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Various studies have suggested a protective effect of HMG-CoA reductase inhibitors, or statins, in reducing the incidence of colorectal cancer, but data is conflicting.1 Statins are indicated for the treatment of hyperlipidemia and to reduce cardiac morbidity and mortality.2 Statins inhibit the conversion of HMG-CoA to melavonate through inhibition of HMG-CoA reductase. This conversion is the rate-limiting step in the synthesis of cholesterol. Statins also inhibit other items within the mevalonate pathway, including the production of farnesyl pyrophosphate and geranylgeranyl pyrophosphate.2 These products are improtant in preylating proteins involved in promotion of cellular growth and proliferation and carcinogenesis. Farnesyl pyrophosphate leads to prenylation of Ras proteins and geranylgeranyl pyrophosphate prenylates Rho and Rac proteins. Mutations in Ras, Rho, and Rac proteins are implicated in many cancers and inhibition of these proteins may be the mechanism of the chemoprotective effect of statins.2   

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In a retrospective, case-control study, Broughton and colleagues evaluated statin use in symptomatic patients undergoing a first diagnostic colonoscopy and compared patients diagnosed with colorectal cancer and with normal results. The patients were in the care of the Gastroenterology Department at the Norfolk and Norwich University Hospital. Information such as demographics, risk factors associated with colorectal cancer, and concomitant medications was collected from patient interviews and verified through medical record reviews. A history of statin use was obtained for each patient, including dose, duration, and type of statin prescribed. Patients undergoing colonoscopies for inflammatory bowel disease, previous adenomatous polyps or cancer, high-risk family history, and acromegaly were excluded from this study. Statistical data was adjusted for known confounding variables.1

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A total of 101 patients diagnosed with colorectal cancer and 132 patients with normal colonoscopies were included. The group diagnosed with colorectal cancer had significantly more males, were older and had more alcohol use; whereas the control group had a greater number of Type 2 diabetics, aspirin use and metformin use (p=0.05). After adjusting for confounding factors, there was a significant inverse relationship between patients who had previously used statins for duration of at least 6 months and a diagnosis of colorectal cancer (OR 0.43, 95% CI, 0.25-0.80, p<0.01). A significant association between duration of statin use and statin dose was evident between both groups. The incidence of colorectal cancer was lower as duration of statin use increased (>5years: OR 0.18, 95% CI, 0.06-0.55, p<0.01) and the dose increased (>40 mg of simvastatin-equivalent/day: OR 0.19, 95% CI, 0.07-0.47, p<0.01). Simvastatin was the most commonly used statin among the patient population (p<0.01), however a benefit was witnessed with all types of statins (including atorvastatin, pravastatin, and rosuvastatin). Aspirin was not found to be protective after adjusting for statin use.1

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This case-control study adds to the evidence showing a chemoprotective effect of statins against colorectal cancer. The study demonstrated a greater protective effect the longer the time on the statin and the higher the dosage. Strengths of this study include medical record reviews that accompanied patient interviews, inclusion of patients that were receiving their first diagnostic colonoscopy, similar demographics and characteristics between the groups, and adjustments for confounding variables. These strengths helped to minimize bias, which is inherent in case-control studies. Case-control studies only determine an association between exposure and a specific outcome, but not cause and effect; therefore randomized controlled trials are needed to confirm that statins are protective against colorectal cancer. The study ...

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