Association between cardiovascular drugs and colon cancer

Abstract

The objective of the study was to determine (1) if cardiovascular drugs (CV) are associated with increased risk of colon cancer (CC), (2) if the risk for any individual agent differs from the risk of the therapeutically class overall, and (3) if the risk differs for patients with CC on right side based on inhibition properties of some CV drugs for bile acid uptake. A population-based case control study was conducted using the HealthCore Integrated Research Database (HIRDSM), a US commercial insurance claims database. Incident cases of CC were patients aged 18 years or older at diagnosis, with first CC diagnostic claim between Jan 1, 2001 to Jan 30, 2011. Each case was matched to one eligible control based on: no diagnosis of CC during study period, actively enrolled at index date of the case, and matched to cases by length of pre-index enrollment (same or greater), sex, and age. Exposure to a CV drug was defined as at least one claim during the risk period. Conditional logistic regression was used to calculate adjusted Odds Ratios (OR). 36,736 cases of CC were identified and successfully matched to controls. Sensitivity analysis were conducted by using alternate case definition, varying lag time between last prescription and CC diagnosis, and setting a required minimum CV drug exposure (12 months).The mean age was 60 years (about 30% were 50-60 years old). Enalapril, labetalol, cholestyramin, diltiazem and furosemide (ORs range:1.07-2.05) were positively associated with CC while atorvastatin, pravastatin and simvastatin (ORs range:0.68-0.94) were negatively associated with CC. In the sensitivity analyses, positive associations remained for just cholestyramine and diltiazem, whereas the negative associations remained for atorvastatin and simvastatin. These results are consistent with beneficial impact of statins on CC risk. Drugs identified as inhibitors of bile acid uptake were not associated with CC on right side. However, the association of individual drugs was not consistent with that therapeutic class as a whole. This suggests that risk may vary by individual agent. Grouping drugs into therapeutic classes for studies of cancer risk may introduce a bias driven by the predominant agents used in a particular population.