Do False-Stable results exist? My latest tests

VascodaGama said:

Another climb in the cycle of my Off-drugs period

For those who have been following my story, I want to inform that the PSA test of this month increased to 1.49 ng/ml. I think this to be more realistic than the previous result of December (1.28) because it comes from an unstained blood sample “clean” of drugs influence, which also excludes 3 months of daily Sinvastatine(s), stopped last December. Statins are known to influence and mask the PSA result.

The increase is not much but an exponential growth calculation indicates a value of 2.0 occurring by August 2015, and probably reaching the 2.5 threshold sometime within this year. I have missed in past calculations, however, I think that the PSA shows cancer growth (not indolence) so that sometime this year I will try having that state-of-art image exam (C11 choline or F18 choline), and then restart the hormonal treatment (IADT).

This accomplishment represents almost 4 years of life without symptoms and the effects of the drugs. I am pleased with the outcome.

Best wishes to everyone in their fights.

VG

Numbers

I have started trying to memorize all of the Threshold numbers in post-treatment PSA, mostly form you yourself, V .  I get my first post-RP psa drawn next week, and am hoping of course for "Undectable."

Impressionistically, your changes do seem very slight.  Plus, the HTs work so efficiently for so many, many years, and have so many variant drugs that is seems you are in for smooth sailing for a long time to come, hopefully decades.

max

VascodaGama said:

Thresholds

Guys,

Thank you for the gentile words.

In systemic cases like mine one has the disadvantage in finding a quick cure but got the advantage of modalities that prolong control over the years while newer technologies establish reliable bases in the “trade”. The way we analyse cancer and treatments today are much more “sophisticated” then what was set as standards back in 2000 (year of my diagnosis).
There is no silver bullet yet and the way to treat is still the “stone age” approach of cutting off the rotten flesh or “burn” it out for good. But these jobs can be done now with precision and lesser risks. Details on cancer behaviour are now known better too and the techniques to find it are wider and more precise. All of this provides better tools in the judgement of a case and in the decision to tackle it.

Thresholds are a set of tools important in sequential therapies. It serves also in the judgement of successes or recurrences. In Max case the traditional PSA=< 0.03 to 0.06 at the two weeks post RP is an important marker of success. In my case the trigger threshold to restart IADT is PSA=2.5 but the common PSA level in IADT is 5.0 to 10.0 ng/ml. This is accommodated when the patient has still the gland in place.

Many guys after failure just give up and try to enjoy life as it comes. Others like me try the sequential where thresholds are important in the management of a certain control. Extending life is important to avail of the advantages I spoken above.
Not to border you with matters of systemic cases (not yours) but to explain an example on the benefits in trying to postpone a treatment or extend control, I can describe about my case. As you know the aim is to check if my PCa case relates to oligometastases. The main job is to get a picture (positive) of the bandit’s location. I know via recent researches and trials that image studies with the choline contrast agent are more reliable than any other contrast agent for recurrence PCa cases. This was not available ten years ago but even now, within the past two years while on my HT vacations (IADT), more progress is seen since researchers identified and set that F18 choline is more practical in exams than the C11.

F18 (FCH) has a half life of 110 minutes whether C11 is 20 minutes requiring a cyclotron machine at the facilities doing the test, otherwise one would risk negative results (with “dead” choline). The F18 (FCH) can use two different substances; the Fluoroethylcholine or the Fluoromethylcholine, which provides higher possibilities in the procurement of the contrast agent. However, both fluors are easier to be lost during the exam due urinary excretion. In this matter C11 choline is a natural product and not easy of being excreted. ADT also interferes with cell's uptake of choline so that the exam must be done in a "clean" status.

These findings provide me the ways to choose the best reliable hospital/clinic where to get a reliable exam and consequently the best oligometastatic diagnosis. From there I can choose my future treatment or step.

Best.

VG

 

A great line
One comment in your post reminds me of a comment the actor Patrick Swazey made in an interview with Barbara Walters, shortly before he died of pancreatic cancer. She asked him about his treatments (which was a horrible chemo) and he said,

"Yea, we have 'medicine' -- cave man medicine, medicine that makes you crawl around on the bathroom floor all night."

He was frustrated, understandably . Things are better now in treatments, but we aint there yet.

VascodaGama said:

Thresholds

Guys,

Thank you for the gentile words.

In systemic cases like mine one has the disadvantage in finding a quick cure but got the advantage of modalities that prolong control over the years while newer technologies establish reliable bases in the “trade”. The way we analyse cancer and treatments today are much more “sophisticated” then what was set as standards back in 2000 (year of my diagnosis).
There is no silver bullet yet and the way to treat is still the “stone age” approach of cutting off the rotten flesh or “burn” it out for good. But these jobs can be done now with precision and lesser risks. Details on cancer behaviour are now known better too and the techniques to find it are wider and more precise. All of this provides better tools in the judgement of a case and in the decision to tackle it.

Thresholds are a set of tools important in sequential therapies. It serves also in the judgement of successes or recurrences. In Max case the traditional PSA=< 0.03 to 0.06 at the two weeks post RP is an important marker of success. In my case the trigger threshold to restart IADT is PSA=2.5 but the common PSA level in IADT is 5.0 to 10.0 ng/ml. This is accommodated when the patient has still the gland in place.

Many guys after failure just give up and try to enjoy life as it comes. Others like me try the sequential where thresholds are important in the management of a certain control. Extending life is important to avail of the advantages I spoken above.
Not to border you with matters of systemic cases (not yours) but to explain an example on the benefits in trying to postpone a treatment or extend control, I can describe about my case. As you know the aim is to check if my PCa case relates to oligometastases. The main job is to get a picture (positive) of the bandit’s location. I know via recent researches and trials that image studies with the choline contrast agent are more reliable than any other contrast agent for recurrence PCa cases. This was not available ten years ago but even now, within the past two years while on my HT vacations (IADT), more progress is seen since researchers identified and set that F18 choline is more practical in exams than the C11.

F18 (FCH) has a half life of 110 minutes whether C11 is 20 minutes requiring a cyclotron machine at the facilities doing the test, otherwise one would risk negative results (with “dead” choline). The F18 (FCH) can use two different substances; the Fluoroethylcholine or the Fluoromethylcholine, which provides higher possibilities in the procurement of the contrast agent. However, both fluors are easier to be lost during the exam due urinary excretion. In this matter C11 choline is a natural product and not easy of being excreted. ADT also interferes with cell's uptake of choline so that the exam must be done in a "clean" status.

These findings provide me the ways to choose the best reliable hospital/clinic where to get a reliable exam and consequently the best oligometastatic diagnosis. From there I can choose my future treatment or step.

Best.

VG

 

Driving a stake!

Driving a stake in the heart of Psa. Is not to wait for prostate cancer to spread with 2.5 psa, but to be pro-active and keep your the numbers to .01or under <1 and getting the "T" number's down too. Your T number's look high and inviting for the cancer to eat. Even at psa of 2.0 in the eye's of MDACC was bad and that was the reason to start Zytiga 3 years ago. Staying ahead of my T and beating back psa, although a active life was not as great as it should been. Got my last number's sent starting Xtandi in December.

December 15 6.1psa at VA hospital

January 20 5.4psa at MDACCFebruary 20 4.7psa at VA hospital

March 20 5.2psa at VA hospital

T number's not detectable <40

AS always, VG stay Strong and Prospers

Ralph

VascodaGama said:

Ralph: Care with refractory

Ralph

Thanks for the opinion and advice.

I think doctors at MDACC are right in keeping T low while controlling the progress with the PSA.
Systemic patients (the ones with failed radicals and salvages) should avoid all means of “whipping” the cancer into activity, “prohibiting” the “free” circulation of testosterone (used in frenzy cancer feeding parties), or should avoid stressful situations in life, or opting for diets and supplements that create environments not beneficial to the cancer. One must be careful with his life style.

However, hormonal treatments have shown to be better if administered intermittently. This on/off methodology allows the body to recuperate from the hypogonadism status with the benefit of a symptom less period and allowing other body systems (that use T) to return to normal functions. It also extends the period of effectiveness of the hormonal treatment (period on drugs) till one becomes refractory, and in need of changing protocols.

My treatment involves this intermittent modality. The thresholds regulating the switches on/off come from cancer activity in PSA terms, ON: PSA=2.5, Off: PSA<0.05 during 12 months. The Testosterone marker serves to certify the hypogonadism status. It also designates refractory status (failure of therapy) when one got increasing PSA in a low T environment. I think this theory has been applied to your case so that when the PSA increased to 7.6 at low levels of T (<40), indicating refractory, the doctor changed protocol from Zytiga to Xtandi.

Your last test has slightly increased (4.7 to 5.2) but nobody can yet judge this result as refractory of the newer drug. If the increase continues (for six months) you will have to stop Xtandi because cells started AR mutation (androgen receptors), and they may be feeding on the Xtandi itself.
This is a period when the bandit survival is not depend on the testosterone your testis may produce. It will feed on the antiandrogen you are supplying freely, and latter it will mutate again to start producing its own androgens. At that time your doctor may suggest again that you restart Zytiga or take as a substitute the old drug Ketoconazole plus prednisone. These second-line HT drugs prohibit cancer to “make” androgens from cholesterol.
When all fails, one may look for control possibilities within the chemo weaponry.

Important note to you: I would like to recommend you to discuss with your MDACC doctor about any possibility in taking Xtandi at the evenings before bed time. This may help you to sustain better the drug’s side effects. Just try it.

Best,

VG

Yes

VG,

When I was taking Gary to the cancer center for his end-stage disease, the NP explained the "intermittant modality" of the HT drugs, almost exactly as you just did.  Sadly, as I have written here before, Gary was NOT a cooperative or "good" patient, -- too hot-headed, and would quit therapies in mid-stream, refusing to even call the doctors for extended periods, sometimes even months ! This undoubtedly reduced the effectiveness of his treatments dramatically.

Played correctly, what I have read and heard explained to me directly (regarding Gary) is that these therapies can, in many cases, work for many years. And, you are the master violinist; play it like Beethoven !

For those who do not know, "Gary" was a friend of mine who died a year ago last September, after a 13-year fight with PCa, which involved surgical removal, months of radiation, hormanal therapies, and finally all of the chemos. The timing or layout of all of this is too complicated to relate here, but I do recall that after surgery he went about five years before beginning radiation, which was his first salvage therapy. 

max

VascodaGama said:

Another twist in my PSA results

I received today a lower PSA value of 1.30 ng/ml. This is a return to the levels of December 2014 after the increase of 1.48 in March 2015. I do not understand the reason for this “seesaw” kind of results but the testosterone is also lower at 252 which could be affecting cancer activity (?).

May 2014; PSA=1.20 ; T=341
Sep 2014; PSA=1.24 ; T=356
Dec 2014; PSA=1.28 ; T=278
Mar 2015; PSA=1.49 ; T=?
Jun 2015; PSA=1.30 ; T=252

As I posted above, my plan is to have an exam (image study) before restarting the hormonal treatment (IADT) to verify any case of oligometastases and to such purposes I want to wait for an increase in the PSA (closer to 2.0) to avail of the best chance for a positive scan. Maybe I should celebrate today’s lower result because it is providing me a longer term off-drugs and therefore off the side effects.
Mean while the cancer is also enjoying the frenzy and that makes me anxious.

The physician looking upon my case has changed in April. I got a younger uro-oncologist who I meet in my last consultation. We discussed the oligometastases treatment concept in my case which he applauded. However he pointed out that in the presence of micrometastases, one should think that not all the metastases will show up in the “sophisticated” image study, because the many still in micro sizes will develop later. More or less it is what occurs in systemic cases.

I am set and signed to participate in a clinical trial for the newer exam named 68Ga-PSMA PET/MRI. This will compare results with the exam F18 (FCH) choline PET/CT, therefore I will take both. I have already discussed with the radiologist that is in charge of the trial at Coimbra University Hospital, so that we are ready only waiting for the increase of my PSA.

This trial is also in execution at the US National Institutes of Health. Please see this;
https://clinicaltrials.gov/ct2/show/NCT02282137?term=68+psma+pet/ct&amp;rank=1

Here are several links regarding the exams, in case someone wants to know details;

http://www.ncbi.nlm.nih.gov/pubmed/24072344

http://www.ncbi.nlm.nih.gov/pubmed/25412869

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311230/

http://www.ncbi.nlm.nih.gov/pubmed/24352789

http://www.researchgate.net/publication/244481682_PETMRI_with_a_68Ga-PSMA_ligand_for_the_detection_of_prostate_cancer

A friend (traveler) send me this article from Dr. Myers Journal in regards to differences between C11 choline and C11 acetate. The main difference seems to be the way our body metabolises the substances. C11 choline requires one to be clean from HT drugs for the test while C11 acetate doesn’t.

I recommend to my friend comrades in particular Hopeful to read the article that also discusses patients in AS;

https://gallery.mailchimp.com/c0d8ce0558462196cd0d62682/files/ProstateForumJune2015.pdf?utm_source=Rivanna+Health+Publications&utm_campaign=c2e53dfd98-Prostate_Forum_June_Attempt_26_2_2015&utm_medium=email&utm_term=0_bc8795358a-c2e53dfd98-149107997&ct=t(Prostate_Forum_June_Attempt_26_2_2015)&mc_cid=c2e53dfd98&mc_eid=10beaa2195

Best wishes,

VGama

Thank you for the update

I wish you the very best through this and find the science fascinating.

VascodaGama said:

Another twist in my PSA results

I received today a lower PSA value of 1.30 ng/ml. This is a return to the levels of December 2014 after the increase of 1.48 in March 2015. I do not understand the reason for this “seesaw” kind of results but the testosterone is also lower at 252 which could be affecting cancer activity (?).

May 2014; PSA=1.20 ; T=341
Sep 2014; PSA=1.24 ; T=356
Dec 2014; PSA=1.28 ; T=278
Mar 2015; PSA=1.49 ; T=?
Jun 2015; PSA=1.30 ; T=252

As I posted above, my plan is to have an exam (image study) before restarting the hormonal treatment (IADT) to verify any case of oligometastases and to such purposes I want to wait for an increase in the PSA (closer to 2.0) to avail of the best chance for a positive scan. Maybe I should celebrate today’s lower result because it is providing me a longer term off-drugs and therefore off the side effects.
Mean while the cancer is also enjoying the frenzy and that makes me anxious.

The physician looking upon my case has changed in April. I got a younger uro-oncologist who I meet in my last consultation. We discussed the oligometastases treatment concept in my case which he applauded. However he pointed out that in the presence of micrometastases, one should think that not all the metastases will show up in the “sophisticated” image study, because the many still in micro sizes will develop later. More or less it is what occurs in systemic cases.

I am set and signed to participate in a clinical trial for the newer exam named 68Ga-PSMA PET/MRI. This will compare results with the exam F18 (FCH) choline PET/CT, therefore I will take both. I have already discussed with the radiologist that is in charge of the trial at Coimbra University Hospital, so that we are ready only waiting for the increase of my PSA.

This trial is also in execution at the US National Institutes of Health. Please see this;
https://clinicaltrials.gov/ct2/show/NCT02282137?term=68+psma+pet/ct&amp;rank=1

Here are several links regarding the exams, in case someone wants to know details;

http://www.ncbi.nlm.nih.gov/pubmed/24072344

http://www.ncbi.nlm.nih.gov/pubmed/25412869

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311230/

http://www.ncbi.nlm.nih.gov/pubmed/24352789

http://www.researchgate.net/publication/244481682_PETMRI_with_a_68Ga-PSMA_ligand_for_the_detection_of_prostate_cancer

A friend (traveler) send me this article from Dr. Myers Journal in regards to differences between C11 choline and C11 acetate. The main difference seems to be the way our body metabolises the substances. C11 choline requires one to be clean from HT drugs for the test while C11 acetate doesn’t.

I recommend to my friend comrades in particular Hopeful to read the article that also discusses patients in AS;

https://gallery.mailchimp.com/c0d8ce0558462196cd0d62682/files/ProstateForumJune2015.pdf?utm_source=Rivanna+Health+Publications&utm_campaign=c2e53dfd98-Prostate_Forum_June_Attempt_26_2_2015&utm_medium=email&utm_term=0_bc8795358a-c2e53dfd98-149107997&ct=t(Prostate_Forum_June_Attempt_26_2_2015)&mc_cid=c2e53dfd98&mc_eid=10beaa2195

Best wishes,

VGama

Comments

I do not think that your 'see saw' PSA results are significant. Rather, I just see statistical variation of the assay around an average (aka mean).

Your conclusion that the cancer is "enjoying a frenzy" is speculative, and in my opinion, erroneous. If so, your PSA would have risen significantly. Hence, you can relax.

PS: I spent many years in biological research and have done (too) many assays...

I would like to give you advice, Vasco

I would love to tell you what I think about all of this, Vasco. Please accept this explanation and my apology. I don't understand it well enough to talk about it! In other words, you are dealing with matters that are above my comprehension and understanding.

Just kidding; trying to get a laugh and have a little fun. You are so very knowledgeable about PC and so willing to share and help the rest of us. Thank you.

Old-timer Jerry

VascodaGama said:

Increased PSA but lower Testosterone

(My RP experience)

This week it makes 15 years since my first attempt to free me from the bandit. My open prostatectomy was done in August 15 of 2000, 3 months after being diagnosed with PCa. I recall well that occasion. On the previous evening the surgeon, Dr. Komatsu, introduced to me and my wife his operating team composed of 5 specialists. He explained the details of the whole procedure, its risks, etc, and requested us to sign an agreement (sort of consent relieving them and the facilities from unpleasant outcomes), recognizing our total understanding of the operation. Later some guy came to my room to shave me from knees up except the head. On the “D-Day” with an empty stomach at noon time one nurse and the doctor in charge of the pre-operative preparations gave me a pill for relaxation, dressed me into a light white gown and then took me on a stretcher to the corridor, to an elevator and down to the surgery theatre. My wife accompanied me all the way and we said good bye when pushed into the hall. There two doctors dressed in green gowns asked me if I knew them. They were the anaesthetists. They informed of their job and asked me to show my back. I was already sort of drudged with the relaxation pill. Then I felt a sort of cold liquid flowing into my spine (epidural anaesthesia, and fall asleep right away. Much later, I recall being awaken at one time (during the operation, I guess) by the doctor calling my name to which I answer (I saw three or four silhouettes over me) He asked me if I was feeling all right and I said that I felt urinating. Then I heard him saying “give him more anaesthesia” and I fallen asleep again and only awaken at around 22H00 at the recovery room, and saw my wife in front smiling at me. She had been the whole time of the operation in a wanting lounge where she was kept informed on the progression of the surgery. She told me that Dr. Komatsu at one time shown her my prostate gland (on the way to the pathologist lab of the hospital) explaining that it looked normal in aspect shape and size. He told me later that the operation took 5 hours and that he had carefully suck/vacuum all liquid and pieces of soft tissue surrounding the organs before stitching me up.

I stayed in the hospital 17 days (5 in preparation for the operation and 12 for recuperating until the catheter was taken out). The hospital facilities (in Tokyo) and staff were excellent. Well looked after, clean and efficient. Two days after operation I was standing and walking in the hospital’s corridor (a squared ring of 350 meters long) pushing a tripod with attached medicine tubes and catheter sac. I never experienced pain and felt good for the physical movements. Five days later I could go out and enjoy the outer fresh air at the hospital‘s gardens.

 

In this anniversary I got the periodical PSA result. It increased to the levels of March 2015 at 1.48 ng/ml. It is higher than the previous but still low and I am not sure if the level is acceptable to the 68ga PSMA PET/MRI trial. I hope Coimbra hospital allows me to wait for another increase.
What surprised me this time is the level of the testosterone. It has been decreasing since September 2014 from T=356 to T=209 ng/dL (Aug 2015). This is considered lower than normal in a 65 years old man. I would appreciate if some comrade here could give some “light” on the incidence. What can be causing the decrease? Should I try TRT?
I recall a survivor in this forum (Jogger; http://csn.cancer.org/node/234869#comment-1207973) commenting about his experience with decreasing levels of Testosterone, but do not know exactly how he managed to control his status at the end.

What can an ADT patient do when his body lowers the testosterone naturally to such levels under the 280 threshold (normal = >280 ng/dL)?

Best wishes to all.

VGama

 

Why Are You Worried?

Why are you concerned about your testosterone level?  What does your doctor say about it?

High testosterone (T) is commonly associated w/PCa growth, so if the higher than expected post-surgical PSA is of concern, I'd think that a low T-level would be the least of your problems.  Low T-level is commonly associated w/ED (or lack of sex drive), depression, fatique and a loss in bone density. Are you experiencing any of these things?  If so, then perhaps some treatment is warranted.  However, such treatment is not normally recommended for PCa patients.

My guess is that if you raise your T-level significantly, it may trigger PCa growth in some way and cause your PSA to rise further. So, I guess it all depends what you consider most important -- raising your T-level or lowering your PSA.  Personally, unless the low T-level is causing a specific identifyable medical/psychological problem, I'd focus on keeping your PSA as low as possible and avoid unncessarily simulating PCa growth by increasing your T-level. 

It's a tricky problem.  Good luck with whatever you decide to do.