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This member is a YANA Mentor This is his Country or State Flag

Frank Pollock lives in Scotland. He was 68 when he was diagnosed in March, 2006. His initial PSA was 9.80 ng/ml, his Gleason Score was 7a, and he was staged T1c. His choice of treatment was Non-Invasive. Here is his story.

In Dr Peter Scardino's 'The Prostate Book - An Owners Manual' (ISBN 0-718-14694-8) he refers to the Prostate Cancer Prevention Trial (PCPT) which found that "...long term use of finasteride [aka Proscar] reduced the overall incidence of prostate cancer by an astounding 25% when compared to a placebo", (p122). He goes on to say "Indeed finasteride may prove to be the first drug capable of preventing cancer", (p123). He also states that "Finasteride is approved for treatment of BPH, but we have long speculated that it might prevent prostate cancer", (p81) [The findings of this study have resulted in considerable debate, because the study also showed "....a slight increase in high-grade disease among men in the finasteride arm (6.4 percent of men in the finasteride group vs. 5.1 percent of men in the placebo group). High-grade tumors (Gleason score 710) are more likely to grow quickly and spread beyond the prostate than lower-grade tumors." One point that seems to be clear from the discussions about the Trial is that finasteride changes the cellular structure of the prostate gland and this raises some questions regarding some of the claims made.]

Seven years ago (March 2004) I was diagnosed with BPH (Benign Prostate Hyperplasia). I was informed that BPH is not prostate cancer. And was prescribed Flomax [This is not finasteride but tamsulosin]. Outcome no symptoms.

1st biopsy carried out after some two years (2006) on Flomax - "no cancer found"

2nd biopsy one month later - "2 x tiny foci, Gleason Score 3+4=7"

Advised 'surgery soonest' was best option but that IMRT (Intensity Modulated Radiation Therapy) was then 'trialling' and would be available soon. There was also talk of brachytherapy becoming an option in the near future

On discussing with oncologist I asked about the PCPT (Prostate Cancer Prevention Trial) outcomes and he somewhat reluctantly said I could have Flomax and Proscar [finasteride] at the same time. I decided on this option to buy time

A 3rd biopsy another 2+ years later (2008) reported "no cancer found" and I am still on Flomax and Proscar to this day with no symptoms or discomfort.

However my PSA has continued to rise. Seven years ago it was 8.6. It is now 18.3 (but the latter value is complicated by use of Proscar for past 4 years or so. [Because Proscar usually reduces the size of the prostate gland, the amount of PSA leaked from a gland which has been enlarged by BPH can diminish. One well known study suggested that men on Proscar would have a PSA reading that was 50% of the 'real' reading. As a result many men double their PSA results if they are on Proscar. This is not a scientifically sound approach as the range of the Proscar effect is quite wide]

PSA doubling time has been constant at 45.43 months over past 4 years; velocity has shown corresponding constant rise of 2.83 ng/ml/yr over same period

I had it at the back of my mind to act as soon as the PSA rate of increase showed signs of acceleration but rate of increase has been constant

Anyway consultant has now booked a 4th biopsy for May 2011

As I see it at age 73 there is statistically a 60/70% probability of PCa but:

If present PSA rate of increase continues and does not accelerate it will be 38.11 at age 80. Megrahi, the Lockerbie bomber, was PSA 363, Gleason 4+5=9, at diagnosis in Sept 2008 - and he is still alive [There are, perhaps, better examples of longevity than the politicised diagnosis of Megrahi in the Experiences pages of this site]

Updated history on my own tale of woe pasted below. All/any responses to my questions in last paragraph and any other relative comment/advice would be much appreciated

My story so far:

12/03 - inc freq, inc urgency, age 66, diagnosed BPH
03/04 - initial PSA 8.6 - Flomax
02/06 - PSA 9.6, biop 1 - no cancer, no size given but "guesstimated" @ 45 cc
03/06 - biop 2 - "2 x "tiny foci" , left lobe, Gleason 3+4, bone scan clear, MRI clear, surgeon advice "prostatectomy"
12/06 - PSA 11.2, oncologist advice IMRT, or can have Flomax and Proscar
10/08 - PSA 10.4, biop 3 - no cancer , size measured @ 76cc (now over 2 years on Flomax and Proscar and dairy free diet, etc)
01/11 - PSA 18.3, no symptoms, no discomfort, now age 73

My comments:

Average PSA range for age 73 is 4.5 to 6.5 [Not too sure where this statement comes from, but since most men of this age may have some enlargement of the prostate gland, this should be factored in to the calculations below.]
Predicted PSA for 76cc prostate is 76 x 0.12 = 9.12 (according to one reliable sounding source) [This has been accepted, but again is indicative not definitive - there are other calculations that produce different results]
Add both together and deduct from present 18.3 (say 5.5 + 9.12=14.62) and notional PSA count becomes 3.68, not the end of the world at 73 [The calculation is unsound as the 'normal' PSA (related to a prostate gland of about 25 cc) would be included in the large (76cc) gland calculation. That calculation should therefore be (76-25) x 0.12 = 6.12 + 5.5 = 11.62 and notional PSA count becomes 6.68]
However Proscar reduces PSA by "half" according to some sources and in my case reducing size of prostate must mainly affect proportion of PSA due to BPH rather than the "2 x tiny foci" cancer seen under a microscope.

This simply shows how easy it is for consultants and patients alike to select and manipulate data to justify almost any action or inaction

My PSA record in tabular form for info:

Date

PSA (Bayer)

PSA (Abbott)

Comment

Age

December-2003

-

-

Inc frequency + urgency

-

March-2004

7.6

8.6 (estimate)

Prescribed Flomax only

66

May-2004

5.5

-

-

-

December-2004

7.7

-

-

-

May-2005

7

-

-

67

November-2005

7.3 (assay change)

8.3

-

-

December-2005

-

9.6

Biop 1, "suspicious"

-

March-2006

-

9.8

Biop 2, "2 x tiny foci, Gl 3+4"

68

May-2006

-

11.6

PSA test after DRE

-

August-2006

-

10.6

Bone scan "clear"

-

October-2006

-

10.4

MRI scan "clear""

-

December-2006

-

11.2

-

-

May-2007

-

16.8

Mountain bike used before test

69

April-2007

-

5.8

No biking for month before test

-

July-2007

-

8.2

-

-

October-2007

-

6.5

-

-

February-2008

-

9.3

-

70

June-2008

-

8.5

-

-

September-2008

-

10.4

Biop 3, "no cancer"

-

March-2009

-

13.1

-

71

June-2009

-

13.3

-

-

September-2009

-

14.6

-

-

February-2010

-

15.6

-

72

June-2010

-

16.7

-

-

September-2010

-

17.2

-

-

January-2011

-

18.3

-

73

May-2011

-

??

PSA test prior to next biop

-

-

-

-

Biop 4 arranged for 05/11

-

June-2011

-

??

PSA test post next biop

-

-

-

-

-

-

-

Decision time?

-

?????

73+

My questions now are:

How does 4 years on Proscar and Flomax affect the appearance of biopsy sample slides under the microscope? [Unequivocally "Yes", according to Dr Gleason, after whom the Gleason grading system is named, and other experts.]

Is use of Proscar and Flomax likely to make perceived Gleason scores higher or lower? [Dr Gleason says that the current grading system cannot be applied to samples from glands where finasteride has been administered.]

Does the pathologist have to be advised in advance to make allowances for this? [Yes]

My thinking was that if PCa was particularly aggressive PSA doubling time would have been much less than 4 years and the rate of increase would have accelerated but latter remained more or less constant. Irrespective of outcome from next biopsy (05/11) I anticipate some pressure to make treatment decision. IMRT is likely to be suggested but at age 73 and PSA 18.3 would skidding by for another few years on Flomax and Proscar be feasible? [This is a very personal decision and there is no clear answer. For a somewhat amusing look at the concept of aggressive treatment at age 70 and above see Lorenzo Q Squarf on the subject.]

If IMRT looms is it worth asking about amifostine? [The use of this drug seems to be more for patients treated with chemotherapy or with head and neck cancers and is aimed at reducing the probability of dry mouth. Dry mouth is not normally regarded as a side effect of prostate cancer radiation therapies.]

Have I lost the plot? [Not in my opinion.]

UPDATED

July 2011

January 2011 - PSA 18.3, no symptoms, no discomfort, now age 73

May 2011 PSA 20.6, biopsy number 4 Gleason 6, size measured at 57cc, 12 samples, longest core 15mm (Right and Left). Microscopy shows a single focus of adenocarcinoma Gleason score 3+3=6 in one left lobe core. Perineural invasion is not identified. The remainder of the left lobe cores show mild chronic inflammation and glandular atrophy. There is no evidence of malignancy in right lobe cores. Tumour involves less than 5% of core total tissues received. Still no symptoms, no discomfort, still 73+

The reduction in measured prostate size was unexpected, as was the "downgrade" to Gleason 6. No matter how well prepared you think you are it is all too easy to be thrown off balance during a consultation and emerge without asking the questions you should have asked.

At 73+ I'm rapidly getting to the position where choices look to be narrowing to continuing on AS or opting for gold seed located IMRT but whether or not IMRT is likely to extend my lifespan by very much is questionable. It might just alter the cause of death from PCa to something else equally unappealing.

With no symptoms skidding by for another year or 2 on Proscar + Flomax (finasteride + tamsulosin) and a change to intermittent Zoladex if PSA gets out of hand (say 50?) might be as good a choice as any.

My strategy throughout has been to weigh up everything after every PSA/biop and to be as objective as possible ln deciding what to do next not as easy as it sounds when it is your own physical well being to weigh up.

On balance though it looks as if tackling the "mild chronic inflammation" is the immediate priority and after that yet another PSA test.

Comment, criticism, advice very welcome. [Regrettably Lorenzo Q Squarf no longer posts on the internet - at least on the subject of prostate cancer, but he did have some strong views on treatment choice as we age - see Squarf on Age]

Frank Pollock

My updated PSA/biop record in tabular form - extending the table above for info:

Date

PSA (Bayer)

PSA (Abbott)

Comment

Age

May-2011

-

20.4

-

-

June-2011

Biop 4, "downgrade" to GL6 from biop 2 March 2006, Prostate now "57cc", it was 76cc at biop 3 October 2008

12 samples, longest cores 15mm (Right and Left). Microscopy shows a single focus of adenocarcinoma Gleason score 3+3=6 in one left lobe core. Perineural invasion is not identified. The remainder of the left lobe cores show mildchronic inflammation and glandular atrophy. There is no evidence of malignancy in right lobe cores. Tumour involves less than 5% of core total tissues received.

-

July-2011

-

??

Will consult onco in coming months

-

-

-

??

-

-

-

Decision time?????

??

more WW/AS? IMRT? ??????

-

Frank Pollock

UPDATED

March 2012

My updated PSA/biop record in tabular form:

Date

PSA (Bayer)

PSA (Abbott)

Comment

Age

June-2011

-

20.4

Pre biop

-

June-2011

-

-

Biop 4 12 samples, prostate 57cc prostate, single focus adenocarcinoma

Gl 3+3=6 in one left lobe core <5%

Perineural invasion not identified, remainder of left lobe cores show mild chronic inflammation and glandular atrophy

No evidence malignancy in right lobe

-

June-2011

-

22.8

Cipro for inflammation - reacted badly, stopped after 2 days

-

August-2011

-

-

MRI = 0

-

September-2011

-

25.1

Trimopethrim for inflammation, no problems

-

October -2011

-

23.1

-

-

February-2012

-

26.7

-

-

March-2012

-

-

MRI = no change

Possibility of anterior right TZ tumour

T1c, N0, M0

74

April-2012

-

-

Next appt with onco

-

Still on Proscar and Flomax

-

-

Change to Avodart and Proscar? Does T1c justify radical at 74?

-

Frank

UPDATED

May 2013

I am still on AS and to be truthful very happy that I was not stampeded into brutal butchery. If you are not taken out in jig time by an aggressive stripe of CaP there is likely to come an age for every one of us where any potential "benefit" from radical intervention is far outweighed by the physical damage it will do to you and at 75+ I reckon I'm there.

The last oncologist consultation I had was with a female radiation oncologist. A hijab wearing tick box merchant who deflected questions and was insistent that I "needed" radiation.

Dutasteride is not approved here (no doubt for financial reasons, fin 8p/tab, dut 79p/tab + private prescription cost) and when I mentioned the possible superiority in enzyme blockage the response was a flat "no"). I went ahead and bought what I needed in southern Europe and I've been taking Tamsulosin and Dutasteride for over a year. PSA change over the full year has been 30.9 to 31.6, ie near enough zilch.

I'm not afraid to undergo treatment, as oncos hinted, but I have to be convinced that on balance it will result in worthwhile benefit. Review situation at regular intervals and if something changes dramatically deal with it then is my intention. The Terry Herbert strategy?

My updated PSA/biop record in tabular form:

Date

PSA (Bayer)

PSA (Abbott)

Comment

Age

March - 2012

-

-

3rd MRI= 0, no change Aug 2011 MRI, oncp "thinks" it may be in right anterior and wants to do a "mapping" biop, 50 samples under anaesthetic. That would bring total no of samples taken to date to 96 and I balked at that.

75

April - 2012

-

30.9

Onco's team now "thinks" it is T3 and I should have radiation

-

May - 2012

-

28.3

Changed from finasteride to dutasteride, against onco advice

-

June - 2012

-

-

Bone scan = 0

-

September - 2012

-

26.9

-

-

February - 2013

-

31.6

-

-

May - 2013

-

-

And that is it. Nearly 10 years on AS and PSA has risen from an initial 8.6 to a present 31.6, now on tamsulosin and dutasteride, with no symptoms or discomfort other than loss of libido which at 75 is par for the course

-

Over past full year PSA has risen 0.7 point from 30.9 to 31.6.

-

June - 2013

Next consultant appointment due. Medics will be even keener to intervene with radiation. But for me at age 75+ I must be near to the time when radical radiation might do more harm than good make no difference to my allotted lifespan and spoil what remains with quite onerous side effects into the bargain.

My gut feeling is that I have already exceeded the local average male mortality age by nearly 10%. I've been gambling on AS for nearly a decade. Does that mean I have already "won"? Time will tell.

Would I do the same again? At present the answer is yes but with hindsight I would not have had any biops at all and I certainly wouldn't have clocked up 4"

Biops are pushed as the 'gold standard', 'only way to be sure', etc. But you find out the hard way that while a positive biop is accepted as certain proof that you have PCa a negative biop is certainly not accepted as confirmation that you don't.

-

Frank

UPDATED

July 2014

Updated assessment of PCa risk/physical cost/potential benefit, etc July 2014

Age 77, on Combodart (dutasteride + tamsulosin)

Known BPH, initial prostate size 76cc, 10+ yrs on AS, PSA initial 7.6 now 38, 4 biops yielded single sample +ve, 3+3, <5% (1of 46 samples), 4 MRIs, 4th in 2014 shows 'new tumour", T3a N0 M0 , tumour size not known

Reasonably fit, eat, sleep and keep well, pee a bit slow 1st thing am, OK thereafter, no pain, no discomfort, no getting up at night. Can live with that, can live with known PCa

All electives come down to what might happen if I choose this, or that, Vs what might happen if I don't

PCa outcome/recurrence/side effects/mortality stats are a mess of contradiction and controversy. Any radical entails absolutely certain physical damage to be weighed against much less than certain benefit

So, what next? How long from T3a N0 M0 to kaput? Will PCa get me before something else does?

@ 77 another decade or so would be good and there is merit in 'if it ain't broke, don't fix it'; or at least not until problems arise and something has to be done

Instinct is to play it to the wire; delay/avoid radical unless/until push comes to shove. Continue present diet/lifestyle/exercise/Combodart regime until symptoms/runaway PSA

Change then to hormones, test PSA low, monitor PSA trend, measure time from low to say doubling, reassess (When is optimum time to start, intermittent or continuous hormones? What is average time from hormone initiation to kaput? Don't' know and I doubt if any medic does)

Radical intervention outcomes vary from unpalatable to downright disastrous and playing for time is a high risk strategy but @ present go with the gut seems like the best option.

PCa has a multitude of individual factors. Pros and cons of this 'what next' assessment inevitably reflect personal outlook and attitude to life.

I know only too well that my preference for minimal intervention is not in line with the standard 'prostate industry' practice of detect early/treat early but I can live with the risk and this assessment looks at it from where I am now.

Decision taken; continue on Combodart, etc as at present for another 6 months, have next PSA test early 2014 and reassess then.

I have looked at it long and hard and at 77 this strategy makes sense to me. On the upside physical damage is negligible on the downside Combodart has carked libido).

Many who read this will dismiss me as a reckless bampot. Maybe I am a nut job but everything in the ephemeral world of PCa is crazy and contradictory. Nothing is quite what it says on the tin and you have to make the best risk/benefit assessment you can all by yourself. No one else will, or can, do it for you.

So that's it for now.

Frank Pollock

UPDATED

August 2015

PSA series since July 2014 reads 48, 50, 48, 65. PSA doubling time, if it means much, is 2.1 years using MSKCC calculator. However PSA has never been 'low'. First ever PSA was 8.6 over 11 years ago and I can live with PSA 65 now

In the always contradictory world of PCa PSA >4 triggers a biop, rising is considered 'ominous'. Recent studies now suggest that falling PSA 'can' indicate aggressive Pca; which is presumably even more 'ominous'.

Not only that I read an article somewhere on a study of autopsies where PSA was already know. Highest PSA with 'NO PCa FOUND' was 300, lowest PSA where 'PCa WAS FOUND' was 1.0

For me that says it all. PSA borders on rubbish (that is MY own 12-year retrospective opinion, medics and those determined to be treated will disagree vehemently).

So what next? At age 78 I'm not going to ruin the few remaining years of my life treating fear.

There is NO radical intervention without onerous 'side effects'; none. As far as I can see absolutely certain physical damage has to be weighed against much less than certain prospect of any real benefit in terms of longevity.

For now I intend to continue on tamsulosin and dutasteride. Have occasional MRI and bone scan, deal with any symptoms that arise if/when push comes to shove.

AS isn't the easy option, minimal drug intervention isn't the easy option, going against the grain of consensus tick box and policy driven guidelines isn't easy either, but I have enjoyed the past dozen year immensely - if I get it wrong so be it.

Frank Pollock

UPDATED

November 2016

Time to update. My previous post was Aug 2015 when my PSA was 65. I am unable to continue table in previous format (hormone brain fog?) so will simply list events in order with comment:

Jul 2015 PSA 65

Aug 2015 CT+bone scans 3 days apart

Aug 2015 sharp PSA increase to 102 at next count a week or so after scans and a very obvious step change in PSA graph gradient. Suspect steep increase due to either scan radiation or to intravenous dyes rather than PCa

Oct 2015 PSA 191

Nov 2015 PSA 204

Feb 2016 PSA 496

Feb 2016 CT+ bone scans, further sharp inc in PSA at next count

Mar 2016 PSA 549

Apr 2016 decision to commence ADT (triptorelin)

Apr 2016 start bicalutamide, to prevent ADT 'flare'

Apr 2016 few days later PSA now 635, start triptorelin (1st injection)

May 2016 PSA 55.3

Jul 2016 PSA 32

Aug 2016 PSA 21

Oct 2016 PSA 6

Oct 2016 PSA 3.2 (prior to triptorelin inj no 8)

Main SE was hot flashes, largely eliminated by low dose cyprostat from Aug onwards

Response to ADT was more or less as anticipated. It may fall a little further, but what next?

A "white male" who has survived to 79 has an "AVERAGE" of around 8 years "remaining"

Few individuals are average but it does give some sort of handle on white male mortality. 8 years would take me to 87, way past my 'sell by'?

Options seem to be:

ADT continuous, ADT intermittent, upfront chemo (docetaxel) followed by further ADT, or simply stop ADT but continue on combodart (ie tamsulosin + avodart)

With something like 13 years behind me I have become a bit blase and I'm inclined towards giving intermittent ADT a go at least once

At 79 duck and dive feels like the way to go - but that's gut instinct and that's me. No doubt readers of this long saga (if any) will see me as a reckless bampot

Frank Pollock

UPDATED

November 2016

My apologies for not updating my tale of woe sooner. I finally succumbed to PSA (prostate specific anxiety) increase in Apr 2016. No real ADT side effects, apart from hot flashes (dealt with by low dose cyprostat).

To me the entire 'prostate industry' is slowly backing away from the gung ho 'get in there, get it out, asap' certainties of a dozen years ago when a young intern was pressing me hard to have the 'big op'; "best for me", no dubiety on his part.

After the past 12 years or so on AS using only tamsulosin + a 5ARI (finasteride, changing to dutasteride when it became available) I have no regrets and I am eternally grateful to Terry Herbert who corresponded with me from time to time. Terry helped me make some sense of the whole confusing and contradictory world of PCa professionals (many are ass covering tick boxers I would class a dishonest - a clapped out old fart like myself can tell it like it is). Terry was a great loss to yananow - and to me.

Frank's e-mail address is: frankpollock@ntlworld.com


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