Jump to content
seafriend40

Merv ALLAN. My Bone Scan.

Recommended Posts

seafriend40

351710-091418.pdf  Hopefully I have done this right, this is the report I got from recent Bone Scan. ALL is looking good at this time, keeping everything crossed.351710-091418.pdf

Share this post


Link to post
Share on other sites
Patrick Turner

What does your bone scan mean? I looked at the report pdf which said there were no bone mets.

Did you have Pca there previously? I am not sure where your post fits into a story about Pca treatment, and I cannot rememeber all histories of everyone at every group.....

Patrick Turner.

Share this post


Link to post
Share on other sites
Kezza2

That's great news Merv.  I would still be pushing for a PSMA PET scan if they are available, even if you have to come to Brisbane for it.  That will show you if there are any small as yet undetectable bone mets or more importantly any soft tissue mets that can be dealt with early rather than later when they can become a bigger problem.  Both PAH and RBWH have PET machines although only RBWH have the machine to manufacture the Gallium 68 tracer at this time.

Share this post


Link to post
Share on other sites
alanbarlee

Hi Merv,

The (upsidedown!) bone scan report showed no lesions - which is good as far as it goes. However, technetium bone scans aren't particularly sensitive, often only responding when PSA levels are 20 or higher. (The same goes for standard CT scans).

You might want to ask your medicos about a 68-gallium-PSMA PET/CT scan, which seems to be the current state-of-the-art, or alternatively, an 18F-FDG PET-CT scan (successfully picked up affected lymph nodes in my case, although FDG scans are generally regarded as not as good).

If there is a well-founded suspicion of bone mets, there are a couple of urine-based bone resorbtion markers that can be ordered , viz NTx and b-CTx. Serum calcium and ALP are other indicators that are usually monitored.

Have a chat with your docs about the relevance of these in your case.

Best wishes,

Alan

 

  

 

Share this post


Link to post
Share on other sites
seafriend40

Alan, Thanx for your interest. My PSA level at this time is 61, yes 61. Am hoping to see Oncologist sometime in October.As report advises I am riddled with Arthritis but NO Metatarsis at this time.

Share this post


Link to post
Share on other sites
seafriend40

Patrick, Thanx to you also for your interest. I posted previously in My Story Forum, which has Full details of my history. If you have trouble finding it I will PM you.

Share this post


Link to post
Share on other sites
alanbarlee

Hi again Merv,

With a PSA of 61, it would be good if you could quote the recent PSA doubling time, i.e. since the last test or two. I'd be concerned that you may not have large enough mets to show up on the bone scan, but rather, a possible proliferation of very small mets (to bone, lymph nodes or visceral) that are causing your PSA to be both high and possibly increasing at a doubling rate of less than 10 months - which would be considered 'high risk'. 

 

If that is in fact what's happening, then early systemic treatment options would be an important topic when you see your medical oncologist next month - e.g. ADT (Zoladex or similar, possibly with Cosudex and Avodart included as 'blockade' treatment. 

 

There's a promising new drug on the scene  - apalutamide ('Erlyand'), that would perfectly fit your current situation of 'non-metastatic castration resistant' PCa with a (possibly rapidly) rising PSA. This drug was approved earlier this year by the TGA for sale in Australia for this patient cohort, and it slated to be discussed at the PBAC's meeting in November for possible inclusion in the PBS (although with approval being at least 6 months away, and quite possibly a lot longer). In the meantime it might be possible for your oncologist to negotiate 'special access' to this new drug through the manufacture, Janssen. (Some years ago, I was a fortunate recipient of such access to abiraterone (Zytiga).

 

You could also google 'apalutamide AND PBAC' to download a PBAC consumer submission form - easy to complete and carrying a lot of weight.

 

Keep us in the loop!

 

Alan   

Share this post


Link to post
Share on other sites
Kezza2

Hi again Merv,  I agree totally with Allan's comments above.  A bit of my history, external beam radiation in 2001 as it was the only option available to me back then, androgen deprivation therapy with Lucrin until it failed in 2015, then an abiraterone plus (or placebo) of apelutimide which held it for two years, a PSMA PET using Galium 68 tracer which showed a proliferation of small bone mets, then enzalutimide which did nothing except make me sick, and a PSA that doubled in 5 weeks.  I have just finished 5 doses of radiation to my T4 to T8 vertebrae in my spine and yesterday had my second dose of docetaxel chemo.  PSA is down from 47 to 34 in three weeks, so here's hoping for a great result. 

Like I said earlier, I would suggest you explore getting a PSMA PET with Gallium 68 tracer.  It might mean a trip to Brissie but the tilt train works OK and there is a regular bus from Roma Street station to either the RBWH or the PAH.  We wouldn't have found the extent of my mets without the PET as only the one on my T7 showed up on the bone scan, but at least the mets are confined to bone and not soft tissue at this stage.

Share this post


Link to post
Share on other sites
Patrick Turner

It seems the PsMa gallium68 scan is best for finding bone mets early which can upset some men because they may have though themselves to be free of bone mets using only CT scan.

But for gallium scan to work, the mets must be PsMa avid, ie, attract the PsMa and gallium and having gather to form a little / big cloud which can be seen. By the time most men have bone mets the Psa is high enough to make gallium scan likely to work. 

Once bone mets are found, then we must decide what to do. I have had 3 such gallium scans, and last May's showed countless bone mets. Psa was less than 7.  

I began Docetaxel 8 weeks ago, Psa was 12.0. Then Psa lept to 36, then down to 26, up to 27, and last one was 30, and before chemo shot 4 next thursday I expect Psa to be 36. So Chemo seems to me to be a dismal failure.

I have read all I can about Cabazitaxel and its hardly any better.

There's a trial for Cabazitaxel OR Lu177 going on now and they are still taking men wanting to take part, but I can't find anyone who knows if the protocol includes a switch from say Cabazitaxel to Lu177 if the former does not work, or vice versa. 

So I could be assigned to have Cabazitaxel and then it fails, and I don't get Lu177.

This may be one reason why they are still looking for patients who are not seeing a possible real benefit that is timely.

So I think I'll just get my onco to refer me to Dr Lenzo, and buy the Lu177. My doc said it would take 6 weeks to get first infusion from Lenzo, probably at St Vincents Sydney. It may be better to have Ra223, because most of my Pca is in bones.

From what I have read, survival time for Docetaxel for Pca bone mets is not so good. 

Hospital doc is saying to give Docetaxel time to work, but this sounds like BS; I could end up having 6 infusions with Psa at 70, bone mets increasing in numwer and size.......... 

Patrick Turner.

Share this post


Link to post
Share on other sites
Charles (Chuck) Maack

Hello seafriend40, Without knowing your history since diagnosis, difficult to offer you suggestions as to where to go from here.  If you were only recently diagnosed with prostate cancer and the bone scan was part of initial development of base points to determine where to go from here then that PSA of 61ng/ml is certainly worriesome and is just part of needing to know more.  Have you had a biopsy?  What did the pathology report tell you as to number of tissue samples extracted, percentage of cancer of those showing such evidence, Gleason Score assigned each such sample?  Is your treating physician trying to determine whether surgical removal is reasonable? Or external beam radiation? Or brachytherapy seed implant? and do you know if your prostate gland is enlarged, and if so what is that size/volume in cc or gm - If known and compared with PSA level can determine how much PSA is related to prostate cancer and how much is related to the enlarged gland size? Certainly if the gland is enlarged a start would be prescribing of androgen deprivation medications would be merited to reduce the size of the gland as well as to bring down PSA level as well as to hopefully stop prostate cancer cell continued growth and proliferation (dividing/multiplying}.  Back to the biopsy, the extent of your cancer as determined by Gleason Score would have an effect on whether it appears your cancer may be significant enough in development within the gland to have possible progressed beyond the gland.  As others have already recommended, you need better forms of imaging to address whether bone or soft tissue shows evidence of prostate cancer cell migration to those areas outside the prostate gland.  If considered likely the cancer may have spread outside the gland, then surgical removal would not serve to rid you of your cancer.  And if appropriate imaging determined bone and/or soft tissue cancer, then radiation to the gland and peripher would serve no purpose, and androgen deprivation would be a first treatment.  And as I explain earlier, in the meantime androgen medications should be considered to immediately halt continued cancer cell growth/proliferation.  Please recognize that none of us are trying to worry you, but rather to look at all areas so that you receive the most appropriate treatment dependent on the most appropriate diagnostics.

Share this post


Link to post
Share on other sites
seafriend40

I was originally diagnosed in 1993, had"aggressive Radiation Therapy" for 17 weeks, with good result. PSA was 20 in 2000 and was told I had A.P.C. and was put on Hormone Therapy, Androcur. Stopped taking Androcur in 2013 on advice from a A.P.C. friend. Was told by Urologist to come back when PSA reaches 60. So here I am, have not, and WILL not be seeing Urologist. Hope to see Oncologist later this year.

Share this post


Link to post
Share on other sites
Charles (Chuck) Maack

Dear Merv,

 

So sorry that you were given ridiculous advice not only by a friend but by a Urologist, as well!  Yes, most certainly, find a Medical Oncologist ASAP - NOT later this year - and get busy getting appropriate treatment.   There are improved androgen deprivation medications that we would hope will arrest continued tumor development and provide you years of control and management.  Advise where you live and hopefully among all these who have posted to you, will be those who know are the better Medical Oncologists in your area who are more conversant with understanding and treatment of recurring/advanced prostate cancer.

Share this post


Link to post
Share on other sites
Charles (Chuck) Maack

I just noticed on your imaging report that you must live somewhere near Bundaberg.  Since I have no idea where that is in Australia (I'm a Yankee bloke in the U.S.A.) hopefully others following this forum can help you find the appropriate Medical Oncologist reasonably near you.

Share this post


Link to post
Share on other sites
seafriend40

Good morning Chuck, 5.30 am Sunday morning here. I have just read your post, Bundaberg is on the East Coast of Australia just below the Tropic of Capricorn. We are famous for Bundaberg Rum made from our locally grown Sugar Cane. We now have a Medical Onco;ogist in Bundaberg, hope to see him in October/November, keeping everything crossed.

Share this post


Link to post
Share on other sites
Patrick Turner
5 hours ago, Charles (Chuck) Maack said:

There are improved androgen deprivation medications that we would hope will arrest continued tumor development and provide you years of control and management.

One might hope there were, but I soon found ADT, Androgen Deprivation Treatments had severe limitations.

Standard ADT is via Eligard, Lucrin, Lupron et all, to shut down testosteone production in testicles and it costs medicare about $5,000 a year, and the drug companies say theit drugs are more effective than having orchiectomey, ie, balls cut out, which would, IMHO, be much cheaper for all concerned. My dad was a vet, and as a kid I helped him do operations in his surgery on animals, and he did many tomcats and dogs. Simple and cheap.

But all the drugs for T suppressions fail because cancer mutates to make its own, and its called di-hydrotestosterone that is 20 times more powerful as a Pca growth agent. Plus the normal ADT does not shut down the adrenal gland which makes small amount of T but that's enough to allow Pca to live quite well, but while mainly asleep. I continue to have monthly injects of Lucrin since 2010, and in 2016 after it failed, docs added blocker drugs to shut down adrenal gland and interfere with DHT production in tumors. Cosadex gave 6 months supression of Pca, then failed, Zytiga (abiraterone) gave 8 months suppression only. But during all this suppression time, my bone mets slowly became big enough to see in PsMa gallium68 scans and by the time countless mets showed up, Zytiga had failed and I accepted the doc's standard treatment of Docetaxel. Psa has nearly tripled in 8 weeks with chemo, from 12 to 30, after only 3 infusions.

So my history demonstrates that getting a lot of suppression of Pca via ADT depends on luck according to your DNA. A friend has gone from diagnosis in mid 50s to end of chemo with Psa at about 40 in only 3 years after RP failed, salavation RT failed, ADT failed, Cosadex made Psa rise rapidly, and docs at "expert care hospital" decided any hormonal manipulation treatment such as abiraterone or enzalutamide would not work. Docetaxel got Psa from 40 to 2 after 3 doses, but then it rose quickly, and no he seeks another espert's advice, someone at Garvin research in Sydney. He is taking enzalutamide even though its hardly working at all.

But it does appear the chemo got rid of or greatly reduced his liver mets. and other visceral mets. But although these mets have vanished off the scans just means they may have been reduced to size that scans cannot see, and they may all increase later. I predict the expert doc my friend is seeing will say to get Lu177 or something else that is provided by Dr Lenzo.  My friend's battle and mine is not over yet, and he and I face a huge expense of money, time, add-on costs, and QOL reductions. It is either that, or I deal with survival time that is frighteningly short, and there will not be any miracles. 

But today, I'll try to cycle 60km to have a coffee at a nice cafe across town. I see the storm clouds gathered, but i am doing life without curling up into a ball of depression.

Patrick Turner. 

 

Share this post


Link to post
Share on other sites
Charles (Chuck) Maack

Hello Patrick,

 

You mention orchiectomy as a less expensive manner of shutting down testosterone production, but in so doing there is no turning back, and in many cases orchiectomy fails to sufficiently shut down testosterone (androgen) production.  I sent the following to many in June and believe I likely sent it to those PCa patients in Australia for whom I have email addresses.  I also believe I may have posted it on this forum to one of the patients who remarked that his testosterone level only dropped to 50ng/ml.  I am providing my post again for readers to review.  A more likely setting for initial move to androgen deprivation is to provide what has been considered “triple androgen blockade.” The means an LHRH agonist or antagonist to shut down testicular production, an antiandrogen (bicalutamide, generic of Casodex most often prescribed) to block the multitude of androgen receptors on prostate cancer cells from testosterone/androgen access (the adrenal glands of which you speak that are not effected by testicular production), and the third medication dutasteride/Avodart whose activity is to stand in the way of any testosterone/androgen that does transit towards the cancer cells where if it comes in contact with 5Alpha Reductase (5AR) enzymes on cancer cells it will convert that testosterone to – as you also note – dihydrotestosterone, a five times or more stronger stimulant to cancer cell growth and proliferation (dividing/multiplying).  For many men this initial triple androgen blockade is very effective and can be successful for many years.  Granted that, unfortunately for many others whose cancer has advanced to metastases, this triple hormonal blockade may not be as successful or for as long.  Fortunately for at least me, I have been successful with androgen deprivation medications for 22 years and counting, but I have run the gamut of most all of them short of chemotherapy to include both abiraterone/Zytiga and enzalutamide/Xtandi.  But I digress, let me include what I sent in June (my apologies for length, but educational never-the-less):

 

ORCHIECTOMY anticipated testosterone level results (also regards Testosterone produced by other than testicular)

 

(A response to “Cam” in Australia with a testosterone level of 1.7nmol (50ng/dl) and still rising PSA post bilateral orchiectomy)

 

The level 1.7 if nmol/L is equivalent to 50ng/dl, and 50ng/dl used to be considered castrate level but no longer so.  20ng/dl (0.68nmol/L) is the level considered castration level that has been achieved with androgen deprivation medications to reduce the testosterone level of active testicular/Leydig Cell production. With bilateral orchiectomy, testosterone, on average, falls to 15 ng/dL (0.5 nmol/L).  Using the explanation as to androgen (testosterone) produced from other sources, your orchiectomy has not sufficiently lowered testosterone to suppress PSA elevation.  An antiandrogen such as bicalutamide/generic of Casodex might suppress adrenal gland produced androgen from accessing cancer cell androgen receptors (AR).  Adding dutasteride/Avodart, a 5Alpha Reductase (5AR) inhibitor prescribed to inhibit androgen/testosterone from conversion to the stronger stimulant to cancer cell growth, dihydrotestosterone/DHT, might serve to inhibit any androgen not suppressed by the antiandrogen while enroute to 5AR and bring PSA down and manageable.  If these are not found effective, then either abiraterone/Zytiga to totally shut down testosterone production from all sources (testicular, adrenal glands, and that produced within cancer cells) or enzalutamide/Xtandi to block androgen access to cancer cell androgen receptors, may be alternatives – since these last two are extremely expensive medications, it would be important that they are covered under your government or private health insurance plan.  Please note that I am only expressing considerations to discuss with your treating physician (Medical Oncologist?). 

 

Testosterone from other sources than testicular:

 

Despite testicular shut down of testosterone production either by LHRH agonists/GnRH antagonist, the adrenal glands still secretes precursors to androgens such as testosterone and advanced androgen independent prostate cancer cells acquire complete steroidogenic ability to synthesize androgens and underline the fact that castration and inhibition of testosterone production in the testes may not achieve androgen deficiency in prostate cancer cells in advanced stages of the disease. (MY NOTE: Though the below reference goes into detail as to how androgen can be produced from other sources (adrenal glands, and cancer cells can produce androgen within themselves which, I believe, is derived from cholesterol) to fuel androgen “independent” cancer cells, the same can occur to continue to fuel androgen “dependent” cancer cells.)

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802176/   (I have emphasized in bold lettering that of interest)

 

 

Results and Discussion

The results described in this study show for the first time that androgen-independent human prostate cancer cells are able to acquire complete steroidogenic potential and are capable of synthesizing testosterone from cholesterol, indicating an intracrine regulation of AR in advanced stages of prostate cancer. Several studies have shown the expression of key steroidogenic enzymes in prostate cancer cells indicating that these cells are able to synthesize androgens from adrenal precursors (El-Alfy, et. al., 1999,Nakamura, et. al., 2005,Stanbrough, et. al., 2006). The presence of functional AR in advanced stages of the disease and the presence of testosterone and DHT, sufficient to activate the AR, in cancer tissues under androgen ablation therapy, also support this notion (Gelmann, 2002,Mohler, et. al., 2004,Titus, et. al., 2005). The purpose of our studies was to determine whether prostate cancer cells in advanced stages of the disease can synthesize testosterone from cholesterol hence making them completely independent of serum testosterone and/or adrenal steroid precursors.

 

In conclusion, our results clearly show for the first time that advanced androgen independent prostate cancer cells acquire complete steroidogenic ability to synthesize androgens and underline the fact that castration and inhibition of testosterone production in the testes may not achieve androgen deficiency in prostate cancer cells in advanced stages of the disease. Our results also explain the essential role of AR in survival and proliferation of androgen- independent prostate cancers under androgen-ablation therapy and suggest that inhibitors of steroid biosynthesis in prostate cancer cells may be required to completely abolish the androgens in these tumors for its therapy.

 

 

Within the past three years the suggestion has been that men initially diagnosed with metastasis begin androgen deprivation medications “accompanied by” chemotherapy with docetaxel/Taxotere since life was extended considerably in doing so.  Initially the medications Zytiga and Xtandi I noted above were reserved to be prescribed following chemotherapy, but more recently they have been approved for prescribing pre-chemo (at least in the USA) for those men whose cancer is not controlled/managed by the usual ADT medications (the triple hormonal blockade I explained) with Zytiga  as the primary testosterone/androgen blocker of testicular, adrenal glands, and that produced with the cancer cells themselves, and Xtandi is pretty much a “super” antiandrogen much stronger in effectiveness than other antiandrogens in blocking the androgen receptors on cancer cells from testosterone access. 

 

Sadly, as Patrick also makes note, these “super” medications are extremely expensive.  Patients can contact the manufacturer of Zytiga and Xtandi to see if they can help in providing their drugs at a much lower cost.

 

Patrick, I sincerely pray that some method of treatment will halt your cancer progression.

 

 

 

Share this post


Link to post
Share on other sites
Kezza2

Hi Merv,

Beautifully explained thanks Chuck.  While I take on board Patrick's position and the failure of several treatments, please remember that we are all different and will respond differently to the various treatments available.  I have previously posted this, but if I were in Merv's position I would urgently be seeking a referral to either Royal Brisbane (RBWH) or Princess Alexandra (PAH) hospitals in Brisbane to the med oncs there who are terrific, with a view to commencing appropriate ADT medication and requesting a PSMA PET scan so you can see EXACTLY what you are up against.  Otherwise you are just guessing.

Share this post


Link to post
Share on other sites
Patrick Turner
3 hours ago, Charles (Chuck) Maack said:

The level 1.7 if nmol/L is equivalent to 50ng/dl, and 50ng/dl used to be considered castrate level but no longer so.

In all the years since I began ADT, my testosterone was not measured often enough, IMHO.

But that it was low enough was considered to be the case because Psa nadir after EBRT and 2 years of ADT was 0.08.

I had no clue just how important testosterone suppression was but a couple of T tests just said <50, low, and of course some believe this is entirely insufficient, and I believe them to be right, and I think T levels should be measured with each Psa measurement. But probably, Medicare protocol does not allow it because its considered an unnecessary cost.  

I am no expert, and only one of thousands of men with Pca, just a brick in the wall, a nobody. 

In your extensive post and repost above you mention  dutersteride addition to control di-hydro-testosterone and I ws able to get that in addition to Tamulosin in the one daily pill, and I took these for most of the time I was on abiraterone, Zytiga. There was not the slightest change to Psa levels when I began dutersteride 3 months after intitial start of Z. Psa went low, then straight back up to same Psa level after 9 months, with failure deemed at 8 months, so I could see no benefit of added dutersteride.

Not one medico was concerned much about these issues. Their attitude is, you get what we do routinely, take it or leave it.

Anyway, I remain unsure about orchiectomy vs ADT injects, which are only ever going to shut down balls. If you ain't got balls, I can't see how T levels could ever be higher than chemical ADT.

Most men who do a multi-year battle with Pca will find that T is their greatest enemy forever, so it just does not matter if you have low T forever after having balls cut out. Remission from Pca, occurs with the same rarity as finding droppings behind a child's rocking horse. If the Psa is undetectable for some years without any treatment AND there is no sign of Pca which does not produce Psa, then OK, a man could take T pills or have injects and its a very simple thing to have T and one of the meds most older men have to take when they go over 60. 

Body builders have generated a huge online source for injectible T and a man can easily self inject if he wants to.

 

Right now, after quitting Zytiga 4 months ago, I guess my adrenal glands are now making some T, but my Pca has probably mutated to be able to make its own DHT and mutated a way to resist any attempt to stop this. Any normal T levels may not matter much any more. Or else my body finally worked out a way to prevent Zytiga doing its job, ie, block its action to get to adrenal gland. Just why did Zytiga fail? I ain't no expert; all I know is that what worked for you or other men will not necessarily work for me or other men, and we can only get what medical care is available, and if we scream we want more, with a pile more blood tests, the docs tend to ignore us. For example, I got from mid 2010 to mid 2016 with ordinary ADT. But a friend got only 4 months. Some men get 20 years. Some men have Pca that is a real weakling, easily controlled with ADT, easily cut out, or easily radiated. But my Pca is a beast which has reared up to show its claws and fangs and Psa flared to triple Psa in a week or two after starting chemo.

Pca which flares up occurs in 14% of most patients who then get OS time of 12.5 months, as against the other 86% where no flare occurs and they get 20.5 months. But all this is theory and nobody really knows what's going to happen to them like my friend who had no flare with chemp, but was back with same Psa of 40 within 7 months, so will he get 20.5 months? I doubt it, but maybe LU177 and Ra223 changes all that.

Any one of us can cling to  pet theory that seems to be So Right, but cancer dances about with different steps and rythyms within different men.

What I do know is that my Puff The Magic Prostate Grenade on which I sit each day is slowly exploding.

Right now, not enough is being done to defuse this explosive device. 

If I tell my onco next Thursday when i have chat before chemo that I want to be referred to Dr Lenzo then I think he will grant me that. At least 2 chemo shots are needed to decide if chemo is working or not, but hospital said 3, and I have had 3, and now 4 is nearly due, and if Psa is up next Wednesday, then probably I get my referral and i get chemo 4 and maybe chemo 5 while the referral is processed. it will take time to confer with Dr Lenzo, he examines if he can give me something worth the expense. I will be on queue of men lining up for treatment; it all takes TIME, and my guess is that after referral is sent, it is 6 weeks before I get first Lu177 infusion. The faster the better I now think, because the bigger the bone mets, the harder it must be to reduce them. 

I am trying to avoid the situtation where my chemo turns out to be an unsuccessful palliative care drug, and then dying within 2 years.

Patrick  Turner. 

 

Share this post


Link to post
Share on other sites

×
×
  • Create New...