14%

10%.

2%.

unknown.

6%.

T bound to sex hormone–binding globulin (SHBG) is active in the prostate.

T is produced by conversion from other androgens such as dehydroepiandrosterone (DHEA).

T is produced by brain cells, but this portion is not measurable in serum.

T is produced in decreased amounts in the presence of hyperprolactinemia.

T is produced by the Leydig cells under the control of luteinizing hormone (LH) only.

Serum T trigger level for symptoms ranges narrowly among individuals.

Recurrence of symptoms is highly reproducible for each individual’s serum T levels, with interruption of therapy.

Signs and symptoms of hypogonadism are specific; biochemical support is desirable but not mandatory.

Sarcopenia and osteopenia/osteoporosis are fundamental elements for the diagnosis of the condition.

Screening questionnaires (Androgen Deficiency in Aging Males [ADAM], Aging Male Survey [AMS]) have high (>75%) specificity.

Salivary T

Total T

Free androgen index

Free T by equilibrium dialysis

Free T by direct radioimmunoassay using a T analog with low affinity for SHBG

Intraindividual variations in serum T levels are less apparent with assays for bioavailable T.

Repeatedly finding borderline serum T levels in the presence of clinical manifestations of T deficiency justifies a trial of T supplementation.

Repeatedly finding borderline serum total T levels in the presence of clinical manifestations of T deficiency is an indication for ordering a direct radioimmunoassay of free T using a T analog assay with low affinity for SHBG.

In older men (>65 years) borderline levels of T with normal gonadotropins rule out the diagnosis of hypogonadism.

Intraindividual variations in serum T levels are insignificant; repeat measurements for diagnosis, therefore, are not necessary.

Growth hormone decreases at a rate similar to T.

Prolactin production is not affected by aging.

Melatonin production by the pineal gland decreases with aging.

SHBG decreases in healthy aging.

Leptin increases with aging and more so in the presence of hypogonadism.

Gynecomastia

Polycythemia

Angina pectoris

Breast cancer

Heart failure

Focus on clinical outcomes with preliminary evidence of benefit.

Conduct long-term studies only if short-term efficacy is established.

Use T for treatment, not for prevention, of disease.

Begin with short-term safety trials.

Focus on populations most likely to benefit.

repeat prolactin assessment.

measure free T by direct RIA.

order MRI of the pituitary.

initiate T replacement therapy.

initiate treatment with cabergoline or bromocriptine.

inform him of the risks and advise him against T therapy.

not consider him a candidate for supplemental T.

inform him of the risks and, with his consent, administer T.

wait for 4 more years (10 since RRP) to consider supplemental T.

consider administration of a weak androgen such as DHEA.