Burnett1948.I know I'm labouring this point. But because I have had different advice from two Urologists: Ond said I should start hormone when my PSA was .9 (which has passed) the other (my current)wants to start when my PSA reaches 8. My latest PSA was 2 last August.After reading more HealthUnlocked Posts I understand that my PCa starts to metastasis at about PSA 1.7 or there abouts. So doesn't it make sense to reduce my PSA with hormone treatment earlier because I have been diagnosed with recurrent PCa. I need help bases on experience please. Should I start hormone treatment now?
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Hi Burnett1948
If you want conventional and up front treatment then go along with your oncologist.
For me my last psa on 2 January 18 is 26.59, it has not doubled yet since the test I did after my 1st Cystoscopy on 10 November 17 at 16.46.
My last CT Scan reports on 2 January 18 shows stable and no further progression.
So with my current treatment I am on status quo.
My body do require time to clean/clear some debris and I will be looking forward to conduct CT & Bone Scans end of this month to confirm the eventual final outcome from my self treatment.
So if you want some personal consultation let me know.
Roland
Roland, That looks like a 10 week doubling time, which truthfully is fairly quick
Burnett1948.Dan59 I have been told its longer than that.You have got me thinking.
I was refering to Rolands doubling time
Hi Dan59
Hope you are feeling better.
Also thanks for your no confidence tick! LOL
Like I mentioned I am all alone in a terrifying journey. So who can I seek help from?
Fortunately luck and Devine intervention prevails I am still left standing/kicking and pain free apart from haematuria which is on going concern. I checked my urine at 5 am this morning and it was clear then I decided to go play 9 holes golf. I made 4 pars and hit my 14 handicap for 9 holes. When I got home the gross haematuria appeared again. Probably caused by my physical over exertion.
Like I said my blood test for other functions is still OK and no infection.
I also post my daily urine combur 10 test to a fully qualified MD.
Next I will talk to an oncologist as scheduled for 15 January 18.
But last and foremost I will do CT & Bone Scan at the end of the month,
My lastest CT on 2 January 18 shows stable/ no further progression,
Thanks for being patience,
Roland
Burnett.
A urologist is not the person you need now it is a oncologist. Cancer is the specialty of a oncologist. The urologist does not specialize in cancer.
Burnett1948.DFZ4835 I am starting to understand that. My Radiation Oncologist told me about 2 years ago she would refer me to her Hospital's Medical Oncologist in about 2019 ( which is only a year away now). I am Australian and I don't think Medical Oncologist have had much to do with treating Prostate Cancer until recently because I don't think Kemo Drugs were used until near end of life at that time. I picked this up at a Prostate Support Group meeting I attended from a Urologist and Radiation Oncologist who attended this meeting about 4 years ago to answer questions. My understanding from my Urologist is that Hormone treatment will be my best chance for another 10 years of life: which sounds okay if this is a reliable prognosis . During the above 4 year period my PSA reduced a couple of times: I get it taken every 6 months. Am I correct in thinking that new Kemo drugs are used earlier in the treatment of Prostate cancer now?. I next see my Radiation Oncologist near the end of February 2018. I will now have a number of questions for her. Thank you all very much.
Hi there,as we are both in OZ & share the same problems i will tell you what i found out yesterday.My psa is now 10.3 & the oncologist said they always start with hormones,mainly Lucrin Depot PDS injections & that will reduce psa levels but it will wear off & that is when chemo starts.My cancer has gone to lumph nodes but no organs luckily & as i have had these injections before i can tell you the side effects are not good. Planning a trip overseas so will take the needle on return.
Hope this helps.
Burnett1948.Bray thanks for replying. I have a couple of questions:-1. When did you first started the Luctin injection; what was your PSA? and 2. Did you have a Pet scan to find find out that your cancer had gone to your lymph nodes and no where else? By the way I'm a Queenslander.
Hello Burnett1948. I was diagnosed with prostate cancer back in 2011 & had radiation in 2012,the psa beign 18 then & after radiation it was 1.4,very good i thought!...2016 psa rising beyond 9.4 then put on Lucrin Depot PDS 3mt injections with Esomeprazole Ec tablets 40mg. This got the psa down again to 1.4 but my mistake was i did not take any repeats because of terrible side effects,tiredness,exhausted & weight gain.
November 2017 psa up to 9.4 again & went to oncologist yesterday,psa 10.4 now so he wanted Lucrin again saying its hormone treatment first then when that doesnt work its Chemo.
I am not impressed with this Lucrin so will go back to the Mater in Newcastle where they talk of geting the imune system to beat the cancer.
The Gallium 68 pet/ct scan was done at the Mater & organised by them showed lymph nodes above the prostate infected but no organs,bones important there.
Hope this helps.
Burnett1948.Bray thanks and Best wishes.
Glad to help
Burnett1948.Roland63217 Thanks
Hi there. I know about the worrying. Hope you can relax.
Can you send a brief reminder of your PCa history? (Sorry if I missed it on an earlier post.) That might help with obtaining more informed input.
Best,
James
Burnett1948. JamesAtlanta. At surgery in 2005 PSA was 7.6 Gleason 3+4: 6mm missed because prostate big(I wasn't told until2012 which I am still cranky about).PSA down to .05 as result of surgery. In 2009 PSA rose to .4 so I had 32 shots of salvage radiation: PSA down to .08. Had PET scan 2016 all clear. PSA up to 2 in August 2017 when I saw my Urologist in Ausgust 2017. I see my Radiation Oncologist on the 27/2/2018. At this stage I see each other alternatively at 6 month intervals. In February 2017 my Radiation Oncologist told me my doubling time was 18 months. I am not confident about working out my doubling time myself. I think about what I read and my thinking is that given that there are new Kemo drugs hormone treatment is now not the last line of defence.
What is your PSADT (PSA Doubling Time)?
Burnett1948 in reply to
Burnett1948. gregg57 twelve months ago it was 18 months.
From what I know (not an MD), prostate cancer is always mutating. If you follow the “wait until it is big enough to treat” you are only giving it time to transform into a resistant form. Hit it hard and hit it early.
But, as a man that I greatly respect says, “what do I know”? (Sorry for taking your line. Will not let it happen again.)
Burnett1948.Dr_WHO thanks; your thinking is becoming mine.
I would definitely not wait til it hit PSA 8. If the doubling time works out to be like a month then you gotta hit it with ADT. Frankly, ADT is tolerable and I would go for it now, just to starve the PCa and have some peace of mind and not worry as much with each PSA test.
All the best to you
Burnett1948. dockam thanks you make sense.
I agree not to wait, I see your gleason was 3+4, which is medium risk. I had read somewhere that with medium risk the cancer spreads somewhere around 10, but why wait , what you want is to get on adt , have psa go undetectable for a period of time some say 14 months to 2 years , Then go off therapy. Nalakrats did it for 2 years and is now going off therapy with hopes it will not return. I wish I had this option, and be done with Prostate Cancer, unfortunately I waited to long to get diagnosed, and start treatment . I agree why wait and let it get mutated and harder to treat, beat it back into complete remission, while the cancer is weak. I wish you the best, I will repeat a quote from a man we all respect “Of course what do I know? “
Dan
Burnett1948. Dan59 Thank you.
in reply to Dan59
I'll second or even third not waiting. I dont see the point if you've made a decision already that you are going to ADT. It might not make much of difference waiting for a PSA of 8 which is still low, but for the sake of peace of mind there's no point in delaying it. It will reduce the stress and anxiety of the Prostate Stress and Anxiety test. And of course there is always a risk asscoiated with delaying any treatment. Why give the little bastards more time to multiply?
Burnett1948 in reply to
Burnett1948.gregg57 Thanks mate.
Since your PSA is 2, you do have the option of a C11-choline scan. (see YouTube)
You might have one or two lymph nodes or bone mets in some unusual spot that can be removed or irradiated, with some chance for a durable remission.
If your prostate is already gone, then you already had "metastasis". ie cancer outside the prosate. I dont think that the number 1.9 is established as much of anything.
Burnett1948 in reply to
Burnett1948.martingugino thanks for replying. I was thinking of asking for a bone scan and CT scan as Roland is doing. I don't know but a Pet scan would be required to detect soft tissue metastasis.
in reply to Burnett1948
The T99 scan ("bone scan") and the CT scan are "standard of care". But they are not good enough, nor is the standard of care in general good enough; that is, not good enough to keep you from dying from prostate cancer.
I believe that the CT scan is to look for cancer in the lymph nodes, and visceral cancer. I do not think that it can tell the different between old dead scar tissue and currently active cancer sites. Very very hard to get anyone to change their ways.
I have a different take than some of those who have responded.
Conventional ADT largely fails within 2 years. That is sufficient reason for delay in most cases, IMO.
What if the cancer becomes metastatic during the delay?
I had a discussion with my urologist some years ago. The wisdom back then, it seems, was that those who had mets had a very poor prognosis, but that most men with PCa do not get mets. I had been confused by (a) patients mostly dying with PCa, but not of it, & (b) metastatic PCa being lethal. I hadn't realized that an increasing PSA did not automatically mean that the cancer was becoming metastatic.
I thought about the bump in the PCa mortality rate that followed adoption of the PSA test. That absolutely should not have happened. It's not a huge bump, but it puzzled me.
At the time, doctors who injected Lupron were getting ~$1,000 a shot. It was common for patients who had failed primary treatment to immediately begin ADT. When Medicare removed the profit motive, there was a change in thinking.
The problem with ADT is that resistance (CRPC) selects for cells that might have increased metastatic potential. I believe that this explains the increase in mortality in the bump. (Suddenly, with the new PSA test, more cancer was being found, more men were being treated, & more men were on ADT because of treatment failure.)
When my prostatectomy immediately failed 13 years ago, I didn't know how to proceed. Was the cancer purely local, or were there mets? Why endure the morbidity of salvage radiation if there were distant colonies? I opted for radiation & I now believe that the odds favored that.
Within a year or two I had read of the idea that altered coagulation, & the appearance of micro-clots, facilitate metastasis. A tumor can send thousands of cells into the bloodstream each day. They have a terrible survival rate. Months can go by before a cell arrives at a favorable destination. The theory is that the only way a cell can avoid being zapped, is if it docks on a circulating micro-clot & becomes invisible to the immune system.
I, stupidly, was not worried about clots. I took vitamin E, 4g omega-3 & a basic nattokinase dose. The double DVT in my left leg was a big surprise. I should have been monitoring D-dimer.
I did end up with metastatic PCa, but only a lesion at L5 so far. I had it treated as an oligo-met.
I keep D-dimer in check with 6 nattokinase caps before bed.
I have less faith in modified citrus pectin, but I have also used that.
I have, unfortunately, found that my cancer does indeed have metastatic potential, but I think I now have that blocked.
I don't believe that "PCa starts to metastasise at about PSA 1.7 or thereabouts". Metastases are a separate issue to PSA rise. I certainly wouldn't begin ADT at 1.7. (The PSA doubling time [PSADT] is a more significant number.)
Best, -Patrick
Patrick, as always you make a lot of sense, and certainly the most educated answer to this thread.
Dan
Burnett1948.pjoshea13.Thank you, I will re-read you post.
in reply to pjoshea13
"Conventional ADT largely fails within 2 years. That is sufficient reason for delay in most cases, IMO."
You mean that that is a reason for delay in starting ADT, right? Or what?
Are you saying that you favor "active surveillance" more than others, possibly? More than Alan Partin, for example? I don't understand the context of this statement.
Oh, you are saying that after treatment to the primary, don't start ADT reflexively.
pjoshea13 in reply to
Almost 14 years ago, when my urologist gave me the bad news that my RP had failed, he said: "There are some who would say that you should start hormone therapy now."
It was clear from his tone that he had doubts. I had been reading a lot of papers that opened with boilerplate wording that ADT failed within 18 to 24 months. I was 56 years old. What options would I have at age 58 with CRPC? No Zytiga, Xtandi, etc, etc. back then.
And so I delayed.
There are more options today, but is there a combination, including ADT, that will reliably result in a durable remission? Under normal conditions, a healthy 56 year old man might reasonably expect to live another 30 years.
ADT is described as being palliative - not curative. With a short mean-time-to-failure, and with failure being associated with more aggressive disease, why rush into it?
I'll give a non-PCa example. My wife had a solitary plasmacytoma in 2014. If there is more than one, they call it multiple myeloma. She had radiation.
In 2015 she had another one. Her oncologist said she had several & needed chemo, stem cell therapy & maintenance chemo forever. & she had to go on a bisphosphonate.
2016 was the year from hell. After chemo, we went to Wake Forest to talk about stem cell replacement.
She was asked why she wanted to do it. Mortality during the procedure was 2.5%. She only had a solitary plasmacytoma (it could have been handled via radiation.) Stem cell replacement was merely palliative. When they harvest the stem cells they hope to get enough for two treatments. They expect to need to do it again. She was warned that the chemo that they give before putting the stem cells back was devastating to the body. "Your blood will never be the same." & so on.
The Wake Forest people understood that palliative treatments that fail quickly need to be reserved. Why rush into a treatment that leaves the patient in a worse state when it fails?
In PCa, the fear is mets. If you start ADT immediately, you don't have to worry about mets for 2 years. But not everyone with PCa will get mets. And if mets occur, deferred ADT will still give one 2 years of effectiveness.
-Patrick
in reply to pjoshea13
There is another benefit to ADT. It is standard treatment before radiation as it is supposed to 'sensitize' the tumor(s) to radiation. I found that it also shrinks the prostate (by shrinking the tumor?). My prostate went from 34 to 27 in only two months, at which time I had HIFU surgery, which provided the 2nd size measurement. The first was at the time of biopsy.
in reply to pjoshea13
"I thought about the bump in the PCa mortality rate that followed adoption of the PSA test. That absolutely should not have happened. "
Mortality rates declined 37% according to this article: drcatalona.com/quest/quest_...
pjoshea13 in reply to
"The NCI reported the following data on prostate cancer death rates by years:
1975 -1987, an annual increase of 0.9%
1987-1991, an annual increase of 3.0%"
1987-1991 was when the PSA test began to be used. How come the increase if PCa deaths jumped from 0.9% to 3% per year? What would explain that - in the context of the PSA test.
-Patrick
in reply to pjoshea13
Well, if the PSA test started in 1987, I don't see how one could feel that a rise in prostate cancer deaths in that year was caused by the test in that year, for example.
You would not expect an immediate effect. When would the effect kick in? Presumably non symtomatic prostate cancer would be the group detected by PSA.
So ... I can't explain that observation.
pjoshea13 in reply to
It was not a one year bump.
& the test was available in early 1986:
"the Hybritech Tandem-R PSA test released in February 1986" [1]
-Patrick
[1] en.wikipedia.org/wiki/Prost...
in reply to pjoshea13
The wikipedia article is for the 1986 date?
in reply to
i did not mean that you said the death rate was higher only in 1987. I meant that i could not see how you could say that the rise in 1987 was caused by testing. Unless the PSA test itself was dangerous (say poison in some magical way), especially in the early days, at least. Hard to think of a mechanism that would work that quickly from a blood draw. Did it precipitate a lot of immediate surgeries by quacks?
In a similar way, I can question each sucessive year. Say if the rise in the death rate in 1988 was the same as the rise in rate in the death rate in 1987, then it probably had the same cause as the 1987 rise , and so also hard to tie to PSA testing
As they say, correlation does not demonstrate causation, although it may provide a clue.
in reply to pjoshea13
" The theory is that the only way a cell can avoid being zapped, is if it docks on a circulating micro-clot & becomes invisible to the immune system."
Citation?
It is not clear what becoming invisible to the immune system has to do with DNA breaks caused by radiation energy (being zapped). DNA repair is separate from the immune system, anti-bodies, and phagocytosis.
Another theory I hear is that (cancer) stem cells are for some reason more resistant to radiation. Possibly they have better repair mechanisms.
Burnett1948 in reply to
Burnett1948.martingugino. Interesting, your reasoning is beyond mine: thanks.
I'd encourage you to seriously consider hormone therapy ASAP. My husband's cancer had already metastasized before his PSA reached 14 with a doubling time of less than two years.
Hi , Confused, to say the least, about the relationship between PSA readings and metastasis. Please read onlinelibrary.wiley.com/doi... and would appreciate comments.
FrankND
The paper has only one reference to the Gleason score:
"Many clinicians now limit bone scans to men with a preoperative PSA level of > 20 ng/mL and/or bony symptoms, provided the Gleason score is <7 (G1 or G2 tumours) [5,6,16]."
Shouldn't that be ">7"?
The 3 papers - all from Oesterling JE - are from 1991-3:
[5] "Five hundred sixty-one patients had a serum PSA concentration of 10.0 micrograms/L or less; only three had an abnormal bone scan result, and one had an indeterminate scan result. Of the 467 men whose PSA value was 8.0 micrograms/L or less (two times the upper limit of the reference range), none had bone scan results that were either abnormal or indeterminate. The rate of false-negative results for an abnormal bone scan result was 0% with a serum PSA value of 8.0 micrograms/L or less and 0.5% with a cutoff level of 10.0 micrograms/L. The 95% upper confidence limit for the rate of false-negative results for all PSA cutoff levels less than 20.0 micrograms/L was less than 2%"
[6] "The findings of these two large-scale clinical studies indicate that serum PSA is an accurate and reliable predictor of the bone scan findings for 40% of the patients presenting with newly diagnosed, untreated prostate cancer. For these patients with no skeletal symptoms and a serum PSA value of 10 ng/mL or less by either the Tandem-R or the IMx assay, a staging radionuclide bone scan is not necessary, as it provides no additional useful information over what is learned from the serum PSA value."
[16] "To evaluate the ability of local clinical stage, tumor grade, serum acid phosphatase, serum prostatic acid phosphatase (PAP) and serum prostate specific antigen (PSA) to predict bone scan findings, a retrospective review of 521 randomly chosen patients (mean age 70 years, range 44 to 92 years) with newly diagnosed, untreated prostate cancer was performed. Local clinical stage, tumor grade, acid phosphatase, PAP and PSA all correlated positively with bone scan findings (p less than 0.0001). Using receiver operating characteristic curves, however, PSA had the best over-all correlation with bone scan results. The median serum PSA concentration in patients with a positive bone scan was 158.0 ng./ml., whereas men with a negative bone scan had a median serum PSA level of 11.3 ng./ml."
...
The Dutch study used data from 1989–1997 - i.e. the start of the PSA era, although the Dutch were not early adopters, as I recall, which perhaps explains the high rate of mets: 30%.
In contrast to Oesterling & his American data, a large proportion of men with high PSA (43% of those with PSA >50) did not have mets, whereas a significant proportion of men with low PSA (16% of those with PSA ≤10) did have mets. Which indicates that PSA was not a useful marker for met risk in that Dutch population.
"In conclusion, ALP levels correlated better than did PSA levels with bone scan results, although not significantly so. ... The use of ALP and PSA is only of benefit in patients who are potential candidates for radical treatment, i.e. generally those who are < 70 years old, with a PSA of < 20 ng/mL and with clinical T2 disease or less."
-Patrick
[5] ncbi.nlm.nih.gov/pubmed/767...
[6] ncbi.nlm.nih.gov/pubmed/?te...
[16] ncbi.nlm.nih.gov/pubmed/170...
Burnett1948.pjoshea13. Your explanation and knowledge is powerful for my understanding & peace of mind: thanks for your 2 posts.
Hi. my husbands cancer was monitored for 2 years...watchful waiting they called it. then when his PSA hit above 10... i think it was only 11., the urologist said he could begin the radiation seeds ...however... they did bone and ct scans and saw that his cancer had already spread to distant parts upper spine and hip and femur so he was not a candidate for the radiation seeds. he started on ADT as his advanced disease is now not curable. ADT has put it into remission after a year. he got off ADT after 14 months and now six months later his PSA is 1.7 (from negligible before that while on ADT) We see his urologist next week and i will ask for an oncologist referral. So.... we learned the hard way that mets and rise in PSA do not always go hand in hand. If we could do it again I would get scans done before two years of watchful waiting -- not after. keep fighting, Anne for Ron.
When I had biochemical recurrence the first time after failed SRT I had an mri when Psa was 1.2 and it found my lymph node mets. After another bcr I waited until Psa reached 2.0 to get a ct pet with axumin and it found a femur met. I treated both recurrences with radiation and ADT. My point is that after bcr you need to wait until Psa is high enough for a scan to detect the point of recurrence so you can hopefully ( if only a few mets) treat them with radiation and ADT not just ADT.
Bob
Burnett1948.Break60. Thanks. My understanding is that they are only starting trials using radiation to kill isolated mets in Australia. But your treatment makes sense to me; I understand same.
Mine were not trials. MY RO's just believed that they could radiate my few mets and forestall progression. If you weight for trials you'll just be subject to standard of care which to me is not aggressive enough.
Bob
Hi! When my 81 year old father was diagnosed with metastasic prostate cancer -one bone met and one lymph node, PSA 4.48 and Gleason 7 (3+4)- the oncologist told him that he need to start the hormone treatment immediately and thoroughout his entire life.
I'm not an expert, heck they wouldn't hire me to scrub floors in hospitals, But if I were in your shoes I would go oncologist hunting (more than one), soon, very soon. I would then begin carpet bombing your cancer with daisy cutters. In other words, beat it down like a rabid dog.
Of course what do I know?
Burnett1948 in reply to
Burnett1948.nameless9999 My Radiation Oncologist has suggested I see a Medical Oncologist. I will talk to her about the need at my end of February appointment.
Burnett, I know you said that you delayed ADT beyond the 0.9 psa that your first urologist recommended. I agree with that appearing to be way too early. But you also said that prostate cancer begins to metastasize at 1.7 or so. That also seems very early. Do you have a reference for that?
Burnett1948.npac I didn't say that or I didn't mean to say that. No I am still coming to terms with when PCa metastasizes. From the feedback I have a better understanding but I now think only the cancer knows.
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