Finasteride is a drug for treating benign prostatic hyperplasia (adenoma). Finasteride is a synthetic 4-azasteroid compound. It is a competitive inhibitor of 5-alpha-reductase type II – an intracellular enzyme that turns testosterone into a more active androgen – dihydrotestosterone. In prostate adenoma, its increase depends on the conversion of testosterone to dihydrotestosterone in the tissues of the prostate gland. Finasteride significantly reduces both circulating and intraprostatic dihydrotestosterone.
In the PLESS study, a safety assessment was conducted in 1524 patients who received proscar at a dose of 5 mg / day, and in 1516 patients who received placebo for 4 years. In 4.9% (74) of patients, treatment was canceled due to side effects attributed to proscar, compared with 3.3% (50) of patients who received placebo. At the same time, in 3.7% (57) patients taking proscar and 2.1% (32) patients taking placebo, treatment was canceled due to impaired sexual function, which was the most frequently observed side effect.
Some researchers suggest using finasteride in HRT M / F-transsexuals.
So, there is an experience of treating distress alopecia in M / W transsexuals with the use of finasteride (2.5-5 mg) and a solution of minoxidil (20 mg) [Lev A. et al., 1003].
The use of finasteride in combination with estrogen and antiandrogen therapy of M / F-transsexuals is inexpedient and not recommended, since the combined effect of estrogens and antiandrogens leads to a rather strong suppression of testosterone levels and the effect of finasteride against this background will be almost imperceptible.
There is little data on the use of GnRH drugs in the treatment of patients with transsexualism [Gooren I., 2005]. Synthetic analogs of natural GnRH after a short initial period of stimulation of the gonadotropic function of the pituitary gland have an inhibitory effect on the secretion of gonadotropin, followed by suppression of the synthesis of female and male sex steroid hormones. These drugs have a direct effect on gonad by reducing the sensitivity of peripheral receptors to the effects of the hormone responsible for the release of gonadotropin. With prolonged use, bone demineralization is possible, which is the risk of osteoporosis.
Some authors recommend the addition of GnRH agonists to the general treatment of M / F-transsexuals in case of excessive estrogen dosage if it is impossible to achieve a sufficient feminizing effect [Moge et al., 2003]. We believe that this therapy is not appropriate, since high doses of estrogen, as well as moderate doses, have an independent antigonanodotropic effect.