T is produced by brain cells, but this portion is not measurable in serum.
T bound to sex hormone–binding globulin (SHBG) is active in the prostate.
T is produced by the Leydig cells under the control of luteinizing hormone (LH) only.
T is produced in decreased amounts in the presence of hyperprolactinemia.
T is produced by conversion from other androgens such as dehydroepiandrosterone (DHEA).
Sarcopenia and osteopenia/osteoporosis are fundamental elements for the diagnosis of the condition.
Signs and symptoms of hypogonadism are specific; biochemical support is desirable but not mandatory.
Recurrence of symptoms is highly reproducible for each individual’s serum T levels, with interruption of therapy.
Serum T trigger level for symptoms ranges narrowly among individuals.
Screening questionnaires (Androgen Deficiency in Aging Males [ADAM], Aging Male Survey [AMS]) have high (>75%) specificity.
Free T by direct radioimmunoassay using a T analog with low affinity for SHBG
Free T by equilibrium dialysis
Free androgen index
In older men (>65 years) borderline levels of T with normal gonadotropins rule out the diagnosis of hypogonadism.
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.
Intraindividual variations in serum T levels are less apparent with assays for bioavailable T.
Intraindividual variations in serum T levels are insignificant; repeat measurements for diagnosis, therefore, are not necessary.
Leptin increases with aging and more so in the presence of hypogonadism.
SHBG decreases in healthy aging.
Prolactin production is not affected by aging.
Melatonin production by the pineal gland decreases with aging.
Growth hormone decreases at a rate similar to T.
Focus on populations most likely to benefit.
Conduct long-term studies only if short-term efficacy is established.
Focus on clinical outcomes with preliminary evidence of benefit.
Use T for treatment, not for prevention, of disease.
Begin with short-term safety trials.
measure free T by direct RIA.
order MRI of the pituitary.
repeat prolactin assessment.
initiate T replacement therapy.
initiate treatment with cabergoline or bromocriptine.
inform him of the risks and, with his consent, administer T.
consider administration of a weak androgen such as DHEA.
inform him of the risks and advise him against T therapy.
not consider him a candidate for supplemental T.
wait for 4 more years (10 since RRP) to consider supplemental T.
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