideas?

Subsequent possible additional treatments discussed: 1. Pluvicto and/or 2. Three cycles chemo

I remember at one time a trial indicated that chemo was better at hi volume Pca vs low volume. Don’t know if that has been superseded. So should I do chemo now, perhaps together with the daralutamide, to create a triple treatment scenario. Or is doing Pluvicto [assuming I am PSMA positive] a better first strategy?

I would appreciate comments and advice as how best to proceed?

[tarhoosier]

podsart I follow you as we have many similarities: Myers, mono enza, Drake and others. You raise several questions i am not competent to opine upon. What I can speak to: You see Charles Drake because he has one of the most advanced backgrounds in our disease. He spends most of his time now in his lab and has broad understanding of the processes involved in this disease. You are not comfortable with his suggestion about thyroid/vit D concerns. If it were me, I would trust him on that. He said “could” as no one can be sure.

If he thinks the rise is due to thyroid/D why remove or add a new drug? I am missing the context of your conversations with him.

He knows my history well and seems comfortable with a standard psa test3x/year and I concur. I am phelgmatic regarding this. This is different than your case.

He ordered a PSMA for me at 0.2-0.3 psa, well below the recommended level. For a baseline he said. A decent size spinal met was found then eliminated by RT.

Chemo at your stage, without evidence of conversion to neuroendocrine status seems premature.

I do not know darolutimide “requirements”. Do you mean prescribing? Clinical trial patient standards? Insurance coverage? Is he prepared to prescribe something not available to you?

I have no experience with his office making an appeal of insurance denial of a drug.

What does he believe is the baseline number for a PMSA scan for YOU?

Might this bone scan /MRI baseline for be his thinking for you?

Your response does not provide a doubling time.

Why does he think a new drug intervention at such an admittedly low psa is warranted?

Those two possible treatments he/you discussed: were they imminent? Future possibilities?

The time span/interval for these possible treatments, what was the discussion about that?

I do not know your age.

I wish you the very best.

JohnC

[podsart in reply to tarhoosier]

Thanks

“if he thinks the rise is due to thyroid/D why remove or add a new drug?” I think he wants drive my PSA to undetectable ASAP. Rebalancing the thyroid is trial and error process, which can take months. Vit D as an oil, which will take time to dissipate.

“I do not know darolutimide “requirements”. I am referring to the typical insurance coverage requirements for this drug.

“What does he believe is the baseline number for a PMSA scan for YOU?” I think like for you 0.2-0.3

“Might this bone scan /MRI baseline for be his thinking for you?” Not sure what you mean by this statement

“Your response does not provide a doubling time.” I don’t have enough PSA detectable data to be able to calculate a true doubling time yet.

“Those two possible treatments he/you discussed: were they imminent? Future possibilities?”

He wants to see what my PSA will be when I start the daralutamide and then a 1 month later to see the impact of the daralutamide. After that I think these other treatments will be then really considered.

“The time span/interval for these possible treatments, what was the discussion about that?” He was vague as to when these 2 possibilities could be implemented. Think he wants to see:1 how my PSA moves between now and the time I start the daralutamide and 2. How the PSA reacts to the daralutamide.

“I do not know your age.” 78 y/o

Thanks Again,

[Tall_Allen]

I can't see any benefit in more therapy when your PSA is only 0.014. IMO, patients should only use the standard PSA test (lowest value 0.1 ng/ml) -- anything else only causes anxiety and there are no treatment changes called for.

[podsart in reply to Tall_Allen]

Thanks

[Justfor_]

"Dr Myers slowly reduced Xtandi dose...." This is just what I have been doing 3 years now with Bicalutamide. They tell you to switch to single decimal place reporting. Analyzers and assays today drill down to the thousands and results are rounded down to the tenths. It is very difficult to find a 30+ year old analyzer still working and if you could find one in a museum any left over assay must have already reached it's expiration date same decades ago. What they really tell you is that up to 0.049 you are good to go because this will be rounded down to less than 0.1, ("undetectable*) but, you don't need to know the exact value as you will start asking questions that your doc doesn't have answers to.

[podsart in reply to Justfor_]

thanks

I am in florida for a couple months, live in NY otherwise. I wonder whether there is a higher ultrasenitive PSA test LabCorp error rate in one part of the country versus another.

[Justfor_ in reply to podsart]

I don't know the specifics in your country, but my best guess is based on the labs turn over on grounds that more tests boost personnel competences and provide financial space for better equipment, maintenance, calibration and consumables inventory. In addition, error rates represent the errors that had been identified and not those that had passed unnoticed. Based on this reasoning, I believe that Florida, being the home of an army of retirees, must have higher demand for PSA tests and thus lower error probability compared to NY. Just a Greek's wild guess.

[NanoMRI]

Offering my thoughts to your asks. Docs' and patients define recurrence with various values and rules; cancer has it's own rules. Prior to my RP nine years ago I chose to rely on uPSA <0.010 as best indicator (no drug involvement). My post RP nadir was 0.051 and cancer indeed remained. I do not need an algorithm to determine 'recurrence'.

I would take your doc up on the imaging - seems willing when many are not. My uPSA has been a slow steady rise from <0.010 since February 2020. I began investigative efforts including liquid blood biopsy testing and imaging at 0.03 - that was in late 2021.

I have 0.050 in mind as value to consider further treatment actions unless LBB and/or imaging indicates cancer sooner. Until 0.050 I am content having regular uPSA testing, scheduled liquid blood biopsy testing and imaging, and focusing on fitness and diet to comeback stem/senescent cells (referencing a previous post of yours). If I need treatment(s) I do not yet know what they might be. As you are, I am educating myself on all my options. Hope this helps. All the best!

[podsart in reply to NanoMRI]

thanks

"I would take your doc up on the imaging" I will get a scan when my PSA is hi enough to give relevant results. The issue is that I dont see value in getting traditional MRi before a PSMA scan, which i more sensitive and can see smaller mets.

[NanoMRI in reply to podsart]

You asked There are varying opinions on when to image and what to image with. The docs I consult with see value in comparative imaging - MRIs, bone scans and other methods. I see no value in giving this beast time to grow and spread so many mets can be seen.

As I share, seven years ago I went to Europe for imaging that was not available to me here in US - actually done at 0.093. Although the PSMA was clear the Ferrotran MRI identified multiple cancerous lymph nodes.

Commenting on your reply to Justfor_ , yes you can get PSA tests reporting to diffent thresholds. You do not have to use ultrasensitive. Yes, some speak out against uPSAt, but they are wrong on their benefit post RP; a benefit not everyone wants. I self-direct my testing at various labs as I travel - use RequestATest and WalkInLabs.

[podsart]

thanks- good point

[CrackerOcala]

I don't understand the concern over one hundredth of a point. Seems overhyped but maybe that's just me.

[podsart in reply to CrackerOcala]

I understand: numerically it seems like a small change

Guess the issue is that it crossed line between undetectable and detectable. Apparently, some, including my Dr feel that going from <.006 to the.014 meant the pca went a totally senescent (sleeping state) to coming out of this “inactive” state.