Simvastatin is a very effective hypocholesterolemic drug which, reducing cholesterol
biosynthesis, can affect normal steroid hormone production. Testes require a continuous
cholesterol supply for testosterone synthesis and this can be derived from low density
lipoprotein receptor-mediated uptake or from de novo local synthesis. The aim of the study was to see if prolonged simvastatin treatment
compromised endocrine testicular function both in basal conditions and after stimulation
by human Chorionic Gonadotropin (hCG) (Profasi 5,000 UI, i.m. at 8 a.m.). Free testosterone
(FT) levels were determined at baseline and after 3, 6 and 12 months of simvastatin
treatment (20 mg/day) in eight hypercholesterolemic patients. At the same time we
performed a hCG stimulation test to evaluate testicular reserve. A significant reduction
of FT, both basal and hCG-stimulated, was observed in the 6th and the 12th month of
the study. However, FT levels remained in the normal range and no patient complained
of gonadal function related symptoms. No significant change was observed in estradiol
response to hCG test. Lastly, there was no variation in LH, FSH, progesterone, 17-OH-progesterone,
a ndrostenedione or dehydroepiandrosterone-sulphate levels. Our study concluded that
the drug causes a mild decline in FT secretion without any clinical sign of testicular
dysfunction.
Key words
Hypercholesterolemia - Simvastatin - Free Testosterone - Testicular Function
