Title:Gonadotropin Treatment for the Male Hypogonadotropic Hypogonadism
Volume: 27
Issue: 24
Author(s): Luca Boeri, Paolo Capogrosso and Andrea Salonia*
Affiliation:
- Division of Experimental Oncology/Unit of Urology, URI, IRCCS Ospedale San Raffaele, Milan,Italy
Keywords:
Gonadotropin, male hypogonadotropic hypogonadism, infertility, FSH, hCG, HPG.
Abstract: Hypogonadotropic hypogonadism (HH) is caused by a dysfunction in the hypothalamus and/or the
pituitary gland and it can be congenital or acquired. This condition is biochemically characterized by low or inappropriately
normal gonadotropin levels along with low total testosterone levels. If fertility is not an issue, testosterone
therapy is the treatment of choice to induce and maintain secondary sexual characteristics and sexual function.
Spermatogenesis is frequently impaired in patients with HH, but usually responsive to hormonal therapy
such as gonadotropin therapy or GnRH supplementary/replacement therapy. When gonadotropins are the choice
of treatment, conventional therapy includes human chorionic gonadotropin (hCG) along with different FSH formulations:
human menopausal gonadotropins (hMG), highly purified urinary FSH preparations (hpFSH) (e.g.,
urofollitropin) or recombinant FSH (rFSH). The combination of FSH and hCG demonstrated to be associated
with better outcomes than single compounds, whereas similar results were obtained with different FSH preparations
in male individuals; both regarding the ability to stimulate spermatogenesis and eventually inducing physiology
pregnancy. Gonadotropins can be administered either subcutaneously or intramuscularly. The combination
therapy with hCG and FSH for a period of 12-24 months was found to promote testicular growth in almost all
patients, spermatogenesis in approximately 80% and pregnancy rates in the range of 50%. Gynecomastia is the
most common side effect of gonadotropin therapy and is due to hCG stimulation of aromatase causing increased
secretion of estradiol. The therapeutic success is higher in patients with post-pubertal HH, in those without previously
undescended testes, in patients with higher baseline testicular volume, who underwent repeated cycles of
therapy and in patients with higher baseline inhibin B serum concentrations. Reversal of hypogonadism can occur
in up to 10% of patients but its physiopathologic mechanism has yet to be elucidated. In conclusion, gonadotropin
therapy is effective in promoting puberty and in supporting spermatogenesis onset and preservation in HH patients
with either hypothalamic or pituitary conditions.
