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Aromatase (EC 1.14.14.14), also called estrogen synthetase or estrogen synthase, is an enzyme responsible for a key step in the biosynthesis of estrogens. It is CYP19A1 , a member of the cytochrome P450 superfamily, which are monooxygenases that catalyze many reactions involved in steroidogenesis .
Ovarian stimulation with the aromatase inhibitor letrozole has been proposed for ovulation induction in order to treat unexplained female infertility. In a multi-center study funded by the National Institute of Child Health and Development, ovarian stimulation with letrozole resulted in a significantly lower frequency of multiple gestation (i.e., twins or triplets) but also a lower frequency ...
[21] [22] [23] Treatment of men with medical castration and add-back testosterone to restore testosterone levels, with or without the aromatase inhibitor anastrozole, showed that prevention of the conversion of testosterone into estradiol partially prevented restoration of sexual desire and erectile dysfunction by testosterone in men. [32]
Antiandrogens, also known as androgen antagonists or testosterone blockers, are a class of drugs that prevent androgens like testosterone and dihydrotestosterone (DHT) from mediating their biological effects in the body. They act by blocking the androgen receptor (AR) and/or inhibiting or suppressing androgen production.
A dosage of two to six 100 μg/day transdermal estradiol patches can achieve mean levels of estradiol in the area of 200 to 400 pg/mL and can be used as a form of high-dose estrogen therapy, for instance to suppress testosterone levels in the treatment of prostate cancer in men and in feminizing hormone therapy for transgender women.
Testosterone levels with 100 to 300 mg/day oral cyproterone acetate and low-dose oral estrogen in men. [160] The estrogen used was 0.1 mg/day diethylstilbestrol (DES), [160] which has been described as an "extremely low" dosage. [87] Levels of testosterone were decreased by about 95% with the combination and by about 61% with cyproterone ...
[10] [15] The beneficial action of testosterone in elevating the HDL fraction can be attributed to its conversion via aromatase activity in adipose tissue into 17-beta estradiol and its subsequent activation of estrogen alpha-receptors; thus, more testosterone leads to greater conversion into estrogen and thus a healthier lipid profile. [10]
It is also less than that achieved by high-dose estrogen therapy, which can suppress testosterone levels into the castrate range similarly to GnRH analogues. [ 222 ] The retroprogesterone derivatives dydrogesterone and trengestone are atypical progestogens and unlike all other clinically used progestogens do not have antigonadotropic effects ...