Hypogonadotrophic hypogonadism is caused either by hypothalamic or pituitary diseases.
The failure of hormonal regulation can easily be determined [3].
Endocrine deficiency leads to a lack of spermatogenesis and testosterone secretion due to decreased
secretion patterns of LH and FSH. The therapy of choice is human chorionic gonadotrophin (hCG) treatment,
with the later addition of human menopausal globulin (hMG), dependent on initial testicular volume [4].
If hypogonadotrophic hypogonadism is hypothalamic in origin, a 1-year therapy with pulsatile gonadotrophin
releasing hormone (GnRH) is as effective as gonadotrophins in stimulating spermatogenesis [5].
Once pregnancy has been induced, patients will go back to testosterone substitution (see below).
Conclusion
Effective drug therapy is available to achieve fertility in men with hypogonadotrophic hypogonadism.
6.2.3 Hypergonadotrophic hypogonadism
Aetiology, diagnosis and therapeutic management
Common conditions associated with hypergonadotrophic hypogonadism in younger men include injury to and
loss of the testicles (e.g. after bilateral testicular cancer) (Table 11). More recently it has been recognized that
hypogonadism may occur after extensive testicular biopsy to recover sperm for IVF/ICSI [6]. Men with Klinefelter's syndrome are at risk for spontaneous hypogonadism with ageing. Those undergoing extensive testicular biopsy in the context of IVF/ICSI will almost certainly have an exacerbated risk [7]. Hypergonadotrophic hypogonadism may occur spontaneously in the elderly, in patients with erectile dysfunction [8], and after LHRH treatment or surgical castration for prostatic cancer [9]. All these conditions are not clinically significant for infertile men. Hypogonadism may be associated with osteoporosis [10]. The laboratory diagnosis of hypergonadotrophic hypogonadism is based on decreased serum testosterone and increased LH levels [2]. Additional prolactin measurement is suggested.
Testosterone supplementation is only indicated in men with levels consistently lower than normal (< 12 nmol/l = 300 ng/dl).
Injectable, oral and transdermal testosterone preparations are available for clinical use [2]. The best preparation is the one that maintains serum testosterone levels as close to physiological concentrations as possible [11].
Conclusion
There is general agreement that patients with primary or secondary hypogonadism should receive testosterone substitution therapy.