Opportunities for Prevention
Hormonal Prevention
The Prostate Cancer Prevention Trial (PCPT), a large randomized placebo-controlled trial of finasteride (an inhibitor of alpha-reductase), was performed in 18,882 men aged 55 years or older. At 7 years, the incidence of prostate cancer was 18.4% in the finasteride group versus 24.4% in the placebo group, a relative risk reduction (RRR) of 24.8% (95% confidence interval [CI], 18.6%-30.6%; P < .001). The finasteride group had more patients with Gleason grade 7 to 10, but the clinical significance of Gleason scoring is uncertain in conditions of androgen deprivation.[1] High-grade cancers were noted in 6.4% of finasteride patients, compared with 5.1% of men receiving a placebo. The increase in high-grade tumors was seen within 1 year of finasteride exposure and did not increase during this time period.[2]
Treating Advanced Prostate Cancer
Prostate cancer occurs when a tumor develops in the prostate gland, which makes the liquid portion of semen. Cancer that spreads outside the prostate gland to the lymph nodes, bones, or other areas is called metastatic prostate cancer. Currently, no treatments can cure advanced prostate cancer. However, there are ways to help control its spread and related symptoms. Treatments that slow the spread of advanced prostate cancer and relieve symptoms often cause side effects. Some patients, often...
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Finasteride decreases the risk of prostate cancer but may also alter the detection of disease through effects on prostate-specific antigen (PSA) and decreased prostate volume (24%), creating a detection bias.[3] In men receiving finasteride, varying adjustment factors may be needed to determine whether PSA is in the normal range.[4] There may be an artifactual histological effect of finasteride on Gleason scoring.
It is possible that finasteride induced the development of high-grade epithelial neoplasia, but this has not been demonstrated.[3] With a finasteride-induced development of high-grade prostate cancer, a gradual and progressive increase in the number of high-grade tumors would have been expected for more than 7 years, compared with placebo; however, this was not the case. The increase in high-grade tumors was seen within 1 year of finasteride exposure and did not increase during this time period.[2] A statistical reanalysis of the PCPT data adjusted for the possible bias of decreased prostate volume in men on finasteride, perhaps making it easier to detect prostate cancer in smaller prostate volume. This reanalysis found that finasteride reduced the incidence of Gleason 5 to 7 and Gleason 3 to 4 prostate cancer, but not Gleason 2 to 3 or Gleason 8 to 10. The reduction in the incidence of Gleason 7 (22%) was less than the reduction in the incidence of Gleason 5 (58%) and Gleason 6 (52%).[5]
The Reduction by Dutasteride of Prostate Cancer Events trial randomly assigned 8,231 men aged 50 to 75 years at higher risk of prostate cancer (i.e., PSA 2.5-10.0) with one recent negative prostate biopsy to dutasteride at 0.5 mg daily or to placebo. The primary endpoint was prostate cancer diagnosed by prostate biopsy at 2 years and 4 years after randomization. After 4 years, among the 6,729 men (82% of initial population) who had at least one prostate biopsy, 25.1% of the placebo group and 19.9% of the dutasteride group had been diagnosed with prostate cancer, a statistically significant difference (absolute risk reduction = 5.1% and RRR = 22.8% [95% CI, 15.2%-29.8%]). The RRR in years 3 to 4 was similar to the RRR in years 1 to 2. The difference between the groups was entirely due to a reduction in prostate cancers with Gleason score 5 to 7. For years 3 to 4 there was a statistically significant increase in the dutasteride group compared with the placebo group in prostate cancers with Gleason score 8 to 10 (12 cancers in dutasteride group vs. 1 cancer in placebo group).[6]
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