Hi all, I've been all over the internet looking for advice on PCa and just found this site. There is some great information here and I look forward to joining in conversations.
A quick update on why I am here:
- Dec 2014 (age 52 years). My lovely wife has for many years suspected I had coeliac disease and finally made me go to GP for blood test. GP gave me a wonderful Christmas present - he confirmed that I have coeliac disease (no more beer, ever) and also told me that I had elevated PSA (7.5) which need a review after Christmas
Feb 2015. PSA review - still elevated (7.8). GP refers me to urologist.
Mar 2015. Urologist gives me the finger. Says 'that doesn't feel good' and books me in for immediate biopsy. Test results are positive for PCa. Bone scans and PET/CT scans are clear. Urologist recommends radical prostatectomy.
Apr 2015. Radical prostatectomy (da vinci robot). Pathology report shows positive margins, seminal vesicle invasion, extra-capsular extension and one positive lymph node out of 20 removed. Now I am really getting worried!
May 2015. Post surgery PSA 0.026. Seems like a good result but the positive margin etc is still in front of mind.
Jan 2016, PSA has risen at each 3 month check and is now 0.1. Urologist refers me to radiologist. I have a PSMA scan, nothing shows up and radiologist recommends salvage radiation to prostate bed to treat positive margin which is likely cause of rising PSA.
May 2016. Post treatment PSA 0.067. We estimate that PSA would have been around 0.2 by now if no treatment had been performed and this is considered a good result. Radiologist advises that PSA will continue to decline over the next 9 months.
Sep 2016. PSA 0.17. I thought that PSA was supposed to be declining?
Dec 2016. PSA now 0.5. Radiologist orders a new PSMA but nothing shows up.
Mar 2017. PSA 2.5. It's rising rapidly, I have another PSMA which shows 1 tumour in pelvis, just outside the previous radiation zone and we discuss stereotactic radiation or surgery or ADT.
April 2017. After another 6 weeks PSA has climbed to 7.5. 300% increase in 6 weeks! Known tumour is very close to rectum and no-one will touch it for fear of rectal damage. So I am out of options. I start 28 days of cosadex, and on day 14 have my first shot of Zolodex (3 month dose).
Aug 2017. PSA has dropped from 7.5 to 2. Any decrease is good news, but Snuffy Myers says that PSA should decline to 0.05 after 3 months of ADT - I have some way to go.
Nov 2017. Next PSA test due in 3 weeks. To say that I am a bit nervous is an understatement.
That's it in a nutshell, you all know the drill. I have some other comments to make about dealing with ADT side effects and I will start a different thread for a discussion on diet and exercise. But I have a 2 questions for my new colleagues hear at Health Unlocked.
1. Prior to ADT, my PSA double time was 1 month. My doctor refuses to be drawn on the matter but this sounds like very fast growing PCa - what have others experienced?
2. How was your response to ADT after 3 months? I suspect that many people here had a much higher PSA than I did at commencement of PSA, I would be interested to understand how others fare (again, my radiologist refuses to comment apart this vague statement "I have seen PSA fall quicker, I have seen PSA fall slower".
3. Which specialist specializes in hormone treatment? My radiologist specialises in radiology (obviously) but at the moment he is managing my hormone treatment - should i be getting another opinion?
Oh by the way, i live in sunny Australia in the beautiful city of Melbourne. Spring is finally here, its been a miserable winter and the sun on my back is making me feel a bit better about life. For those in Northern hemisphere - you've only got 6 months to wait!!
Regards to all, Hazard
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Hazard
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Sorry that you joined the club, but you came to the right place. We have lots of knowledgeable members here - much more so than me
As for PSA, mine was 227 and I had one bone met in my T 8 vertebra. Age 53, Gleason 4+4=8. Started ADT immediately - I was in a lot of pain. Also had radiation for palliative treatment of my spine.
PSA went down to 9 the first month, 3 in month 2, 0.1 in month 3. Then undetectable for about a year. I also began chemo during month 3 (6 rounds of taxotere) - due to findings from the Stampede study recommending early chemo.
My PSA is now up to 1.4 and is climbing 0.1 points every month or two. My oncologist said I’ll start Zytiga when it reaches 2.0.
As for who you should consider treating you, seems like you would want an oncologist who specializes in proatate cancer as your team leader.
Best of luck! We are pulling for you! I’m sure you will get a lot of sage advice from our fellow members.
Glad you found us, but sorry you have to be here. You'll find lots of support here and kindred souls. We are all pretty much in the same boat.
I started in late February of this year with an off-the-hook PSA of 463, bone scan with more lights than a well lit Christmas tree. Lots of pain to go with that, had just started opiate meds and was hobbling around in constant pain. Diagnosed at stage 4.
Started Lupron in early March, followed by 6 rounds of Taxotere chemo. PSA went down to 12 the first month, then to .5 and slowly made it's way to 0.19 where it is now. I was pain free in around 4 weeks after the start of treatment.
On my second life now, and appreciate everything so much. Not sweating the small stuff any more.
Hope we can all help to you keep your chin up. ADT is very effective for most PCa so hope you continue to improve.
I hope "out of options" means "out of radiation options." You still have lots of options. As James suggested, you want to add a medical oncologist with PCa specialty to your team. The ADT side effects suck, but they will help add good years.
Thanks Yost, you are are correct, I really meant to say that i was out of 'curative' options - radiation or surgery. That was an initial discussion with doc, but he abandoned the idea after consulting with other specialists.
Hazard: Please get in touch with Jim Marshal in Melbourne. He is a wonderful advanced Prostate Cancer advocate and can be very helpful to you. He has a website under JimJimJimJim.com You will find this to be an excellent resource for you "down under" You really need a good genitourinary oncologist managing your case. Probably should have consulted one some time ago, but water under the bridge now. You never mentioned your Gleason score. I only mention this because I was wondering why hormone therapy was not begun around the time of your IMRT. Anyway, there is some really good help over there. Look for it.
Hi Peter, I've had a look at JimJimJimJim and i will explore it further. Thanks for the guidance.
GS was 7 (3+4). I assume that ADT was not commenced at time of IMRT as PSMA scan showed nothing, and given that I had positive margin, it was reasonable to assume that this was the cause of rising PSA. Maybe they forgot that I also had a positive LN ....
Hi Hazard sorry your here but welcome, im from Sunny Perth but live in the UK.
I was told a PSA would continue to drop for approx 6 weeks after radiotherapy 9 months is stretching it a bit, still your very similar to me my RP & RT failed my PSA doubling time is 4 weeks ive been on early Chemo & Zolodex since August my PSA so far has only dropped from 8.7 to 6.6 with blood test from 3 cycles of chemo so mine is coming down slowly.
When I had third occurrence after Gleason 4+3 prostatectomy and salvage IMRT, my Plan C was ADT, Taxotere, and radiation of abdominal lymph nodes. PSA was only 0.06 but doubling in 6 months.
My body tolerated Taxotere better than ADT. Still waiting for testosterone to get high enough for PSA < 0.01 to be meaningful.
I agree with the guys who say get an oncologist who specializes in prostate cancer.
I was 54 when first diagnosed in 2006, and have been using every tool in the toolbag at each step. Every doctor I've met says the sooner you have a particular treatment, the better it works.
I think I should give my story here briefly hoping you will enjoy reading it in some way whilst also learning from my experience as always we do in this group from each other.
I am living in an Asian country. My daughter and son are living in Melbourne. Before visiting them in December 2014 I did my routine labs which included a PSA test. My PSA was 7.9 and I cut short my holiday returning in February 2015 for further investigations with a urologist. In March 2015 I was diagnosed with aggressive prostate cancer at the age of 68, without any symptoms. We decided to follow an aggressive treatment course since my biopsy confirmed it was Gleason 9 although the cancer was organ contained ( confirmed by DRE and MRI ). Immediate treatment:
March 2015 - Radical Retropubic Prostatectomy ( RP )
Pathology : Cancer within the capsule, seminal vesicles not involved, nodes not involved, perineurial invasion present, Positive Surgical Margins, Gleason Score : 4+5=9, Cancer Staging : T2c No Mo. ( Micro metastasis is always a possibility ). I was continent after surgery and did't have any other complications. PSA went down to 0.025 after RP before taking any other treatment. No time to waste on GS: 9 PCa being most aggressive. Thus I followed :
April 2015 - 2 year continuous course of ADT 2 ( Zoladex 10.8mg + Bicautamide 50mg )
May 2015 - Radiation ( IMRT - Total 74Gy ) 36 sessions ) - Radiation is said to be more effective when combined with ADT.
My ADT treatment ended in April 2017.
My PSA was checked every 3 months during the treatment period and also now. Trough out the whole period up to now it has remained at 0.008 ( undetectable ). To support my primary treatment and also to remain in remission I have done the following additional things :
- Rarely eat red meat and dairy products, keeping to a heart/PCa healthy diet
- Do regular physical exercise
- Take 4000IU Vitamin 3 daily
- One tomato cooked with olive oil and black pepper with breakfast ( For Lycopene )
- Cruciferous vegetables such as Broccoli and Cauliflower rich in antioxidants
- 3 cups of Green Tea daily
- Plenty of water of course
I also take one capsule of Avodart .5mg daily although my primary treatment regimen ended in April this year because Dr.Myers is of the opinion that it will help to stabilize remission when you are off main ADT treatment.
People speak of various foods, supplements and alternative treatments for PCa but personally I count only on scientifically proven treatment protocols practiced by expert/good medical oncologists who specialize in treating PCa.
My suggestions to you :
- Learn as much as possible on PCa. I learned a lot by reading the books : "Guide to Surviving Prostate Cancer by Dr.Patrick Walsh" and " Beating Prostate Cancer : Hormonal Therapy and Diet" by Dr.Charles "Snuffy" Myers. I also learned immensely and continue to do so by sharing the knowledge and experience with the members of this unique HealthUnlocked PCa Support Group. Some are really brilliant and all are very compassionate and helpful.
- Join the Advanced Prostate Cancer Support Group in Australia ( JimJimJimJim.com ) headed by Jim Marshal ( I am a member too ) especially because you live in Melbourne.
- Early enough, be mindful of the fact that PCa is heterogeneous meaning that it has different types of cells. Only some cell populations are sensitive to hormone therapies and that too is for a limited period ( short or long depending on the individual and the pathological status ). Some cells totally ignore the hormonal treatments and continue their growth even without producing PSA. ( H.Refractive cells ) . This is a dangerous reality when your GS is high ( 8,9 or 10 ) and also your staging is advanced at the time of diagnosis. Therefore in choosing treatments think of killing the enemy without merely trying to arrest. It is like a battle situation: "kill or be killed".
- Learn about the important Trials - STAMPEDE, CHAARTED and LATITUDE concluded recently on the early use of Chemotherapy upfront combined with primary ADT or Zytiga/Extandi which can destroy a wide spectrum of PCa cells which may result in a cure or long term remission, if executed at the right time.
- Your Gleason Score ( GS ) is a critical factor among other things ( Not given by you )
- At the age of 55 be a brave soldier. Take all the weapons into your hands. There is a battle ahead. We are all there with you and YOU ARE NOT ALONE.
I hope that your PSA is lower in Nov, but it might be useful to know your testosterone [T] & dihydrotesterone [DHT] levels. You mention Dr. Myers. He was a DHT producer even at castrate T.
You might be interested in the paper below.
"Incomplete Testosterone Suppression in Prostate Cancer"
"According to the Food and Drug Administration, the target testosterone level for androgen-deprivation therapy involving the use of LHRH agonists and antagonists is less than 50 ng per deciliter (1.7 nmol per liter). The typical testosterone level in men after orchiectomy is 14 ng per deciliter (0.5 nmol per liter). Yet Morote and colleagues noted that 25% of men receiving continuous androgen-deprivation therapy (given as a depot injection every 3 months) had a serum testosterone level above the recommended threshold of 50 ng per deciliter, and only 44% had a level that was consistently below 20 ng per deciliter (0.7 nmol per liter).3 In the same study, there was a direct correlation between the time to development of castration-resistant prostate cancer and the serum testosterone level. In another study, Perachino and coworkers reported a significant association between the serum testosterone level 6 months after initiation of androgen-deprivation therapy and overall survival."
N Engl J Med 2010; 363:1976November 11, 2010DOI: 10.1056/NEJM
To the Editor:
We have witnessed a new renaissance in the treatment of castration-resistant prostate cancer,1 but the progression of this disease beyond a form treatable by means of hormone deprivation still begs scientific and clinical inquiry. The adverse events associated with androgen-deprivation therapy are well characterized.2 Risks of cardiovascular-related side effects, skeletal-related events, loss of libido, and depression — among others — that are associated with androgen-deprivation therapy are major concerns for physicians and patients alike. An adverse event that is frequently overlooked, however, is the failure to lower or maintain levels of testosterone that would be present after castration. The package insert for all current luteinizing hormone–releasing hormone (LHRH) agonists and antagonists recommends periodic monitoring of serum testosterone levels. When we ask an audience at meetings the question, “Do you routinely measure testosterone levels in men who are receiving androgen-deprivation therapy?,” approximately 85% say no (though among these respondents, 80% do state that they would measure testosterone levels if the level of prostate-specific antigen were rising).
According to the Food and Drug Administration, the target testosterone level for androgen-deprivation therapy involving the use of LHRH agonists and antagonists is less than 50 ng per deciliter (1.7 nmol per liter). The typical testosterone level in men after orchiectomy is 14 ng per deciliter (0.5 nmol per liter). Yet Morote and colleagues noted that 25% of men receiving continuous androgen-deprivation therapy (given as a depot injection every 3 months) had a serum testosterone level above the recommended threshold of 50 ng per deciliter, and only 44% had a level that was consistently below 20 ng per deciliter (0.7 nmol per liter).3 In the same study, there was a direct correlation between the time to development of castration-resistant prostate cancer and the serum testosterone level. In another study, Perachino and coworkers reported a significant association between the serum testosterone level 6 months after initiation of androgen-deprivation therapy and overall survival.4
The failure of androgen-deprivation therapy to lower testosterone to “castrate levels” is itself a side effect. If it is recognized as such, we hope that physicians will then monitor testosterone levels, patients will request testing, and additional treatment options can be considered.
As everyone can quickly figure out, the purpose of ADT is literally to deprive PCa of androgen. It follows that less might probably be better. Men with T < 20 ng/dL do better than those 20-50 ng/dL, but perhaps 15 is better than 20, & so on. We don't have a tool where we can plug in our attained nadir & get a mean or median time to failure. If we did, most here would probably advise to ignore such a group statistic - it says nothing about the individual.
In a 2000 study of bilateral orchiectomy patients [1], "the median testosterone value in this patient cohort was 15 ng/dL." The authors concluded that "castrate testosterone should be defined as less than 20 ng/dL".
Subsequently, following dissatisfaction with the 50 ng/dL definition of castrate, 20 ng/dL began to look like a reasonable & attainable target.
In a 2006 study [2], "the mean serum testosterone level was 29.1 ng/dl in patients undergoing {maximal androgen blockade} and 29.5 ng/dl in patients treated with the LH-RH agonist". i.e. perhaps not so easy to get below 20 ng/dL.
A 2007 study [3] involved "73 patients with nonmetastatic prostate cancer treated with medical castration, 28 (38.4%) of whom also received bicalutamide (maximal androgen blockade)."
"Testosterone was less than 20 ng/dl in all determinations in 32 patients (43.6%). Breakthrough increases between 20 and 50 ng/dl were observed in 23 patients (31.5%), and increases greater than 50 ng/dl were observed in the remaining 18 (24.7%)."
"The lowest testosterone level with a significant impact on survival free of androgen independent progression was 32 ng/dl. Mean survival free of androgen independent progression in patients with breakthrough increases greater than 32 ng/dl was 88 months ... while it was 137 months ... in those without breakthrough increases" A 4 year difference!
With so many men not attaining <32 ng/dL - let alone <20 ng/dL - makes sense to add Zytiga if the target isn't reached within 3 months (if not starting ADT & Zytiga together).
{& an anti-androgen (e.g. Casodex), DHT inhibitor (e.g. Avodart) & a cholesterol inhibitor (e.g. Simvastain), of course.}
like you my main goal is to control PCa and NOT develop crPCa. I have a protocol I call Xtandi/BAT that I plan to start shortly. 3 months Xtandi on and 3 months Xtandi off...so the cancer is alternately exposed to T for 3 months, then deprived of access to T for 3 months. What is your opinion of this protocol.
BAT alternates between ~no T & supra-high T. You are presumably in the middle. T is growth-permissive at lower levels.
As we know, ADT selects for cells that can survive with very low T. The monthly BAT T shots shock cells bact to normality. It's a device to prolong the effectiveness of ADT.
Xtandi is an anti-androgen. It's not clear how intermittent use would extend its effectiveness. I don't know if there is literature on intermittent use of Casodex as monotherapy. That would offer a clue.
I hope you keep & report details of your protocol effects.
Thanks, I did ask my doc what T level was after 3 months and all he said was - its at castrate levels. I will ask for a specific number when i see him in Nov.
Also, he has only tested for 'Free Testosterone'. I assume that this doesn't measure DHT. Its a bit strage that 10 years after Snuffy Myers wrote a book stressing how important it is to measure and manage DHT that it's still overlooked.
And yes - I have male pattern baldness which is linked to DHT - so maybe there is a pattern here....
Free T is actually more relevant than T. What that means, is that if T is a bit higher than one would wish, an elevated SHBG could take enough T out of circulation that the effect is the same as lower a T with normal SHBG.
Unfortunately, studies related to ADT & optimum nadir androgen continue to use T as the target.
If you your knew free-T, I doubt that you would find a useful study.
On the other hand, a target free-T can be inferred from a target T, by assuming a normal ADT SHBG.
Mostly, labs measure T & SHBG to back into an assumed free-T.
You will find a lot of recommendations here. I would suggest you read the NCCN Guidelines for Prostrate Cancer: nccn.org/professionals/phys.... These are the latest physician guidelines for treating Prostate cancer Version 2.2017 for the United States. It will ask you to register. You can register as a patient and see the same guidelines as a physician. There is also a guide for Patients which is easier to read and follow.
I would also suggest you see a Medical Oncologist, if you are not using one, now. He/She will guide you between Urologists, Surgeons and Radiologists, as needed. I would suggest Chemo at this point, with or without ADT. The current treatment protocol, in the US is attack hard with Chemo initially, then resort to Abiraterone/enzalutimide/ADT, to pick up the stragglers that are missed by the chemo. The opposite of the protocol five years ago, when I started. Stage 4 Survivor since 2012, castration-resistant, metastases to pelvis, spine, ribs. liver, lymphs, spinal nerve root collapse, Osto Necrosis of the Jaw (ONJ). Currently in round 8 of docetaxel/carboplatin. You can read my tribulations elsewhere on this website. I have been thru many options except surgery.
Thanks to everyone for the warm welcome and generous support. I'm very glad to have found this site.
I can't reply to every post, but 2 things stand out
1. Most people are getting rapid decrease in PSA to very low levels in first 3 months of ADT.
I am concerned that i don't show a rapid response and I need to have a good talk to my doc about combined blockade or perhaps early chemo, but then again i have just found this research:
"To our knowledge, this is the first report to show that a faster time to reach a PSA nadir post-ADT initiation is associated with shorter survival duration in men with metastatic HSPC. These results need confirmation, but may indicate that a rapid initial response to ADT indicates more aggressive disease."
Now this dates from 2010. Does anyone know of any more research along these lines to either support to contradict this finding?
2. I need to find a medical oncologist. I know that my hospital has multi-disciplinary team meetings, and my radiologist advises that my case has been reviewed by a panel of PCa specilialists, but given that radiotherapy is now off the table it would make sense to make oncologist my primary contact.
My appointment is 15 Nov so nothing will happen until then - except hopefully a continued decline in PSA . I will let you know how it goes.
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. I will let you know how it goes.
Should/Can I take zytiga/xtandi et al without metastasis diagnosis
Help! Grappling with treatment choices.
