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Medical Forum / Diseases and Disorders / Prostate Cancer / June 2006BPH story of a PCa patient
I, similar to many of you, have both benign prostatic hyperplasia (BPH) and prostate cancer (PCa). Some of you may be interested in my new, non-commercial BPH website, which describes my experiences with BPH and presents what I have learned about it. The site's address is: http://www.ljblgb.com/ Here's a digest of my two prostate disorders: Currently 75 years old, PCa dx'd Nov 2000 with PSA of 5.7 and Gleason of 3 + 3, read by Dr. D. Bostwick. Active Surveillance supervised by Dr. M. Scholz. Diet, Avodart, & Flomax. No other intervention. PSA on 4/20/06 was 2.60. BPH--my enlarged prostate is 84 cc, last measured on 2/3/06 by a color-doppler/black-and-white ultrasound scan by Dr. D. Bahn. Best Wishes, Lawrence J. Bookbinder > I, similar to many of you, have both benign prostatic hyperplasia > (BPH) and prostate cancer (PCa). Some of you may be interested in my [quoted text clipped - 13 lines] > Best Wishes, > Lawrence J. Bookbinder It is interesting that your PSA has dropped significantly. Presumably your previous PSA level resulted primarily from your BPH rather than the cancer, and the Avodart apparently reduced the BPH. In any event, it seems that active surveillance is working well for you. At your age, there is a very good chance you will never be bothered by your prostate cancer. The BPH may be more of a problem but it seems under control for now. Good luck! You might consider posting to alt.support.cancer.prostate. Leonard Evens wrote...snip... > It is interesting that your PSA has dropped significantly. Presumably > your previous PSA level resulted primarily from your BPH rather than the > cancer, and the Avodart apparently reduced the BPH. Not sure I'd agree that the PSA dropped significantly. Avodart (dutasteride) will cut PSA's roughly in half. Doubling the current value of 2.6 takes us to 5.2 which, given test variation, is pretty close to the 11/00 value of 5.7...ron. Hi Ron, It would depend if the action of Avodart included activity against prostate cancer tissue. They are starting to recognize the value of 5-AR inhibitors in the treatment of PCa. Not widely accepted as things go in the world of PCa, but nevertheless more used than ever before. In this case, where BPH and PCa are known to be present, a PSA reduction of almost 50% seems to be significant. At the very least it tells us that there is androgen dependence. That is in my estimation reassuring to the patient who is conservativly managing his disease. Best regards, RalphV > Leonard Evens wrote...snip... > > It is interesting that your PSA has dropped significantly. Presumably [quoted text clipped - 5 lines] > value of 2.6 takes us to 5.2 which, given test variation, is pretty > close to the 11/00 value of 5.7...ron. Hi Ralph...I thought that when Leonard said, "It is interesting that your PSA has dropped significantly"; he meant this in the sense that we track PSA as a monitor of prostate and tumor volume, and that in this sense there was a significant change. Often we operate under the assumption that PSA level correlates with prostate size and tumor size, and usually that's a fair assumption for tracking purposes. However, sometimes when certain drugs are administered (for example avodart, some LHRH agonists, etc.) the PSA level can change significantly without a corresponding change in prostate / tumor volume. In the case of avodart it is known that it will reduce the pre-avodart PSA level by about 50%; but the prostate and tumor volume haven't decreased 50%. The avodart has probably reduced the PSA level by affecting some protein, enzyme, etc involved in PSA expression so that the same cells are now simply expressing less PSA. The net result is that the PSA has dropped "significantly" but for PSA tracking purposes (again, the way I thought Leonard was using the term), the PSA remains, for all intents and purposes, unchanged...Ron Hi Ron, I agree that the correlation of PSA with prostate volume is not necessarily accurate and there are important reasons for that lack of correlation. These are related to the way and zone location where the PSA leaks into the bloodstream. The use of 5-AR inhibitors has been mostly ignored to treat or prevent PCa even when the med lit supports its use. These 5-AR inhibitors promote apoptosis, a reduction of blood flow to the gland and antiangiogenic activity causing a reduction of microvessel density. Treated glands demonstrate reduced cell proliferation and in time a reduction in gland volume. In patients with known PCa (along with known BPH) there is no reason to double PSA when treating with a 5-AR. Why? Because the morphological and histological changes are real and the PSA level measured is representative of such changes. DHT is the most potent androgen and its inhibition cause cell death, reduced cell proliferation and other physical changes that reduce PSA production. The doubling of PSA to avoid missing a diagnosis of PCa when treating a patient with BPH does not apply in the case under discussion. This patient had a positive PCa diagnosis and is managing his cancer with the least objectionable form of androgen suppression. Below, some references. Best regards, RalphV 1: Sutton MT, Yingling M, Vyas A, Atiemo H, Borkowski A, Jacobs SC, Kyprianou N. Finasteride targets prostate vascularity by inducing apoptosis and inhibiting cell adhesion of benign and malignant prostate cells. Prostate. 2006 May 1; [Epub ahead of print] PMID: 16652387 [PubMed - as supplied by publisher] 2: Rittmaster RS, Norman RW, Thomas LN, Rowden G. Evidence for atrophy and apoptosis in the prostates of men given finasteride. J Clin Endocrinol Metab. 1996 Feb;81(2):814-9. PMID: 8636309 [PubMed - indexed for MEDLINE] 3: Maria McCrohan A, Morrissey C, O'keane C, Mulligan N, Watson C, Smith J, Fitzpatrick JM, Watson RW. Effects of the dual 5 alpha-reductase inhibitor dutasteride on apoptosis in primary cultures of prostate cancer epithelial cells and cell lines. Cancer. 2006 Jun 15;106(12):2743-52. PMID: 16703599 [PubMed - in process] 4: Andriole GL, Humphrey P, Ray P, Gleave ME, Trachtenberg J, Thomas LN, Lazier CB, Rittmaster RS. Effect of the dual 5alpha-reductase inhibitor dutasteride on markers of tumor regression in prostate cancer. J Urol. 2004 Sep;172(3):915-9. PMID: 15310997 [PubMed - indexed for MEDLINE] > Hi Ralph...I thought that when Leonard said, "It is interesting that > your PSA has dropped significantly"; he meant this in the sense that we [quoted text clipped - 13 lines] > thought Leonard was using the term), the PSA remains, for all intents > and purposes, unchanged...Ron ralphv_in_az@yahoo.com wrote...snip... The doubling of PSA to avoid missing a diagnosis of PCa when treating a patient with BPH does not apply in the case under discussion. Hi Ralph...I thought that anyone taking a 5-AR inhibitor, whether they have PCa or not, should double their PSA value to get a "true" (non-medicated) PSA reading. Am I understanding you to say that men with PCa using 5-AR inhibitors need not do this "doubling"? Are you saying that, in such cases of men with PCa using finasteride or dutasteride, the tumor kill and prostate shrinkage due to the 5-AR inhibitor use is what is causing the PSA to fall to half of the pre-5-AR inhibitor value?..Ron Hi Ron, The question of Proscar (finasteride) reducing PSA by 50% has confused many. That included me for a number of years until I did some research on that matter. 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 other words, Merck wanted to ensure that a man treated for BPH would have a biopsy triggered if his PSA exceeded 2.0 ng/ml and had no claim against them for masking their PSA with Finasteride. 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. 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 when the product is used off label in someone diagnosed with PCa. 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 such PCa patients, PSA results are what they are and need not to be doubled. Best regards, RalphV Sources: Damber JE et al. Effects of finasteride on vascular endothelial growth factor. Scand J Urol Nephrol 2002;36(3):182-7 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 > ralphv_in_az@yahoo.com wrote...snip... > The doubling of PSA to avoid missing a diagnosis of PCa when treating a [quoted text clipped - 8 lines] > inhibitor use is what is causing the PSA to fall to half of the > pre-5-AR inhibitor value?..Ron > Hi Ralph...I thought that when Leonard said, "It is interesting that > your PSA has dropped significantly"; he meant this in the sense that we > track PSA as a monitor of prostate and tumor volume, and that in this > sense there was a significant change. My original thought was that some portion of his orininal PSA was from BPH rather than from prostate cancer. In that case, it would be true that the PSA drop didn't indicate any significant change in the prostate cancer. The good part of that, if it were true, would be that his PSA, due to prostate cancer, was pretty low to start, which would have been another argument for trying watchful waiting in a man his age with a small tumor and Gleason 6. I didn't think and certainly never would suggest that his teatment actually caused the cancer to regress. But so far at least, there doesn't seem to be any strong reason to believe that WW is beginning to fail for him. > Often we operate under the > assumption that PSA level correlates with prostate size and tumor size, [quoted text clipped - 10 lines] > thought Leonard was using the term), the PSA remains, for all intents > and purposes, unchanged...Ron Actually, that was what I meant in my original comment. The important thing was that there was no reason to believe, based on PSA, that his cancer was growing significantly. |
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