AUA: Studies Link Cholesterol to Prostate Cancer Recurrence

By Charles Bankhead
ORLANDO, 29 may 2008-- Controlling serum cholesterol may help reduce the risk of prostate cancer as well as heart disease, two studies reported here suggest.
Men with the highest cholesterol levels had more than a two-fold greater risk of biochemical relapse after radical prostatectomy compared with men who had the lowest cholesterol levels, Lionel L. Banez, M.D., of Duke University, reported at the American Urological Association meeting.
"These findings suggest that cholesterol may play a role in prostate cancer progression," said Dr. Banez. "Cholesterol-lowering drugs, such as statins, should be investigated for a possible role in the treatment of prostate cancer."
A second study, presented by Robert J. Hamilton, M.D., of the University of Toronto, showed a correlation between higher cholesterol levels and higher PSA values.
Those findings support previous evidence that men treated with statin drugs to lower their cholesterol levels also had reductions in PSA levels, Dr. Hamilton said.
Dr. Banez and colleagues analyzed data from 471 men who underwent radical prostatectomy from 1998 through 2007. Lipid profile and prior exposure to statin therapy was available for all of the participants. The multivariate analysis controlled for variations in prostate cancer features and history of statin therapy.
The researchers found that higher cholesterol levels and higher levels of LDL predicted an increased risk of biochemical relapse (P=0.001, P=0.007).
HDL was not associated with recurrence risk.
Men in the highest cholesterol quartile (≥217 mg/dL) had a 2.5 times greater risk of relapse compared with men in the lowest quartile (<167 mg/dL) with a hazard ratio of 2.49, 95% CI 1.28 to 4.86, P=0.007.
The intermediate quartiles were not associated with recurrence risk.
How cholesterol might influence prostate cancer risk is unclear, said Dr. Banez. However, he pointed out that cholesterol is a precursor to testosterone, which fuels prostate growth and function.
Another mechanistic explanation posits that cholesterol interferes with signal transduction associated with normal cell growth, he said.
Dr. Hamilton and colleagues did a longitudinal study involving 1,214 men prescribed a statin from 1990 through 2006. At baseline the men were free of prostate cancer, had not undergone prostate surgery or taken medications that alter androgen levels, and had PSA values of 0.1 to 10 ng/mL.
The primary outcome was the association among total cholesterol, LDL, HDL, and PSA levels in the two years before starting statin therapy.
After adjusting for age, ethnicity, and body mass index, investigators found that the pre-statin PSA level associated with pre-statin total cholesterol (P=0.02) and LDL (P=0.04) levels, but not HDL.
For each 10 mg/dL increase in total cholesterol or LDL, PSA levels increased by 0.02 ng/mL.
Among men who had baseline PSA values ≥3 ng/mL, each 10 mg/dL rise in total cholesterol or LDL corresponded to increased PSA levels of 0.7 and 0.08 ng/mL, respectively.
Dr. Banez disclosed that he has been an investigator for AstraZeneca. Dr. Hamilton had no disclosures.
Primary source: Journal of UrologySource reference:Banez LL, et al "Higher cholesterol increases the risk of biochemical failure after radical prostatectomy: Results from the SEARCH Database Group" J Urol 2008; 179(suppl): 68. Abstract 192. Additional source: Journal of UrologySource reference: Hamilton RJ, et al "The association between cholesterol and PSA" J Urol 2008; 179(suppl): 721. Abstract 2094.