Dr Strum: When to start HT and recommended tests.

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John T
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Date Joined Nov 2008
Total Posts : 4225
   Posted 6/27/2011 6:59 AM (GMT -6)   
There has been a lot of discussion on when to start HT and the testing one should have. This is Dr Strums advice on P2P.
 

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Material posted here is intended for educational purposes only, and must not be considered a substitute for informed medical advice from your own physician.

**********

From: Stephen Strum, MD, FACP

Board-Certified Medical Oncologist

Specializing in Prostate Cancer since 1983

To: Frank S.

TIME 9:30 PM to 10:20 PM

On Jun 24, 2011, at 3:34 AM,

<mailto:franks@prostatepointers.org>franks@prostatepointers.org wrote:

>**********

>

>Material posted here is intended for educational purposes only, and

>must not be considered a substitute for informed medical advice from

>your own physician.

>

>**********

>Frank S.

>Dear Doctors,

>I was diagnosed 3 years ago at age 49. PSA 13.6; GS 7 (3+4); 6/10

>positive cores;

<Stephen Strum, MD> always crucial is need for VALIDATION of key information such as Gleason score. Michael Kattan MD, now at the Cleveland Clinic, has nomograms relating to PC of which one predicts the likelihood of an upgrade to a higher Gleason score at RP.

See <http://rcalc.ccf.org>http://rcalc.ccf.org

Frank S.

08/2008 RRP; Pathology GS7 (3+4); clear nodes; positive margin; no SV invasion;

<Stephen Strum, MD> "clear nodes" does not cut it. Number of nodes from what anatomic nodal areas. Details such as these are critical to appraise STATUS or What's Going On. The bottom line in assessing any biological system in the universe is "You Gotta Do Your Homework". --Stephen Strum, MD along with "What are the facts?

"The facts, maa'm, just the facts." --Jack Webb in Dragnet

Even the (3,4) does not cut it since the amount of grade 4 is so important and can vary from as little as 5% grade 4 to as much as 49%. So, what was it?

 

Frank S.

>07/2009 SRT 78 Gy

<Stephen Strum, MD> and given your RP findings of a positive margin without waiting to see what the PSA is one month post RP, your MDs went ahead with RT. Given that the RP was in 8/08 and the RT in 7/09, perhaps there was a rise in PSA and you are just not presenting data chronologically.

Frank S.

>PSA history:

>Post RRP:

>

>10/08: 0.04

>

>11/08: 0.06

>

>12/08: 0.06

>

>3/2009 0.1

>

>6/2009: 0.2

<Stephen Strum, MD> Present your data in context with what is going on since this the more logical and rational way to understand cause and effect.

Frank S.

>Post SRT:

>10/2009: 0.1

>11/2009: 0.03

>2/2010: 0.04

>5/2010: 0.04

>8/2010:0.05

>11/2010: 0.07

>2/2011: 1.4

>3/2011: 2.1

>4/2011: 2.6

>5/2011: 3.2

>6/2011: 5.2

<Stephen Strum, MD> you have had a steady rise in PSA with PSADT of about 2 months which is consistent with metastatic disease.

 

Frank S.

>In spite of the RRP and SRT I have an active sex life with my wife of

>27 years. Consulted with my urologist who wants to start hormone

>therapy immediately. When asked about the benefit of immediate over

>postponed, he is rather ambiguous. My medical oncologist is of the

>opinion that there is no benefit and there is potential harm. What is

>the latest medical opinion about immediate or postponed HT for

>someone with my present status?

<Stephen Strum, MD> Definitely agree with the urologist more than the

fellow medical oncologist. What you do not want is bulky and mutated

PC to deal with. One issue is where is the PC?

I would want the following:

DRE (digital rectal exam) report.

CBC, CMP (comprehensive metabolic panel)

bone resorption markers to include serum b-CTX (C-Terminal

Telopeptide, b-Crosslaps) & urine DpD (deoxypyridinoline) since

these are associated with metastases and also since if one or both of

these markers are high normal or elevated i would want to begin Xgeva

medication.

I would want an MRI-A (MRI axial skeleton) to rule out bone mets.

Lecouvet FE, Geukens D, Stainier A, et al: Magnetic resonance imaging

of the axial skeleton for detecting bone metastases in patients with

high-risk prostate cancer: diagnostic and cost-effectiveness and

comparison with current detection strategies. J Clin Oncol

25:3281-3287, 2007; PMID:

17664475.

PURPOSE: To evaluate the diagnostic performance, costs, and impact on

therapy of one-step magnetic resonance imaging (MRI) of the axial

skeleton (MRIas) for detecting bone metastases in patients with

high-risk prostate cancer (PCa). PATIENTS AND METHODS: Sixty-six

consecutive patients with high-risk PCa prospectively underwent MRIas

in addition to the standard sequential work-up (SW) of bone

metastases (technetium-99m bone scintigraphy [BS] completed with

targeted x-rays [TXR] in patients with equivocal BS findings and with

MRI obtained on request [MRIor] in patients with inconclusive BS/TXR

findings). Panel review of initial and 6-month follow-up MRI

findings, BS/TXR, and all available baseline and follow-up clinical

and biologic data were used as the best valuable comparator to define

metastatic status. Diagnostic effectiveness of MRIas alone was

compared with each step of the SW. Impact of MRIas screening on

patient management and costs was evaluated. RESULTS: On the basis of

the best valuable comparator, 41 patients (62%) had bone metastases.

Sensitivities were 46% for BS alone, 63% for BS/TXR, 83% for

BS/TXR/MRIor, and 100% for MRIas; the corresponding specificities

were 32%, 64%, 100%, and 88%, respectively. MRIas was significantly

more sensitive than any other approach (P < .05, McNemar). MRIas

identified metastases in seven (30%) of 23 patients considered

negative and eight (47%) of 17 patients considered equivocal by other

strategies, which altered the initially planned therapy. Economic

impact was variable among countries, depending on reimbursement

rates. CONCLUSION: MRIas is more sensitive than the current SW of

radiographically identified bone metastases in high-risk PCa

patients, which impacts the clinical management of a significant

proportion of patients.

 

Tombal B, Rezazadeh A, Therasse P, et al: Magnetic resonance imaging

of the axial skeleton enables objective measurement of tumor response

on prostate cancer bone metastases. Prostate 65:178-187, 2005; PMID:

15948151.

BACKGROUND: There is currently no technique to image quantitatively

bone metastases. Here, we assessed the value of MRI of the axial

skeleton (AS-MRI) as a single step technique to quantify bone

metastases and measure tumor response. METHODS: AS-MRI was performed

in 38 patients before receiving chemotherapy for metastatic HRPCa, in

addition to PSA, computed tomography of the thorax, abdomen, and

pelvis [CT-TAP]; and Tc-99m bone scintigraphy. A second AS-MRI was

performed in 20 patients who completed 6 months of chemotherapy.

Evaluation of tumor response was performed using RECIST. RESULTS:

Only 11 patients (29%) had RECIST measurable metastases in

soft-tissues or lymph nodes on baseline CT-TAP. AS-MRI identified a

diffuse infiltration of the bone marrow in 8 patients and focal

measurable metastatic lesions in 25 patients (65%), therefore,

doubling the proportion of patients with measurable lesions.

Transposing RECIST on AS-MRI in 20 patients who completed 6 months of

treatment, allows the accurate estimation of complete response (n =

2), partial response (n = 2), stable disease (n = 5), or tumor

progression (n = 11), as it is done using CT-TAP in soft tissue solid

metastases. CONCLUSIONS: MRI of axial skeleton enables precise

measurement and follow-up of bone metastases as it is for other

soft-tissue metastasis.

Pending the results of the above would then make treatment decisions

re ADT (androgen deprivation therapy) and how best to give.

If Combidex were still available would do after a normal MRI-A (MRI

axial skeleton) study. If MRI-A (MRI axial skeleton) could not be

done then I would opt for PET/CT using F18 but NOT FDG isotope.

I would also want baseline testosterone level as well as prolactin

level and given the uncertainty of the Gleason score would want

neuroendocrine (NE) markers that are more often seen with high

Gleason scores of 8-10 such as CGA (Chromogranin A), NSE (Neuron

Specific Enolase) and CEA (Carcinoembryonic Antigen). Read The

Primer on Prostate Cancer by Strum & Pogliano and see page 64

regarding markers in high GS situations.

Assuming all has been done, ADT should be at least ADT with 3 drugs

to include anti-androgen (AA) e.g. Casodex or Flutamide followed one

week later by an LHRH agonist like Lupron or Trelstar or Eligard. I

also use Avodart along with the anti-androgen (AA). I monitor the

CBC, ultrasensitive PSA, CMP (comprehensive metabolic panel) &

testosterone monthly until stable values. My goal in PSA is < 0.05 x

12 months and then off ADT but staying on Avodart.

Our published paper used finasteride (Proscar) but dutasteride

(Avodart) appears to be a more appropriate 5ARI (5-alpha reductase

inhibitor) for higher Gleason score PC.

Hope this helps.

If you appreciate the time I have spent in helping you, please

consider paying it forward by making a charitable donation to one of

the following worthy organizations:

SmileTrain: To help a child obtain surgery for correcting a cleftlip

deformity:

<http://www.smiletrain.org/site/PageServer>http://www.smiletrain.org/site/PageServer

$240 changes one child's life with surgery.

Habitat for Humanity: To help rebuild a home for someone that has had

their home destroyed by a natural disaster:

<http://www.habitat.org/ap/>http://www.habitat.org/ap/

Partners in Health: to help a medical team deliver medical care to

unfortunate people in low income areas of the world:

<http://www.pih.org/home.html>http://www.pih.org/home.html

Stephen B. Strum, MD, FACP

Board Certified: Internal Medicine, Medical Oncology

Specialist in Prostate Cancer since 1983

Member: ASCO, AUA, ASTRO

Member: International Strategic Cancer Alliance (ISCA)

********

Material posted here is intended for educational purposes only, and must not be considered a substitute for informed medical advice from your own physician.

**********

From


JNF
Veteran Member


Date Joined Dec 2010
Total Posts : 3745
   Posted 6/27/2011 7:49 AM (GMT -6)   
Thanks John, excellent information.   My urologist and oncologist are both proponents of early intervention when it is apparent that the cancer is progressing.   They want to deal with it in its smallest least aggressive form.   They both tell me that if you allow the cancer to grow unfettered it will also continue to mutate and both conditions allow it to become more resistant to treatment.   I have not understood how some will put a future PSA threshold of say 10 before starting HT.   It seems like that could be a lot of cancer advancemet particularly if it is higher gleason that puts off much lower volumes of PSA relative to it size.


PSA 59 on 8-26-2010 age 60. Biopsy 9-8-2010 12/12 positive, 20-80% involved, PNI in 3 cores, G 3+3,3+4,and 4+3=G7, T2b.
Eligard shot and daily Jalyn started on 10-7-2010.
IMRT to prostate and lymph nodes 25 fractions started on 11-8-2010
HDR Brachytherapy December 6 and 13-2010.
PSA <.1 and T 23 on 2-3-2011.
PSA <.1 on 4-7-2011
Second Eligard shot on 4-7-2011

Post Edited (JNF) : 6/27/2011 8:06:31 AM (GMT-6)


An38
Veteran Member


Date Joined Mar 2010
Total Posts : 1148
   Posted 6/27/2011 7:55 AM (GMT -6)   
Thanks John, very interesting.

I don't understand why he believes that a fast doubling time is consistent with metastatic disease. I am not sure I have heard this before. High Psadt was in my mind related to aggressive disease and not necessarily metastatic. Thoughts?

An
Husband's age: 52. Sydney Australia.
Family history: Mat. grandfather died of PC at 72. Mat. uncle died of PC at 60. He has hereditary PC.
PSA: Aug07 - 2.5|Feb08 - 1.7|Oct09 - 3.67 (free PSA 27%)|Feb10 - 4.03 (free PSA 31%) |Jun10 - 2.69. DRE normal.
Biopsy 28Apr10: negative for a diagnosis of PC however 3 focal ASAPs “atypical, suspicious but not diagnostic” for PC. Review of biopsy by experienced pathologist, 1/12 core: 10% 3+3 (left transitional), 1/12 core: ASAP (left apex)
Nerve sparing RP, 20Aug10 with Dr Stricker. Post-op path: 3+4 (ISUP 2005). Neg (margins, seminal vesicles, extraprostatic extension). Multifocal, with main involvement in the fibro-muscular zone. T2C.
Post RP PSA,
Lab 1: Sep10 – 0.02|Nov10 – 0.03|Dec10 – 0.03|Feb11 – 0.03
Lab 2: Nov 10 - 0.01|Dec10 – 0.01|Feb11 – 0.01|Apr11 – 0.01

John T
Veteran Member


Date Joined Nov 2008
Total Posts : 4225
   Posted 6/27/2011 10:03 AM (GMT -6)   
An,
You will notice that the fast PSAD was post SRT. This would be indicative of systemic disease. I would think that any fast PSAD post treatment would be a very likely indicator that what is generating the psa is not local.
Also any fast PSAD indicates agressiveness, the tumor is growing at a rapid rate. An aggressive tumor has much more of a chance of going systemic than a slow growing tumor.
JT
66 years old, rising psa for 10 years from 4 to 40; 12 biopsies and MRIS all negative. Oct 2009 DXed with G6 <5%. Color Doppler biopsy found 2.5 cm G4+3. Combidex clear. Seeds and IMRT, 4 weeks of urinary frequency and urgency; no side affects since then. 2 years of psa's all at 0.1.

Purgatory
Elite Member


Date Joined Oct 2008
Total Posts : 25380
   Posted 6/27/2011 11:22 AM (GMT -6)   
John, I agree with your original post and followup post, its in line with what my new oncologist has discussed with me concerning my numbers.

david
Age: 58, 56 dx, PSA: 7/07 5.8, 10/08 16.3
3rd Biopsy: 9/08 7 of 7 Positive, 40-90%, Gleason 4+3
open RP: 11/08, on catheters for 101 days
Path Rpt: Gleason 3+4, pT2c, 42g, 20% cancer, 1 pos margin
Incont & ED: None
Post Surgery PSA: 2/09 .05,5/09 .1, 6/09 .11. 8/09 .16
Post SRT PSA: 1/10 .12, 4/8 .04, 8/6 .06, 2/11 1.24, 4/11 3.81, 6/11 5.8
Latest: 6 Corr Surgeries to Bladder Neck, SP Catheter since 10/1/9, SRT 39 Sess/72 gy ended 11/09, 21 Catheters, Ileal Conduit Surgery 9/10

ralfinaz
Veteran Member


Date Joined Jan 2011
Total Posts : 735
   Posted 6/27/2011 11:54 AM (GMT -6)   
Dr, Strum said in his response to Frank:
"<Stephen Strum, MD> and given your RP findings of a positive margin without waiting to see what the PSA is one month post RP, your MDs went ahead with RT. Given that the RP was in 8/08 and the RT in 7/09, perhaps there was a rise in PSA and you are just not presenting data chronologically."

From the data presented, it seems to me that Frank waited some 11 months after RP to get SRT and not one month after surgery when it was evident that recurrence was present.

RalphV
Phoenix, Arizona
Disclaimer: I am a long-term prostate cancer survivor. My comments are not intended as medical advice. The intent is to provide information. Seek direct recommendations from your medical team.
Surviving prostate cancer since 1992 at age 58. RP; Orchiectomy; GS (4 + 2); bilateral seminal vesicle invasion; tumor attached to rectal wall; Stage T4; Last PSA September, 2010: <0.1 ng/m

142
Forum Moderator


Date Joined Jan 2010
Total Posts : 6947
   Posted 6/27/2011 12:01 PM (GMT -6)   
Ralph,
 
That 11 months has me confused as well - I can't see anyone starting adjuvant RT without there having been time for at least one psa. Sure, you could make the call to do it (I did), but there were two psa tests before enough healing time had passed to even start the RT process.

ralfinaz
Veteran Member


Date Joined Jan 2011
Total Posts : 735
   Posted 6/27/2011 12:14 PM (GMT -6)   
Hi 142,
Frank had 5 PSA tests after RP; A PSADT of some 2 months. It seems to me he made the right decision to try salvage radiotherapy then. I think Dr. Strum"s comment was based on misinterpreting the dates...

RalphV
Phoenix, Arizona
Disclaimer: I am a long-term prostate cancer survivor. My comments are not intended as medical advice. The intent is to provide information. Seek direct recommendations from your medical team.
Surviving prostate cancer since 1992 at age 58. RP; Orchiectomy; GS (4 + 2); bilateral seminal vesicle invasion; tumor attached to rectal wall; Stage T4; Last PSA September, 2010: <0.1 ng/m

Carlos
Regular Member


Date Joined Nov 2009
Total Posts : 486
   Posted 6/27/2011 1:00 PM (GMT -6)   
John,  Thanks for the very interesting post.  I do have a question about ADT3.  Strum, Scholz, Myers and Sartor are strong advocates for ADT3.  Yet, in a recent paper Scholz mentioned that there had not been any clinical trials evaluating the efficacy of ADT3.  Sartor also mentioned in an older paper that there wasn't any data showing lower T levels provided any benefit.   Have you come across any studies that show a benefit such as longer survival times or longer holiday periods?  I have seen some data showing the benefit of adding finasteride to the mix.
 
Carlos

Dx 2/2008, at age 71, PSA 9.1, G8, T1c
daVinci surgery 5/2008, G8(5+3), pT2c,N0,MX,R0
BCR 2 1/2 yrs after surgery
IMRT, 68.4 Gy, 12/2010 - 2/2011
PSA 0.07 three months after IMRT

zufus
Veteran Member


Date Joined Dec 2008
Total Posts : 3149
   Posted 6/27/2011 1:49 PM (GMT -6)   
John-Good example of what a classy oncologist might investigate for a patient

Carlos- I don't have a link but consider this also Dr. Leibowitz and some others have patient histories on alot of patients that probably cover almost 20 yrs. experience in patients receiving ADT3, friend of mine used ADT3 as his primary treatment back in 1996 and was gutsy enough to be his own gineau pig. (psa was 11.0 2 cores positive, low Gleason (2+3) back then, today that is considered Gleason 6's). He has had biopsies 3 times during all these 15 yrs., recently one with color doppler by Dr. Fred Lee and no cancer is found (thus far). He could still receive any treatment if and when he felt compelled, isn't that interesting???

There are many patients treated by Dr. Leibowitz with interesting histories, maybe comparable to this. Those oncologist do share info and meet at annual meetings, etc. Perhaps some of that kind of info is what they look at and their own patients histories and then abstracts or whatever can be found.

In Dr. Strums book Wheeler, et al compared Lupron+Casodex to Casodex+Proscar and useage as found in hormone naivee or non-hrpca patients, the results were almost identical as to effectiveness. The big difference would be the costs/profits, and side effects less on casodex+proscar (CAB). I find that very interesting and speaks alot about what goes on in the name of patients. Then there are the choices of other PCa drugs even as first line useage. Many ways to jump into HT therapies.

John T
Veteran Member


Date Joined Nov 2008
Total Posts : 4225
   Posted 6/27/2011 2:59 PM (GMT -6)   
Carlos,
I believe you are correct in that there are no studies comparing ADT3 to mono HT. It's a tenent in oncology that combinations of meds are more effective than only one med. When 9 out of 10 of the most experienced oncologists use ADT3 vs a mono treatment there must be something to it. These oncologists combined have tens of thousands cases of advanced PC and I think that this experience trumps any small clinical trial done by a researcher with little experience in actually treating advanced PC.
The way medicine used to be practiced is that a doctor would do something and observe what happened; this is how he learned. Today with the large institutions and their protocols nothing happens unless there is a clinical trial to suppport it. This is one reason that the major instituations are far behind the private practice oncologists in dealing with advanced cases.
The main thing I get out of Strum's posts are all the tests and measurements he takes to first identify the individual biology and the futher testing to see what the meds are actually doing. This is a far cry from the "normal shot of Lupron and see you in three months" treatment that a lot of advance cancer patients get.
JT
66 years old, rising psa for 10 years from 4 to 40; 12 biopsies and MRIS all negative. Oct 2009 DXed with G6 <5%. Color Doppler biopsy found 2.5 cm G4+3. Combidex clear. Seeds and IMRT, 4 weeks of urinary frequency and urgency; no side affects since then. 2 years of psa's all at 0.1.
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