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Medical Forum / Diseases and Disorders / Prostate Cancer / March 2007Bounce vs. Recurrence
This point is not at all clear to me. How can one determine iniiatially whether an increase in psa post treatment is a bounce, or the disease on the move. At what point is it prudent to start HT. > This point is not at all clear to me. How can one determine iniiatially > whether an increase in psa post treatment is a bounce, or the disease on > the move. > At what point is it prudent to start HT. I believe what the docs look for is three consecutive increases in PSA results. Even then, it seems to be good practice to rule out other possibilities. For example, in Prostate Cancer for Dummies, Lange mentions that there can be delayed inflammation that occurs long after the initial seeds implant for patients who elected brachytherapy. --charlie >> This point is not at all clear to me. How can one determine iniiatially >> whether an increase in psa post treatment is a bounce, or the disease on [quoted text clipped - 8 lines] > > --charlie My understanding is the same as Charlie's. One standard for determining recurrence is three consecutive rises in PSA, each three months or more apart. However there have been at least a few cases where even that wasn't conclusive and after three rises the PSA still went down on the next reading. Bounces are most common in the first 3 years, with a peak in months 18-24, but bounces after 5 years have been recorded. Experts seem to disagree about what to do. My own inexpert thoughts are: 1. Starting hormone therapy (HT) prematurely is bad. HT has powerful effects on the body that nobody would want unless they had to have HT to hold their cancer in check. HT also drastically lowers PSA. If you suspect that you may just have a bounce but start taking HT, you won't know whether it was just a bounce until you stop taking HT and it wears off. Any PSA readings you take while undergoing HT will not reflect your pre-HT situation. 2. Starting HT late may also be undesirable. The experts disagree on this one. a. Some say that it can never be a good thing to allow cancer cells to divide and multiply. Start HT as soon as you know you have a recurrence. b. Some say HT can be started any time before the beginning of metastasis with equal effects on outcome. c. Some say HT can be started any time before the beginning of symptoms with equal effects on outcome. I seem to recollect reading that c. is no longer in high favor, but I don't know how strong the evidence is for each of the above positions. So, it seems to me that, like so much else in this disease, you have to make a personal choice. After my PSA rises I decided not to go on HT. I had had HT once and had some problems with it (elevated liver enzymes and arthritic like symptoms). I didn't want to take it again unless I really had to. My doctor told me that there was a small amount of evidence indicating that early HT was better than later HT. He would like me to stay off because I was in a clinical trial and HT would, in effect, take me out of the trial since my PSA measurements would no longer be meaningful for the trial. But he told me the choice was mine. I was lucky. I stayed off the HT. But after each of my up tics the next reading went down. I resolved that I wouldn't even consider HT unless and until I had three up readings in a row. And even then I'd think hard about it. If my PSA starts to really zoom, that's another matter. But there are some cases where even a real zoom may not be definitive. Ron Figueroa (Heather's Ron) had a real zoom, but it's beginning to look like even it was a bounce. Alan > This point is not at all clear to me. How can one determine iniiatially > whether an increase in psa post treatment is a bounce, or the disease on > the move. > At what point is it prudent to start HT. That is a major subject of expert debate even in the broader scope of immediately post-treatment, at biochemical failure (PSA rise), at clinical failure (mets detected by lab work), or actual met symptoms. Trying to pin it down to a small PSA level or duration is *really* splitting unknown hairs, and, according to many leading experts, more dependent on the individual's SEs than on statistical disease prognosis. Similarly, it's *prudent* to live on blueberries, stewed tomatoes'n'broccoli, and whatever other superfoods and supplements one wants, but the benefit isn't likely to be worth the sacrifice. i.e., HT is still a judgment call prior to symptoms. I.P. On March 25, Bob wrote: > This point is not at all clear to me. How can one determine > iniiatially whether an increase in psa post treatment is a bounce, or > the disease on the move. At what point is it prudent to start HT. I am dealing with this dilemma right now, my monthly PSA results having increased from 0.01 to 0.1 between November '06 to March '07. Here is some information: A PSA "bounce" (aka bump) is a term of art referring to a "temporary rise in PSA after first having a decline in PSA after completion of brachytherapy." Others expand it to include any form of RT. It is defined as an increase of 0.1 ng/mL or more above the previous level, followed by a decline to less than that level. See: Strum & Pogliano, _A Primer on Protate Cancer_ 2nd ed. p. 103 et seq. "The “bump” follows a benign clinical course and usually resolves itself within a year. The main danger of the PSA “bump” comes when physicians mistakenly conclude that the rising PSA represents recurrent cancer and decide to start ADT when no cancer is present." See: Prostate Cancer Research Institute at: http://www.prostate-cancer.org/education/localdis/scholz_newlydiagnosed2.html or http://tinyurl.com/2os6n5 The definition of biochemical failure per ASTRO (American Society for Therapeutic Radiation and Oncology) is three consecutive rises in PSA over a period of months. Note: It is related to radiation therapy, not other tx modes. There is authority for restarting treatment when the PSA rises from nadir to 0.2 ng/mL, but as usual there is also controversy. Opinions vary all over the place. I have decided to continue to observe the PSA results until they reach 1.0 (if they do) at which point I will probably restart ADT. This is anecdotal and should therefore be viewed with caution. Note: I have been off ADT (Trelstar) since March '06. Presently only on Avodart 0.5 mg qd plus Zometa 4 mg q 90 days and calcium and vitamin D3. A rise in PSA was expected. Question is when it will stabilize. Regards, Steve J "The thing is to expect nothing in particular, but (to) be aware of the lack of enforceable guarantees or enforceable contracts with nature/god/entropy as to the condition or durability of our bodies." -- Brian Brunner, PCa survivor, December 12, 2005 on The Prostate Problems Mailing List Thank you, Brian. > On March 25, Bob wrote: > I am dealing with this dilemma right now, my monthly PSA results having > increased from 0.01 to 0.1 between November '06 to March '07. Damn, Steve! Did I miss this in another post? > I have decided to continue to observe the PSA results until they reach > 1.0 (if they do) at which point I will probably restart ADT. This is > anecdotal and should therefore be viewed with caution. This is anecdotal, too, but I think you have selected a good course of action. ADT has worked for you before and there is a reasonable expectation that it will reduce your PSA at 1.00 pretty much as it would for 0.10.  SignaturePSA 16 10/17/2000 @ 46 Biopsy 11/01/2000 G7 (3+4), T2c RRP 12/15/2000 G7 (3+4), T3cN0M0 Neg margins PSA <.1 <.1 <.1 .27 .37 .75 EBRT 05-07/2002 @ 47 PSA .34 .22 .15 .21 .32 Lupron 07/03 (1 mo) 8/03 (4 mo), 12/03, 4/04, 09/04, 01/05, 5/05, 10/05, 2/06, 6/06 PSA .07 .05 .06 .09 .08 .132 .145 Casodex added daily 07/06 PSA <0.04, <0.05 Non Illegitimi Carborundum >> On March 25, Bob wrote: > [quoted text clipped - 12 lines] > expectation that it will reduce your PSA at 1.00 pretty much as it > would for 0.10. Just to assure that there is no confusion, I was referring to myself when I wrote the ¶ beginning, "I am dealing...." This is the first time I have mentioned it here. I rarely mention my own situation because it is (so far as I know) unique due to my tx history, which is failed cryo then IMRT with adjuvant ADT. Gleason 4+5 and 4+4. I suppose I was spoiled by > a year of 0.01 PSAs. Now, I must realize that an increase that I anticipated when I stopped ADT is actually happening. Or is it the "bump?" No way to know. Thanks for the inquiry! Regards, Steve J Black dang it. I just posted > Just to assure that there is no confusion, I was referring to myself > when I wrote the ¬∂ beginning, "I am dealing...." The weird symbol was supposed to be an abbreviation for "paragraph." Sheesh. Regards, Steve J On Mar 25, 12:53 pm, Steve Jordan <mycrofts...@cox.net> wrote...snip... > I am dealing with this dilemma right now, my monthly PSA results having > increased from 0.01 to 0.1 between November '06 to March '07. > I have decided to continue to observe the PSA results until they reach > 1.0 (if they do) at which point I will probably restart ADT. This is > anecdotal and should therefore be viewed with caution. > > Note: I have been off ADT (Trelstar) since March '06. Presently only on > Avodart 0.5 mg qd plus Zometa 4 mg q 90 days and calcium and vitamin D3. Hi Steve...Have you been tracking your T level? Whether it has plateaued or is continuing to rise, along with the PSA, might provide an indication of what's going on. Also, since you're on Avodart your checkpoint of PSA=1.0 is roughly equivalent to PSA=2.0 for a man not taking it, but I suspect you already know this...Best wishes and good health, ron On March 25, ron replied to me: > Hi Steve...Have you been tracking your T level? Yes. T on March 20 was 437, about the same as last September. (snip) > Also, since you're on Avodart your > checkpoint of PSA=1.0 is roughly equivalent to PSA=2.0 for a man not > taking it, but I suspect you already know this... This doubling idea is controversial. It applies when one is on a 5AR inhibitor such as Proscar or Avodart for tx of BPH. Reduction of the PSA expression is genuine and is not a "masking." It is caused by reduction in the size of the gland. After primary PCa tx, the doubling is inapplicable. The PSA is what it is. For a detailed discussion, see the following essay by Ralph Valle, whose PCa expertise is unequaled by any other layman, and IMO is greater in scope and depth than that of many medics. It was written before advent of Avodart (dutasteride), also a 5AR inhibitor.. "The question of Proscar (finasteride) reducing PSA by 50% needs review. Finasteride was developed by Merck to treat BPH. Since BPH and PCa are two diseases that could cause a PSA elevation and those prostate conditions can and do coexist in many males, Merck promoted studies known as The Finasteride Group Study to ensure that men treated with finasteride for BPH would not be at increased risk of PCa by having reduced levels of PSA. "In those studies, men treated with Proscar for prostate enlargement experienced a blood serum PSA reduction of approximately 50%. There is ample evidence that this PSA reduction is related to a reduction in gland volume (maximized by one year of treatment) caused by cell death and reduced cell proliferation. In other words, the PSA reduction is not an artifact causing a masking effect on the measuring test, but simply an effect caused by definitive biological factors induced by the inhibition of DHT. "In Dominican Republic there are several families of men born with a genetic disorder by which they do not convert testosterone to dihydrotestosterone (DHT). These men all have prostate atrophy, do not experience either BPH or prostate cancer and are capable of procreation. It is a medical fact that DHT is recognized as the androgen involved in the development of the prostate gland. "Finasteride is medically used to treat BPH and there was a prostate cancer prevention study using Proscar in which 18,000 men participated. There is no question that inhibiting the formation of DHT has a significant impact in the prostate gland. This trial resulted in nearly 25% reduction on PCa for the participants on the active arm pf the study. "The use of Proscar to treat prostate cancer is not a recognized label use for this product. In spite of this, Proscar is used in hormone suppression protocols when maximal suppression is intended. It is used in intermittent androgen suppression during the off-cycle period to extend the time off medications. Drs. Leibowitz, Strum/Scholz and Bruchovsky have successfully used Proscar to effectively extend the off-cycle period. Dr. William Fair studied the use of Proscar in treating stage D PCa and concluded that a decrease in serum PSA in the finasteride treatment group suggests that finasteride exerts a minor effect in patients with prostate cancer. This effect does not approach that seen with medical or surgical castration, but it is important because finasteride's lack of toxicity. "JE Damber and coworkers in Sweden showed that finasteride treatment decreases VEGF expression in the human prostate. Vascular endothelial growth factor (VEGF) is a potent regulatory factor of angiogenesis in human prostate tissue. Also Wang and coworkers at New York University demonstrated that the level of androgen receptor was dramatically decreased in the cells treated with finasteride. "Merck's action to demonstrate that the use of finasteride in BPH does not result in an impairment of prostate cancer detection by a 50% reduction in PSA level has caused much confusion. The PSA reduction is real and caused by the action of Proscar in inhibiting DHT, VEGF expression and down regulation of the androgen receptor and not by a PSA masking effect without a direct biological effect on androgen dependent cancer cells. In other words,in the treatment of prostate cancer the 50% PSA reduction factor is not applicable. In such PCa patients, PSA results are what they are. Sources: "Fair WR et al.Multicenter, randomized, double-blind, placebo controlled study to investigate the effect of finasteride (MK-906) on stage D prostate cancer. J Urol 1992 Oct;148(4):1201-4 "Damber JE et al. Effects of finasteride on vascular endothelial growth factor. Scand J Urol Nephrol 2002;36(3):182-7 "Bruchovsky N et al Intermittent androgen suppression for prostate cancer: Canadian Prospective Trial and related observations. Mol Urol 2000 Fall;4(3):191-9;discussion 201 "Wang LG et al Down-regulation of prostate-specific antigen expression by finasteride through inhibition of complex formation between androgen receptor and steroid receptor-binding consensus in the promoter of the PSA gene in LNCaP cells. Cancer Res 1997 Feb 15;57(4):714-9" Thanks to anyone who got this far ;-) Regards, Steve J This is a bit off-topic from the original intent of my post, but you've raised some points, so I've responded within the text of your response...Best wishes and good health, ron > On March 25, ron replied to me: snip > > Also, since you're on Avodart your > > checkpoint of PSA=1.0 is roughly equivalent to PSA=2.0 for a man not > > taking it, but I suspect you already know this... > > This doubling idea is controversial. In what way is it controversial? The articles I've read seem to agree that the PSA of someone on a 5AR inhibitor would be roughly doubled if the individual were not taking the 5ARi. >It applies when one is on a 5AR > inhibitor such as Proscar or Avodart for tx of BPH. Reduction of the PSA > expression is genuine and is not a "masking." It is caused by reduction > in the size of the gland. I'm not sure what you (and Ralph) mean by "masking", but it turns out that the gland size is typically reduced about 20% by the 5ARi, leaving about 30% of the PSA reduction to be explained. Presumably some mixture of decreased cell membrane permeability resulting in reduced PSA leak, reduced (by the 5ARi) PSA precursor availability or downregulation of the enzymes that assist in the manufacture of PSA contribute to explain this 30% portion of the overall 50% PSA reduction. > After primary PCa tx, the doubling is inapplicable. The PSA is what it is. Well yes, the PSA is what it is, but why do you posit that doubling is inapplicable after primary Tx? Why wouldn't it apply to anyone on HT? Strum uses the doubling factor when he compares the PSA of men using a 5ARi during their HT off-period, to the PSA of men not using a 5ARi during their HT off-period. On March 25, ron responded to me: > This is a bit off-topic from the original intent of my post, but > you've raised some points, so I've responded within the text of your > response... >> On March 25, ron replied to me: > snip [quoted text clipped - 6 lines] > that the PSA of someone on a 5AR inhibitor would be roughly doubled if > the individual were not taking the 5ARi. Please refer to Ralph Valle's essay, which I quoted in full. >> It applies when one is on a 5AR >> inhibitor such as Proscar or Avodart for tx of BPH. Reduction of the PSA >> expression is genuine and is not a "masking." It is caused by reduction >> in the size of the gland. > > I'm not sure what you (and Ralph) mean by "masking", I have seen people (not including Ron) refer to it as "masking," thus my mention of it. The term is not related to reality. > but it turns out > that the gland size is typically reduced about 20% by the 5ARi, > leaving about 30% of the PSA reduction to be explained. That is not what Andriole et al. say in their seminal report. See, "Treatment with finasteride preserves usefulness of prostate-specific antigen in the detection of prostate cancer: results of a randomized, double-blind, placebo-controlled clinical trial. PLESS Study Group. Proscar Long-term Efficacy and Safety Study." This study, published in 1998, involved 3040 men *with BPH* and concluded, "In men treated with finasteride, multiplying PSA by 2 and using normal ranges for untreated men preserves the usefulness of PSA for prostate cancer detection." (emphasis added) See, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed ...and search on PubMed ID 9697781. > Presumably > some mixture of decreased cell membrane permeability resulting in > reduced PSA leak, reduced (by the 5ARi) PSA precursor availability or > downregulation of the enzymes that assist in the manufacture of PSA > contribute to explain this 30% portion of the overall 50% PSA > reduction. Would Ron please cite his source? I'm trying to learn, and prefer to study primary sources. Tnx. >> After primary PCa tx, the doubling is inapplicable. The PSA is what it is. > > Well yes, the PSA is what it is, but why do you posit that doubling is > inapplicable after primary Tx? See above. The doubling applies to *BPH* patients. > Why wouldn't it apply to anyone on > HT? Strum uses the doubling factor when he compares the PSA of men > using a 5ARi during their HT off-period, to the PSA of men not using a > 5ARi during their HT off-period. Ron does not cite a source, so I've done my best to ferret it out. Strum & Pogliano referred to advanced PCa pts for whom ADT was their *primary tx*. And they were hormone-naive. See, _A Primer on Prostate Cancer_ 2nd ed., subtitled "The Empowered Patient's Guide" pages 145-146. Ralph Valle is the expert upon whom I based what I wrote, and I quoted his essay in full. I rely upon his qualifications as a scientist. I am not as qualified to debate the issues that Ron raises as Ralph is. I would be interested to see a debate between Ron and Ralph. It would be educational. Regards, Steve J > ... > I am dealing with this dilemma right now, my monthly PSA results having > increased from 0.01 to 0.1 between November '06 to March '07. > ... Steve, Your situation is unusual in that you had the cryotherapy first, then the radiation. So the generalizations made for radiation patients may or may not apply to you. However, for whatever it's worth, it is my understanding that an undetectable PSA is not the most common outcome for successfully treated radiation patients. I was told by my rad onc that there is usually some measurable PSA. Also, your previous ADT may make the interpretation of your previous PSA tests somewhat problematic. Production of testosterone returns at different rates for different men and, although you cited sources in your reply to Ron that in your case PSA measures are accurate inspite of the dutasteride, I don't know if we don't know for sure it has no influence on the return to pre-treatment testosterone levels, or pre-treatment reactions to testosterone, when combined or following ADT. All of this is just to say that I am hoping that you do not have a recurrence, and that my hopes are based on more than just wishful thinking. Also, for whatever it's worth, my PSA levels have stabilized for the last year at around .2 (the lab did not report hundredths.) I was told not to expect an undetectable PSA, and that it's looking like my treatment was successful. Alan On March 25, Alan Meyer replied to me: > Your situation is unusual in that you had the cryotherapy first, then > the radiation. So the generalizations made for radiation patients [quoted text clipped - 4 lines] > successfully treated radiation patients. I was told by my > rad onc that there is usually some measurable PSA. Maybe so, but post IMRT and with adjuvant ADT, I clocked UDPSAs for > a year. Even during most of the time after I stopped ADT , which was in March 2006. First noted rising PSA in December 2006. Did the fact that my tumor(s) had been damaged though not destroyed by the cryo influence this? Who knows? > Also, your previous ADT may make the interpretation of your > previous PSA tests somewhat problematic. Production of [quoted text clipped - 4 lines] > the return to pre-treatment testosterone levels, or pre-treatment > reactions to testosterone, when combined or following ADT. FWIW, my 10/06 T test after stopping ADT (3/06) was 463 ng/mL, well within the (then) range of 181 - 758. Nothing remarkable. > All of this is just to say that I am hoping that you do not have > a recurrence, and that my hopes are based on more than just > wishful thinking. I appreciate the thought. > Also, for whatever it's worth, my PSA levels have stabilized > for the last year at around .2 (the lab did not report hundredths.) > I was told not to expect an undetectable PSA, and that it's > looking like my treatment was successful. Yes it is. Good! Regards, Steve J > On March 25, Bob wrote: > [quoted text clipped - 4 lines] > I am dealing with this dilemma right now, my monthly PSA results having > increased from 0.01 to 0.1 between November '06 to March '07. Here is what my doctors and I are doing, FWIW. My last 3 PSA measurements were 0.75, 1.7 and 3.29, roughly 3 months apart. I'm just finishing a four-week course of a broad-spectrum antibiotic, after which we'll do another PSA. If that's still rising I suspect a biopsy will be the next step; PSA alone is not sufficiently unambiguous after brachytherapy, at least not in the first 3 years when, as you (Steve) pointed out, the bounce may be to blame. Biopsies in the first 2 years after brachy can also give false positive results, but I'll be at 30 months by the time that decision is taken. (Medical info is from Wallner et al, Prostate Brachytherapy Made Complicated, 2nd ed., 2001 -- 3rd ed. coming in August, I'm told, and I'm looking forward to reading it!) And then, if it appears the cancer's back, comes the HT decision. It won't be easy, but I'll cross that bridge if I come to it. SignatureGreg Louis At age 58, PSA 5.4 rising triggered biopsy 2004-06-22, Gleason 3+3, T1c, prostate volume 27 cc. Monotherapy, 55 I-125 seeds implanted 2004-11-16. Nadir 0.59 (8 mo); then 0.62, 0.85, 0.75, 1.7, 3.29 (27 mo). |
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