Abstract
TO THE EDITOR: Gutt et al documented fewer recurrences among men with radiation-treated prostate cancer who had received statin therapy during or after their radiation therapy. They interpreted their observations to indicate a favorable influence by statins on prostate cancer behavior, a conclusion that is not appropriate unless observations are controlled for host factors that may have influenced tumor behavior. Most studies examining relationships between smoking and prostate cancer recurrence or tumor-related mortality demonstrate smoking-related increases in both, even after controlling for multiple factors including the more advanced malignant disease at presentation and the smaller prostate size characteristic of smokers. In a study similar to that of Gutt et al, Pantarotto et al reported follow-up data from 434 patients after external-beam radiation therapy with curative intent. In patients who had been current smokers at the time of therapy, they found a recurrence rate 5.2 times greater than the rate of life-long nonsmokers, and in former smokers, the recurrence rate was 2.9 times greater. Studies examining relationships between obesity and prostate cancer recurrence or tumor-related mortality have demonstrated an inconsistent pattern. Gong et al retrospectively analyzed tumor characteristics, body mass index (BMI), and smoking habits in 752 patients with prostate cancer and reported that prostate cancer–specific mortality was doubled in men with a BMI 30 kg/m compared with men who were less obese and that this mortality was 2.3 times as great in smokers compared with nonsmokers. Freedland et al reported a 2.09-fold increased risk of prostate-specific antigen failure in severely obese men (BMI 35 kg/m) and, in a recent review, concluded that obesity may reduce the risk of nonaggressive disease but increase the risk of aggressive disease, especially in those with BMI 35 kg/m. These observations suggest that if smokers in the study by Gutt et al had been less likely to receive statins either because of their lower average weight and associated lower lipid values or because of a lower level of interest in maintaining optimal health, then statin consumers would have included lower percentages of smokers, contributing to a lower frequency of tumor recurrences among them, and that the distribution of obese men might also have influenced recurrence rates. Analysis of BMI and smoking habits of their patients would increase the value of their analysis, while adding to the body of information that eventually should help to define any influence that statin therapy might have on prostate cancer behavior.
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