T is produced by the Leydig cells under the control of luteinizing hormone (LH) only.
T is produced by conversion from other androgens such as dehydroepiandrosterone (DHEA).
T bound to sex hormone–binding globulin (SHBG) is active in the prostate.
T is produced in decreased amounts in the presence of hyperprolactinemia.
T is produced by brain cells, but this portion is not measurable in serum.
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.
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 equilibrium dialysis
Free T by direct radioimmunoassay using a T analog with low affinity for SHBG
Free androgen index
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 insignificant; repeat measurements for diagnosis, therefore, are not necessary.
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.
In older men (>65 years) borderline levels of T with normal gonadotropins rule out the diagnosis of hypogonadism.
Growth hormone decreases at a rate similar to T.
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.
Prolactin production is not affected by aging.
Use T for treatment, not for prevention, of disease.
Conduct long-term studies only if short-term efficacy is established.
Focus on populations most likely to benefit.
Begin with short-term safety trials.
Focus on clinical outcomes with preliminary evidence of benefit.
measure free T by direct RIA.
repeat prolactin assessment.
initiate treatment with cabergoline or bromocriptine.
order MRI of the pituitary.
initiate T replacement therapy.
wait for 4 more years (10 since RRP) to consider supplemental T.
inform him of the risks and advise him against T therapy.
inform him of the risks and, with his consent, administer T.
consider administration of a weak androgen such as DHEA.
not consider him a candidate for supplemental T.
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