Do False-Stable results exist? My latest tests

13

Comments

  • tonycue
    tonycue Member Posts: 39
    Best of Luck in All of the Above

    The Headline says it all

        Best wishes    Tony

  • Max Former Hodgkins Stage 3
    Max Former Hodgkins Stage 3 Member Posts: 3,767 Member

    Keep the Faith

    In March of 2014 I posted here a thread under the title “IADT- vacations period very close to its end”. I did it because of PSA fast increasing results since the end of the effectiveness of the last Eligard shot (Leuprolide). I was freaking out and anxiety has set in.

    Since then the PSA has maintained a sluggish advancement in a sort of plateaued pattern. The last PSA (Sep 2016) at 1.56 ng/ml again confirms the situation (Jun 2016 PSA=1.59). Another interesting aspect of the results is that the testosterone which has been decreasing since Sep of 2014, has now double the previous (T=181) increasing to T= 364, meaning that I have more T-serum in circulation very opportune and tempting for the bandit to start a T frenzy cocktail party again.

    This result marks the period of vacations away from hormonal drugs in 4 .5 years and 5 years (58 months) since my last Eligard 45mg shot. I am still far from the PSA=2.0 trigger threshold to restart HT. Before that I will have the expected image study so much discussed in above posts. The length on vacation have provided me with chances in getting better image exams that were still on the drawing boards before starting this thread.

    In the last blood tests I also have verified an increase in liver‘s function indicators (AST, ALT, GGT) which have double now at AST=47 UI/L; ALT=83 UI/L; GGT=78 UI/L. ALP has decreased to 63 (indication of other enzymes proliferation). The Microalbuminuria,Creatinine and Glomerular filtration rate (GFR) maintain the higher levels now making me to believe that I am experiencing pre-diabetes. The best I can do is to change diets, giving up with sweets, animal protein and animal fat, and give preferences to fruits, vegetables, and whole grains products, in other words, trying to become healthy again. Can I do it?

    Best to all survivors in their journeys,

    VG

    Poker

    You continue to show your mastery over PCa at the poker game of HT, Vasco.  It sounds like things will remain stable and managable for a long time to come.

    I have had elevated AST-ALT levels for decades, much higher than your current numbers.   I attribute part of this to earlier liver trauma, part to fatty liver.  Fatty liver (which I suspect you do NOT have) is indeed controllable with diet.  The statin drugs  (Lipitor, etc.) can also control it in many situations.  And alcohol is to be taken in moderation, if at all.

    Keep winning and we will keep being impressed,

    max

  • Old Salt
    Old Salt Member Posts: 1,003 Member
    edited October 2016 #44
    Looking good!

    In my simple mind, that's a great result, especially considering the testosterone uptick.

  • Will Doran
    Will Doran Member Posts: 207
    Same Path

    VG,

    Congratulations, again.

    It sounds like we are on the same treatment path.  My PSA has been holding at <0.010 for three years (post surgery and radiation) while my Testosterone has been at 17 (normal being 250 - 1,100). I was on Lupron. I month ago I had blood work done and my testosterone has made a slow climb to 170 and I'm now back to 320, in the normal range. My PSA is at 0.035 at this time.  I've been off the Lupron for 10 Months now.  Last shot was Oct. 2015.  Doctors say as long as I stay below a PSA of 2, I can stay off Hormone therapy.  If not then I will go back on some sort of Hormone Therapy.

    Let's hope for the best, and that we can continue to stay off the hormone treatments.  However, if I need to go back on those treatments, then I will do it.  As you said.  We will "Keep the Faith".

    Love, Peace and God Bless

    Will

  • Josephg
    Josephg Member Posts: 326 Member
    Keep the Faith

    Vasco,

    Your management work of your PCa, your complete transparency and candor through your continuing journey, along with your informed perspectives and thought-provoking recommendations, are truly inspirational to all of us.

    You are ESSENTIAL to the continuing success of this forum.

  • VascodaGama
    VascodaGama Member Posts: 3,581 Member
    Let’s talk about statins and its influence on kidney function

     

    I appreciate all the good wishes laid here from my buddies. I am keeping the faith and hope you do it as well.

    Max’s comments on statins, has awaken my long curiosity in the action of these drugs. I am taking Simvastatin 20mg on On/Off intervals periods of: two months On three months Off, with the intent of controlling high blood pressure (high but not super high).
    From researches, I know that statins can mask the PSA to certain extent, as well as influence the lipids levels. They also reduce cholesterol by eliminating the HMG-CoA reductase, an enzyme in liver for the production of cholesterol; however, one of the side effects of all statins is to increase ALT. The drug’s manufacturer cautious and recommends to stop the drug if ALT levels rise above 10-fold the upper limit of normal (61 UI/L), or persist in being above 5-fold elevated. Fortunately this is not my case now with ALT=83 UI/L. I wonder if statins also increase AST, the other marker for liver function impairment.

    Dr. Myers and famous PCa oncologists use statins in their protocols of drugs-cocktails as protective means against drugs side effects. In one of Myers video, he comments on his preference for Crestor (Rosuvastatin) which is a newer statin class drug, seems to be the best in handling hypercholesterolemia. It also increases the level of HDL, the good cholesterol, and it seems to be friendlier to liver than the other statins (comparing with past experiences). I do not know if Crestor is preferred by Myers because of lesser interaction with HT drugs, in particular with Ketokonazole, one of the common HT drugs of his arsenal. How far is it better than the others in regards to keep ALT within normal levels is unknown as it also metabolizes in the liver via CYP 2C9, (the same coenzyme used by the other statins).

    Lipitor (Atorvastatin) is known in lowering the lipids (therefore its trade name).but it is similar to Simvastatin regarding the increase of ALT. It is also known to be linked to the causes of type 2 diabetes. I wonder what would be its actions in liver enzymes. The lipids (hydrocarbons) are the little parts making the cells, which, similarly to these, become the building blocks of our body.

    Most probably all the above effects have something to do with kidney function impairment (?). This is of concern to me because malfunction of kidney limits the use of contrast agents, even prohibiting PET exams. I have a lower creatinine at 1.61 ng/dL but still high above the normal of 1.20. Last year it was 1.77 which could turn my oligometastases treatment adventure into jeopardy. I have no evidences but I read about some guys being refused the PET exam because of their creatinine set above 1.70 ng/dL. This is the main reason for my interest in verifying/regulating liver and kidney functionality.

    I would appreciate any note from you about this subject. It would help me to understand better the waters I am sailing in.

    Thanks again.

    VGama

  • Max Former Hodgkins Stage 3
    Max Former Hodgkins Stage 3 Member Posts: 3,767 Member
    edited October 2016 #48
    Josephg said:

    Keep the Faith

    Vasco,

    Your management work of your PCa, your complete transparency and candor through your continuing journey, along with your informed perspectives and thought-provoking recommendations, are truly inspirational to all of us.

    You are ESSENTIAL to the continuing success of this forum.

    Wow

    Joseph,

    You said to Vasco what I meant to say, but couldn't.  Perfectly stated.

    max

  • Old Salt
    Old Salt Member Posts: 1,003 Member
    edited October 2016 #49
    About statins

    First of all, statins are not used to lower blood pressure. They are used to lower LDL and possibly raise HDL; triglycerides may also be lowered.

    Secondly, statins do not eliminate HMG-CoA reductase; they inhibit the enzyme.

    Statins (all of them) have well known side effects, and it's recommended to have period checks of liver enzymes etc.

    To my knowledge, simvastatin was one of the early statins. Lipitor is a later one, marketed by Pfizer, but now available as a generic (atorvastatin). Crestor is yet a newer statin, still under patent protection. I don't know if there is evidence that it is 'better' than atorvastatin. It is used at a lower dose than atorvastatin, but that doesn't necessarily mean that it's 'better'. It's conceivable that the side effects are less, but I haven't looked.

    With respect to scans, it is practice (in the US) to determine kidney function (creatinine) prior to administering certain imaging agents.

    As an aside, I have been a long-term statin (initially Lipitor but now the generic) user; as recommended by my highly-qualified cardiologist.

  • VascodaGama
    VascodaGama Member Posts: 3,581 Member
    edited October 2016 #50
    Old Salt, Thanks for the comment

    Old Salt,

    Thank you for tunning in. You are right regarding the statins not being used for lowering the blood pressure. My mistake. I am taking Adelat 35 daily for the blood pressure and aspirin 100mg since 2001 at recommendation by JH oncologist. Simvastatin is to control the cholesterol which has been good even when off the drug, now at 180 mg/dL. Regarding the PET scans do you know what is the upper limit of creatinine for acceptance to the tests?

    Thanks in advance.

    VG

      

  • Swingshiftworker
    Swingshiftworker Member Posts: 1,013 Member
    My Experience w/Simvastatin and Atorvastatin

    I have a long history of high cholesterol which I believe to be genetic, not dietary, because the quality of my diet is very low in any form of fat and I also exercise -- lifting and cardio -- actively 3-5x's a week.

    I was a long time user of simvastatin which kept my cholesterol in check for many years but my current PCP switched me to atorvastatin a couple of years ago, which reduced my "bad" cholesterol and improved my "good" cholesterol levels noticeably even further.  So, at least in my case, atorvastatin seemed to be more effective than simvastatin. 

    Just recently had a complete blood array done and there were no red flags -- everything w/in expected levels -- including liver and kidney function.  I've also not noticed any negative side effects from taking either medication.

  • Old Salt
    Old Salt Member Posts: 1,003 Member

    Old Salt, Thanks for the comment

    Old Salt,

    Thank you for tunning in. You are right regarding the statins not being used for lowering the blood pressure. My mistake. I am taking Adelat 35 daily for the blood pressure and aspirin 100mg since 2001 at recommendation by JH oncologist. Simvastatin is to control the cholesterol which has been good even when off the drug, now at 180 mg/dL. Regarding the PET scans do you know what is the upper limit of creatinine for acceptance to the tests?

    Thanks in advance.

    VG

      

    Dear Vasco

    I don't know the answer to the above question, but I did find out that hospitals have protocols to make sure the kidney can handle the imaging (agent). Patients with renal insufficiency and/or diabetes mellitus are especially at risk.

    I did find a paper which stated that some institutions regard a creatinine level >1.5 mg/dL as 'abnormal'; while others use a level above 2.0 as 'abnormal'. It looks like you may be somewhere in between. But as I wrote, the radiological institute should be able to tell you what they find acceptable for YOUR scan, using YOUR health data.

     I hope this is somewhat helpful

  • VascodaGama
    VascodaGama Member Posts: 3,581 Member
    edited January 2017 #53
    Hibernation; What is going on?

    With no apparent justification my cancer decided to hibernate. This week's PSA test returned to 1.47 ng/ml, lower than the previous of Sep 2016 (PSA=1.56) indicating a complete plateau since March of 2015. My uro has no idea for the fact and I wonder what is going on. Testosterone has fluctuated alot since Sep of 2014. This time it is 262 ng/dL, lower than the previous of 364. This variation could have some influence on the PSA level but the values are still indicative of a sort of hibernation by the bandit.

    My vacations away from hormonal drugs continue, however, I am now trying to regulate the creatinine levels which increased to 1.65 ng/dL. As commented before, this marker may be problematic for my expected PET exam. I am scheduled for a CT scan this week to verify any kidney mal function. All markers have increased above normal and I have no clue for the causes. Have I diabetes? Is there any problem with the liver?
    I hope to sort out the facts the soonest.

    Best to all,

    VGama

  • Will Doran
    Will Doran Member Posts: 207
    Good for you

    VGama,

    Glad your PSA has settled in.  That's what my doctors are hoping will happen to me.  If so then I can hope to not have to go back on HT either drugs or Orchiectomy.  They said my Testosterone could come up and then go back down a little and settle in. That was because I had been on Lupron for 2 years.   

    If I may ask---Do you have pain in your testicles from time to time?  I do and I have been told that is the hormones changing.  There are times that I can barely touch myself. The pain comes and goes.  Some days it's really uncomfortable.

    As to the Creatinine levels,  My last test showed a level of 0.98, which is the correct range.  I guess I really don't know anything about those numbers, but I do know that my Doctors check that every time they do blood tests.  My level has always been in the proper range, so We don't talk about that much.  In my last blood work, I showed my Serum / Plasma Urea Nitrogen/creatinine mass/volumn to be 24 with normal being 7 - 18, and my mass ratio for the same being 24.9 with normal being 10 - 20.  So, those are up a little.  I guess I'll have to see what that means.  I'm going to look at my tests from last year to see where those levels were. 

    Went back and looked at my levels from the last two years on my medical potal through the hospital.  The serum plasma urea nitrogen mass volumn was 17, then 21.2 and is now 24. The mass ratio was 22.4 and is now 24.9.  So, not sure what that means.  Do you know?  I guess I will find out when I get to my rescheduled appointment on Jan 27.

    Good Luck

    Love, Peace and God Bless

    Will

  • Old Salt
    Old Salt Member Posts: 1,003 Member

    Hibernation; What is going on?

    With no apparent justification my cancer decided to hibernate. This week's PSA test returned to 1.47 ng/ml, lower than the previous of Sep 2016 (PSA=1.56) indicating a complete plateau since March of 2015. My uro has no idea for the fact and I wonder what is going on. Testosterone has fluctuated alot since Sep of 2014. This time it is 262 ng/dL, lower than the previous of 364. This variation could have some influence on the PSA level but the values are still indicative of a sort of hibernation by the bandit.

    My vacations away from hormonal drugs continue, however, I am now trying to regulate the creatinine levels which increased to 1.65 ng/dL. As commented before, this marker may be problematic for my expected PET exam. I am scheduled for a CT scan this week to verify any kidney mal function. All markers have increased above normal and I have no clue for the causes. Have I diabetes? Is there any problem with the liver?
    I hope to sort out the facts the soonest.

    Best to all,

    VGama

    January PSA

    Whatever the reason, your recent PSA test result should be comforting.

    I hope that the other tests (creatinine etc) won't raise any alarms.

  • VascodaGama
    VascodaGama Member Posts: 3,581 Member

    Please read my new thread on the above subject.

    https://csn.cancer.org/node/307433

  • VascodaGama
    VascodaGama Member Posts: 3,581 Member
    edited July 2017 #57
    Another PSA and another suspicious result

    For those interested or following my story, I want to inform that I am now celebrating my fifth year on vacation from the HT drugs. I am glad for successfully being able of reaching this mile stone in such long period free from the side effects, but not all was like a smooth walk in the park. I was not free from anxious moments at each time I did the PSA or experienced suspicious symptoms. In fact I am wary of the results with sharp increases and decreases since Dec 2014, when I started this thread.

    The last PSA was again lower than the previous, returning to the levels of 2016. The histology goes as follows;

    Dec 2014; PSA=1.28 ; T=278
    Mar 2015; PSA=1.49 ;
    Jun 2015; PSA=1.30 ;
    Aug 2015; PSA=1.48 ; T=252
    Nov 2015; PSA=1.46 ;
    Feb 2016; PSA=1.41 ; T=181
    May 2016; PSA=1.59 ;
    Sep 2016; PSA=1.56 ; T=364
    Jan 2017; PSA=1.47 ; T=262
    Apr 2017; PSA=1.81 ; T=377
    Jul 2017; PSA=1.57 ;

    Apart of the PSA there is no other fact that could deny or imply other than a sort of indolence by part of the cancer, I only worry if these results relate to a false pretention that the cancer is not spreading in its advancement. My doctor has no idea of what is occurring but recommends to restart HT as soon as the PSA gets to 2.0 ng/ml. In our last meeting in the beginning of this month he gave the referrals for a PET scan with F18 Flurocholine (discussed in above posts) and scheduled my next appointment to September. This exam is covered by the national health services (NHS). The 68Ga PSMA PET clinical trial in which I was enrolled is no more available but I also could not do it due to the limitations in renal insufficiency (high creatinine levels) imposed by the CT image that makes part of the trial's protocol. I will try still to do it at my own charge if I manage to get a referral letter from another doctor. In any case, the 18F (FCH) PET may be sufficient for my purposes. The only worry is if a PSA of 1.5 can assure a positive result. I am not interested in another false negative.

    According to the doctor the F18 substance is not Nephrotoxic so that I have not to worry with my CKD case. The only minus is that the CT image that complements the exam cannot use the iodine based contrast. Our good friend survivor Denistd has suggested the same in one of his posts.

    Best wishes to all,

    VG

  • Old Salt
    Old Salt Member Posts: 1,003 Member
    Looking good!

    Time for some celebration...

  • desperate for hope
    desperate for hope Member Posts: 44
    edited July 2017 #59
    I hope it's good news!

    I wonder, when the primary has been treated, if PSA can fluctuate with diet and activity in the same was as it does for men on active surveillance. 

    I don't mean to scare you but here's an article about low PSAs and met. PCa. 

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873892/

    What was your initial Gleason?

  • ramaka
    ramaka Member Posts: 55
    Very happy for you and your

    Very happy for you and your family, VG! Thanks for ALL the help and wishing you only the best!

  • Max Former Hodgkins Stage 3
    Max Former Hodgkins Stage 3 Member Posts: 3,767 Member
    Better

    Lower PSA is always better.  You have the best doctors, who will figure your pattern out.

    Blessings,

    max