SUSTAINED THERAPY WITH 3-HYDROXY-3-METHYLGLUTARYL-COENZYME-A REDUCTASE INHIBITORS DOES NOT IMPAIR STEROIDOGENESIS BY ADRENALS AND GONADS

Plasma lipoproteins are a major source of cholesterol for steroid horm one synthesis. 3-Hydroxy-3-methylglutaryl-coenzyme-A (HMG-CoA) reducta se inhibitors, which reduce both intracellular cholesterol synthesis a nd serum cholesterol levels, thus have a potential negative impact on steroidogenesis. In this study, we evaluated basal and maximally stimu lated adrenocortical and testicular steroidogenesis in 24 hypercholest erolemic male subjects during 6-36 months of statin treatment. One gro up was evaluated before treatment and after 6 months of treatment. A s econd group, which received long term treatment, was evaluated after 2 4-36 months and then 2 months after treatment had been discontinued. F ourteen subjects were given simvastatin, and 12 were given pravastatin , both at the maximum therapeutic dosage of 40 mg/day. During statin t herapy, serum cholesterol was lowered by about 30%. Basal serum and ur inary cortisol levels as well as serum cortisol response to ACTH were not influenced by statin therapy. Basal serum testosterone and its res ponse to hCG were also unchanged by statin treatment. In addition, ste roid hormone urinary metabolites were strikingly similar when patients were given HMG-CoA reductase inhibitors and when they were not. These results indicate that maximum therapeutic doses of statins have no ne gative impact on adrenocortical and testicular steroidogenesis even wh en these glands are maximally stimulated.