Male hypogonadism is characterised by androgen deficiency and infertility.
Hypogonadism can be caused by disorders at the hypothalamic or pituitary le
vel (hypogonadotropic forms) or by testicular dysfunction (hypergonadotropi
c forms). Testosterone substitution is necessary in all hypogonadal patient
s, because androgen deficiency causes slight anemia, changes in coagulation
parameters, decreased bone density, muscle atrophy, regression of sexual f
unction and alterations in mood and cognitive abilities. Androgen replaceme
nt comprises injectable forms of testosterone as well as implants, transder
mal systems, sublingual, buccal and oral preparations. Transdermal systems
provide the pharmacokinetic modality closest to natural diurnal Variations
in testosterone levels. New injectable forms of testosterone are currently
under clinical evaluation (testosterone undecanoate, testoterone buciclate)
, allowing extended injection intervals. If patients with hypogonadotropic
hypogonadism wish to father a child, spermatogenesis can be initiated and m
aintained by gonadotropin therapy (conventionally in the form of human chor
ionic gonadotropin (hCG) and human menopausal gonadotropin (hMG) or, more r
ecently, purified or recombinant follicle stimulating hormone (FSH)). Apart
from this option, patients with disorders at the hypothalamic level can be
stimulated with pulsatile gonadotropin-releasing hormone (GnRH). Both trea
tment modalities have to be administered on average for 7-10 months until p
regnancy is achieved. In individual cases, treatment may be necessary for u
p to 46 months. Testosterone treatment is interrupted for the time of GnRH
of gonadotropin therapy, but resumed after cessation of this therapy. (C) 2
000 Elsevier Science Ireland Ltd. All rights reserved.