TY - JOUR
T1 - Minimal detection bias in the inverse association between statin drug use and advanced prostate cancer risk
T2 - A simulation study
AU - Mondul, Alison M.
AU - Caffo, Brian
AU - Platz, Elizabeth A.
N1 - Funding Information:
Dr. Mondul was supported by the National Institutes of Health National Research Service Award T32 CA009314. This analysis was supported by Public Health Service Research grant P50 CA58236 from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services. The content of this manuscript is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
PY - 2011/8
Y1 - 2011/8
N2 - Background: Prospective studies support that statins may protect against advanced prostate cancer. Detection bias arising from higher PSA screening rates among statin users vs. non-users could produce an inverse association for advanced disease. Thus, we conducted simulations to assess whether this source of bias is explanatory. Methods: 3000 datasets with 100,000 men without prostate cancer were simulated for populations with high (65%) or low (15%) PSA screening. We investigated three scenarios: RR true=1.0, 0.75, and 0.5 for statins and advanced disease (1.0 for localized). We set the statin prevalence to 10% and varied the percentage of users who were PSA screened (0-100%). We assumed an annual total prostate cancer incidence of 1%, with risk in screened men twice that of unscreened men, and an advanced stage at diagnosis in 20% and 40% of cases in screened and unscreened men, respectively. Results: As PSA screening and statin use became more coincident, the RR observed for local and total prostate cancer was biased upward from the RR true of 1.0, especially when the prevalence of PSA screening was low. However, in all simulated scenarios, there was little downward bias for advanced disease (e.g., if RR true=1.0 and 70% of statin users and either 65% or 15% of the population overall was PSA screened, then RR observed=0.98 for both). Conclusions: Given our assumptions, this simulation suggests that this source of detection bias is unlikely to explain the reported inverse association between statins and advanced prostate cancer, but may explain the positive association for total prostate cancer that has been reported in some studies.
AB - Background: Prospective studies support that statins may protect against advanced prostate cancer. Detection bias arising from higher PSA screening rates among statin users vs. non-users could produce an inverse association for advanced disease. Thus, we conducted simulations to assess whether this source of bias is explanatory. Methods: 3000 datasets with 100,000 men without prostate cancer were simulated for populations with high (65%) or low (15%) PSA screening. We investigated three scenarios: RR true=1.0, 0.75, and 0.5 for statins and advanced disease (1.0 for localized). We set the statin prevalence to 10% and varied the percentage of users who were PSA screened (0-100%). We assumed an annual total prostate cancer incidence of 1%, with risk in screened men twice that of unscreened men, and an advanced stage at diagnosis in 20% and 40% of cases in screened and unscreened men, respectively. Results: As PSA screening and statin use became more coincident, the RR observed for local and total prostate cancer was biased upward from the RR true of 1.0, especially when the prevalence of PSA screening was low. However, in all simulated scenarios, there was little downward bias for advanced disease (e.g., if RR true=1.0 and 70% of statin users and either 65% or 15% of the population overall was PSA screened, then RR observed=0.98 for both). Conclusions: Given our assumptions, this simulation suggests that this source of detection bias is unlikely to explain the reported inverse association between statins and advanced prostate cancer, but may explain the positive association for total prostate cancer that has been reported in some studies.
KW - Hydroxymethylglutaryl-CoA reductase inhibitors
KW - Prostate-specific antigen
KW - Prostatic neoplasms
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U2 - 10.1016/j.canep.2010.11.005
DO - 10.1016/j.canep.2010.11.005
M3 - Article
C2 - 21167804
AN - SCOPUS:79960592736
SN - 1877-7821
VL - 35
SP - e6-e11
JO - Cancer Epidemiology
JF - Cancer Epidemiology
IS - 4
ER -