TESTIS FAILURE III: SECONDARY HYPOGONADISM
VARIANTS
Eunuchoid features common to primary (hypergonadotropic) and secondary (hypogonadotropic) hypogonadism are presented here in the classic physical phenotype (see Plates 3-16 and 3-17). However, most males with hypogonadism do not develop into such exaggerated, tall, lean individuals. Most exhibit “in-between” morphogenetic types, as the onset of clinical hypogonadism occurs at various ages and has various degrees of influence. For example, many hypogonadal men are shorter than normal, although with skeletal proportions still characterized by long radial skeletal bones associated with delayed maturation of the epiphyses. Indeed, not all prepubertally hypogonadal men develop disproportionately long extremities, as additional factors are necessary for excess linear growth, including growth hormone status, nutritional and environmental factors, and thyroid balance.
Hypogonadal males with
partial androgenic deficiency show all degrees of penile and testicular
development. Many cases of secondary hypogonadism are not genetic but acquired
and present after puberty as a result of extreme physical stress, anabolic
steroids, chronic opiates, sickle cell disease, acquired pituitary cysts,
diabetes mellitus, and hemochromatosis. These patients tend to have normal volume testes and normal phallic length and may present with symptoms of
sexual dysfunction such as erectile dysfunction, low libido, or infertility.
Hair development in
hypogonadal men varies with responsiveness to both testicular and adrenal
cortical androgens. More hair can develop when testicular failure is incomplete
and abundant; fine pubic hair may be present due to pituitary
adrenocorticotropic hormone (ACTH) and resultant adrenocortical androgens.
Hypogonadal men tend to be obese and have relatively undeveloped muscle and
bone. In addition, fat tends to accumulate on the anterior abdominal wall,
above the symphysis in the mons pubis area, around the mammary glands, and on
the outer thighs and buttocks. Obesity can also be explained by dietary habits
or other familial traits.
The treatment of
hypogonadism is testosterone replacement. Testosterone can be given
intramuscularly with depot injections (monthly), by transdermally absorbed gels
(daily), buccally absorbed tablets (daily), dermal patches (daily), and
implantable pellets (biannually). Such replacement can be
important to prevent the complications of long-term hypogonadism that include
osteoporosis, anemia, depression, heart disease, muscle wasting, memory loss,
and possibly even higher rates of prostate cancer and metabolic syndrome. Cases
of secondary hypogonadism may also respond to pituitary replacement with human
chorionic gonadotropin (hCG) that acts as luteinizing hormone (LH) and
stimulates interstitial Leydig cell function and testosterone production.
In the vast majority of hypogonadism cases, testosterone replacement will
reduce pituitary follicle-stimulating hormone (FSH) and LH secretion by
negative feedback homeostasis and induce sterility. The addition of injectable
FSH therapy along with hCG can restore natural fertility to the majority of
secondarily hypogonadal men. This is an important issue in secondary
hypogonadism induced by anabolic
steroid use by athletes and
body builders.
