ANAHEIM, CA (UroToday.com) - Dr. Carl Olsson moderated a point-counterpoint "PCPT Trial: Why is No one Using Finasteride?"" at the Tuesday Plenary Session of the AUA in Anaheim, May 22, 2007. Dr. Ian Thompson debated that the PCPT is a good study and Dr. Patrick Walsh argued that it is a bad study.

Dr. Olsson reviewed the PCPT, which included over 18,000 men randomized to finasteride 5mg daily or placebo for 7 years. It excluded those with CaP, a PSA greater than 3ng/ml or an abnormal DRE. It was closed 15 months early due to its positive findings. The problem was that although the incidence of CaP was lower in the treatment group, there were more high risk cancers.

Dr. Thompson argued that it was a good trial and should be offered to men. PSA screening has decreased the incidence of CaP from 19% to about half that over the last 10 years. In men with an initial negative biopsy, men often get repeat biopsies due to the worry that cancer was missed. Finasteride would alter this, he said. He discussed that in the PCPT the high-grade tumors were most commonly in those with an abnormal DRE or rising PSA. He referred to finasteride's ability to reduce the amount of benign tissue, thus improving the sensitivity of the DRE and prostate biopsy. Undergrading is more statistically common in a large as compared to a small prostate gland. Furthermore, finasteride decreases BPH risk, reduces the risk of high-grade PIN and is well tolerated.

Dr. Walsh argued against finasteride use for chemoprevention. He stated that the trial design was ok. He first argued that DHT is not strongly a causative factor in CaP initiation, rather it is testosterone that is causative. In fact, androgen levels in the prostate go up inside of CaP cells. Thus, testosterone is most important and finasteride does not affect this. He said that this was not truly a prevention trial due to its short time course, rather a trial of early hormonal therapy. The effect of finasteride treated only the small tumors due to the effect on stroma. In the clinical setting the reduction was only 10%, not 24.8% as finasteride actually decreased the likelihood of a patient getting a prostate biopsy. Is the increase in high-grade tumors artifact? It doesn't matter he stated, as finasteride did not decrease in the number of high grade tumors, which are the most lethal to the patient. Cost savings really are not true, since only low risk cancers are treated and the costly high-risk tumors are unaffected. Finally, finasteride is not approved by the FDA and he quoted Dr. Olsson as saying that the cost would be astronomical.

Dr. Thompson rebutted that the risk reduction is 4-fold better with finasteride than using statins to reduce the risk of a cardiovascular event. He said that the goal is to reduce the burden of the disease, not just look at survival benefit. He stated that Dr. Walsh's radical prostatectomy population was 81% low risk, so how could he argue that finasteride was unnecessary in these patients when he was operating on them! Dr. Walsh countered that a recent report from Johns Hopkins of his patients shows that low risk CaP is cured in 95% and only 5% of these are pathologically insignificant. He again argued that finasteride was treating early, occult CaP that didn't need treatment and that it is not really chemoprevention. Dr. Olsson concluded with a slide that showed that finasteride sales have not increased much since the publication of the PCPT. This was a very dynamic session!

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Written by Christopher P. Evans, MD, a Contributing Editor with UroToday.

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