The goal for<unk>  therapy is to induce pubertal development, sexual function, fertility, bone health, and psychological wellbeing Testosterone therapy for males and estradiol therapy for females is used to improve genital development, develop secondary sexual characteristics, allow for the growth and closure of the epiphyseal plate, as well as improving sexual function. This therapy does not restore fertility as gonadotropins are required for spermatogenesis and folliculogenesis. If fertility is desired, pulsatile GnRH therapy or gonadotropin therapy is necessary. Gonadotropin therapy involves the use of human chorionic gonadotropin (hCG) and FSH. In the male, hCG stimulates Leydig cells to produce testosterone so that plasma and testicular levels increase. With the increased levels of testosterone, sexual activity, libido and overall wellbeing should improve. Administration of FSH is required to induce spermatogenesis by acting on Sertoli cells. FSH is required for maintaining the production of high numbers of good quality sperm. Gonadotropin therapy in<unk>  men usually is able to generate enough sperm for fertility to occur, however sperm count is still lower than normal. In the female, the goal for gonadotropin therapy is to obtain ovulation. This is obtained with FSH treatment followed by hCG or LH to trigger ovulation. FSH will stimulate granulosa cells for follicular maturation while LH will act on luteal cells to produce steroids aiding follicular maturation and preparing the endometrium for pregnancy. For hyperprolactinaemia-caused AHH, dopamine agonists are used to improve GnRH secretion. Dopamine binds to D2 receptors on lactotrophs within the anterior pituitary This results in the inhibition of secretion of prolactin resulting in less direct and indirect inhibition of GnRH secretion. In up to 10-20% of cases, patients can exhibit sustained fertility and steroid production after therapy, resulting in<unk>  reversal. The mechanism for this reversal is unknown but there is believed to be some neuronal plasticity within GnRH releasing cells.
Hypogonadotropic hypogonadism
Hypergonadotropic hypogonadism
Late-onset hypogonadism
Isolated hypogonadotropic hypogonadism
Polyorchidism
Hypergonadotropic hypergonadism
Microorchidism
Dual-role transvestism