4.3 Article

Statin drugs, serum cholesterol, and prostate-specific antigen in the National Health and Nutrition Examination Survey 2001-2004

Journal

CANCER CAUSES & CONTROL
Volume 21, Issue 5, Pages 671-678

Publisher

SPRINGER
DOI: 10.1007/s10552-009-9494-9

Keywords

Prostatic neoplasms; Hydroxymethylglutaryl-CoA reductases; Cholesterol; Prostate-specific antigen; Cross-sectional studies

Funding

  1. National Cancer Institute, National Institutes of Health [T32 CA009314]
  2. National Institutes of Digestive, Diabetes, and Kidney Diseases, National Institutes of Health [K01 DK076595]

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We evaluated the associations of statins and serum cholesterol with PSA to understand whether the inverse associations of statins and low cholesterol with aggressive prostate cancer are explained by detection bias. We analyzed data from 2,574 men aged a parts per thousand yen40 years without prostate cancer in The National Health and Nutrition Examination Survey 2001-2004. We estimated multivariable-adjusted geometric mean PSA by statin use and cholesterol quintiles. To limit the influence of correlates of statin use and cholesterol on PSA, we stratified by comorbidities. Statin users had a non-statistically significantly lower PSA than non-users (0.90 vs. 0.95 ng/mL, p = 0.22), especially in men without comorbidities (n = 1,680; 0.86 vs. 0.99 ng/mL p = 0.02). In men with comorbidities, statin users had a non-statistically significantly higher PSA than non-users (0.91 vs. 0.83 ng/mL, p = 0.14). Men with lower cholesterol had lower PSA (bottom vs. top quintile: 0.92, 1.02 ng/mL, p-trend = 0.06). Statin users and men with lower cholesterol may have lower PSA. If so, the probability of detecting asymptomatic prostate cancer might be lower at present, but these cases might be more likely to be diagnosed at an advanced stage in the future. Thus, PSA-associated bias is unlikely to explain the inverse association of statins with advanced prostate cancer.

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