The hypothesis that increased
estradiol production may be the cause of impaired spermatogenesis in infertile men with idiopathic
oligozoospermia was tested by administering the
aromatase inhibitor,
testolactone, and by assessing its effects on sperm output and fertility. Our study was a randomized, placebo-controlled double-blind crossover trial. Subjects (n = 25) with
infertility due to unexplained
oligozoospermia were given
testolactone (2 g/day) or placebo for 8 months followed by crossover to the other treatment for an additional 8 months. Total
estradiol and
testosterone levels during
testolactone exposure did not change from basal and placebo values. However,
sex hormone-binding globulin binding capacity consistently decreased (30%, p less than 0.01) and free
testosterone levels increased (36%, p less than 0.01). Free
estradiol values increased but not significantly. Additionally, LH and FSH serum levels increased by 15% and 20%, respectively (p less than 0.05), and
17 alpha-hydroxyprogesterone values increased by 90% (p less than 0.05) during
drug administration. Sperm output and semen quality remained unchanged during either
testolactone or placebo treatment, and no pregnancies occurred during the 16-month study. These data suggest that chronic administration of
testolactone at this dose fails to maintain
aromatase inhibition despite depression of
17,20-desmolase activity with elevated
17 alpha-hydroxyprogesterone and depressed SHBG binding capacity with elevation of free
testosterone.
Testolactone is not efficacious in the treatment of idiopathic oligozoospermic
infertility.