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proscar does not cause cancer

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Here is more evidence that Proscar does not cause prostate cancer.

" Men with severe BPH should approach testosterone replacement cautiously. It

would be prudent for those with BPH who are taking testosterone replacement

therapy to also use the drug Proscar (finasteride) to inhibit

5-alpha-reductase levels, thereby suppressing the formation of

dihydrotestosterone (DHT) (171- 182). "

-Life Extension Disease Prevention and Management, third edition.

The first citation at the end of the above quote is a reference to the

research abstract I've included below. In this study 3,040 men with BPH were

given either placebo or finasteride (Proscar) for up to four years. Prostate

cancer was later diagnosed in about 5% of the men in both groups. Note

there was no difference (p=0.7) in the incidence of prostate cancer between

the placebo group and the finasteride group. The 1500+ men who took

finasteride were no more likely to get prostate cancer than the 1500+ men

who did not take finasteride.

171. 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.

Andriole GL, Guess HA, Epstein JI, Wise H, Kadmon D, Crawford ED, Hudson P,

CL, Romas NA, L, Cook TJ, Waldstreicher J

Division of Urology, Washington University School of Medicine, St. Louis,

Missouri 63110, USA.

Urology 1998 Aug;52(2):195-201; discussion 201-2

OBJECTIVES: To evaluate prostate cancer detection and prostate-specific

antigen (PSA) among men with benign prostatic hyperplasia treated with

finasteride for up to four years.

METHODS: Three thousand forty men 45 to 78 years of age with PSA less than

10 ng/mL and no history of prostate cancer were randomized in a

double-blind, placebo-controlled trial to finasteride (n = 1524) or placebo

(n = 1516) for up to 4 years. A prerandomization biopsy negative for

prostate cancer was obtained in 98% of patients with a screening PSA of 4.0

ng/mL or more, and an end-of-study biopsy was requested of all such patients

without a recent second negative biopsy or a prostate cancer diagnosis.

RESULTS: Overall, 644 patients (21%) underwent biopsy and 201 (6.6%)

underwent transurethral resection of the prostate. Prostate cancer was

diagnosed in 4.7% of men on finasteride and 5.1% on placebo (P = 0.7).

Elevated PSA prompted diagnosis in 35% of cases on finasteride and 34% on

placebo. The area under the receiver operating characteristic curve for last

PSA was 0.84 on finasteride and 0.79 on placebo (P = 0.07). Use of an upper

limit of normal for last PSA of 2.0 ng/mL for finasteride and 4.0 ng/mL for

placebo yielded similar sensitivity (66% versus 70%, P = 0.6), higher

specificity (82% versus 74%, P < 0.0001), and a higher likelihood ratio (3.6

versus 2.7, P < 0.05) for finasteride than for placebo.

CONCLUSIONS: 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.

-gts

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