© The Canadian Journal of Urology™; 21(Supplement 2); June 2014
profiles. Primaryhypogonadismismarkedby increased
luteinizing hormone (LH) and follicle-stimulating
hormone (FSH), the result of reduced feedback from
testosterone; secondary hypogonadism is characterized
by low or low-normal levels of LH and FSH; and the
mixed form varies according to the predominance of
primary or secondary hypogonadism. All forms also
involve impaired spermatogenesis.
11,43
The clinical
guidelines of the Endocrine Society recommend
measurement of LH and FSH in hypogonadal men
to distinguish between primary and secondary
hypogonadism.
11
Amore rational approach is to reserve
FSHmeasurement for hypogonadal patients who have
fertility concerns. LH is directly relevant to testosterone
production and, in the absence of fertility questions, is
the only gonadotropin of interest for TD classification.
Measurement of serumprolactin, for insight onpituitary
function, is appropriate when the serum testosterone
level is < 150 ng/dLor when secondary hypogonadism
is suspected.
13
Identifying candidates for screening
There is lack of agreement on the relevance of TD to
ED—that is, whether ED is sufficiently symptomatic of
hypogonadism to prompt screening and testosterone
measurement. The Endocrine Society guidelines
11
do
not specify ED as suggestive of TD. The American
College of Physicians does not recommend for or
against routine hormonal blood tests or hormonal
treatment for ED, citing the wide-ranging prevalence
rates of ED in hypogonadal men (12.5%-35%) and
the lack of conclusive evidence about the impact
of testosterone therapy on ED.
29,44
On the other
hand, several other international medical societies
13
recognize ED as among the hallmark symptoms of TD
requiring biochemical corroboration. Most primary
care physicians will know from their own experience
that ED is the portal to testosterone measurement. It
should by no means go unappreciated as a possible
manifestation of TD.
TABLE 3.
Primary and secondary forms of hypogonadism
14,39,40-42
Primary hypogonadism
Congenital anorchidism
Cryptorchidism (undescended testes)
Mumps orchitis
Genetic and developmental conditions: Klinefelter’s syndrome (1 in 1000 live births. Most patients have 47,
XXY genotype anomaly; however, mosaicism is also seen); androgen receptor and enzyme defects
Sertoli-cell-only syndrome
Noonan syndrome: phenotypic and genotypic males with physical signs of classic female Turner syndrome
Radiation treatment ⁄chemotherapy
Testicular trauma/surgical procedures
Autoimmune syndromes (anti-Leydig cell disorders)
Secondary hypogonadism
Kallmann syndrome (pituitary macroadenoma)
Pituitary tumor, granulomas, abscesses
Genetic conditions: Kallmann’s syndrome, Prader-Willi syndrome
Hyperprolactinemia
Cranial trauma
Radiation treatment
Various medications
Mixed hypogonadism (seen chiefly in men aged 50-70 years old)
Alcoholism
Aging
Chronic infections (eg, human immunodeficiency virus [HIV])
Corticosteroid treatment
Hemochromatosis
Systemic disease (liver failure, chronic kidney disease sickle-cell disease
44
Miner ET AL.
