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.