PSA Rising even with Fastineride...

I found out last December that I had prostate cancer. A twelve core biopsy revealed only one core at 5% cancer with another one suspicious. I had the slides reviewed at Hopkins for a second opinion. An MRI was ordered and it too showed Gleason 6 low grade cancer. I chose to do AS for the time being. My PSA last December was 2.4 after being on the Fastineride since last September. My most recent PSA test revealed 3.4 and am still taking the Fastineride. According to my UR, you have to double these figures to get the real PSA value. So, I'm now at 6.8. I sent the test results to my UR up at Hopkins and he wrote back advising to have another biopsy done if my PSA was rising while taking the Fastineride. The UR here in town didn't act concerned. I'm scheduled to do another biopsy 5-Dec-14 up at Hopkins, but may end up doing another one sooner than that.

So, the roller coaster continues and I'm left wondering what to do. I read so much and see videos of guys who opt for surgery with the same stats as me. Am I being stupid for waiting when sooner or later surgery will be a reality? I just turned 60 and am second guessing the AS. Not 30 minutes of each waking hour passes without me thinking of doom and gloom. I'm tired of it. I feel guilty for worrying about the PC as my stats are far better than some guys. I just have not felt normal since I received the diagnosis. Should I be so concerned?

Foxbo,

When I was kicking around my treatment plan my Uro told me AS was an option but all it takes is a small jump in a patient's PSA to opt for an immediate treatment plan. I was one to just do it and get it over with.
No regrets either. Good luck!

I was on finasteride for over ten years , PSA suddenly jumped to 2.1 from. .9 then to 5.4 in two years. Bx showed low volume but high grade Pca , GL 9. I had RP three months later and was stage pt3b. So the fact that ur GL 6 and low volume is a good thing but I guess I would get another bx if I were you if it keeps rising because velocity is a key determinant of progression.
Bob

Thanks for the replies fellows. I plan on following up with Hopkins to do another biopsy.

" When used with active surveillance in PCa patients there is no need to double the value of a PSA test result because there is no occult cancer" What does this mean? My UR says to double the PSA # to obtain the true reading.

I'm thinking, "snatch it out" and be done with it. I'm having a tough time thinking of something evil growing inside of me.

I had to look up occult cancer, see below; (more fun cancer facts)

Cancers often spread from their primary site (the part of the body where the cancer started) to one or more metastatic sites (other parts of the body). Cancers are named based on their primary site, regardless of where in the body they spread. For example, a lung cancer that spreads to the liver is still classified as lung cancer and not as liver cancer.

Sometimes it’s not clear where a cancer may have started. When cancer is found in one or more metastatic sites but the primary site cannot be determined, it is called a cancer of unknown primary (CUP) or an occult primary cancer. This happens in a small portion of cancers.


I am under the assumption that Finesteride will suppress the PSA numbers and that as a general rule, your PSA number would read twice as high if not suppressed by the drug, is that incorrect?

The question of Proscar (finasteride) reducing PSA by 50% needs an explanation. Finasteride was developed by Merck to treat prostate enlargement (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 medical 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 was developed to treat BPH, but Merk conducted 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 a 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 ADT 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 of finasteride's lack of toxicity in most cases.

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. The PSA reduction is caused by 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. Unfortunately the confusion continues…

RalphV

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