Abstract

Most steroid hormones are produced from cholesterol contained in low-density lipoproteins, which is uptaken by the gonads and adrenal cortex, and used as a substrate for steroidogenesis. Theoretically, in states associated with very low-density lipoprotein (LDL) cholesterol levels, cholesterol conversion to steroid hormones may be impaired. The study included 15 men with coronary artery disease, in whom initial statin treatment had been unsuccessful and therefore was replaced with rosuvastatin (20-40mg daily). Although in 11 patients, rosuvastatin decreased plasma LDL cholesterol levels to below 70mg/dL, the drug only moderately reduced testosterone levels and increased gonadotropin levels, as well as insignificantly increased plasma ACTH levels. Aggressive rosuvastatin treatment did not affect plasma cortisol and dehydroepiandrosterone sulphate levels, and urine free cortisol. Our results suggest that intensive rosuvastatin treatment is associated with only small changes in adrenal and testicular steroidogenesis.

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