disease, ectopic ACTH-producing tumors, female acne and hirsutism, oligomenorrhea in female athletes, polycystic ovarian syndrome, Stein-Levinthal syndrome, and virilizing congenital hyperplasia.
From Leydig cells, the testis elaborates testosterone,
androstenedione, and dehydroepiandrosterone (also
from adrenal cortex). Luteinizing hormone from the
pituitary stimulates the formation of testosterone, which
is inactivated and conjugated in the liver and excreted as
glucuronide. Testosterone production rates in men are
2-8 mg/day; in women, 0.5-2.5 mg/day.
Testosterone maintains sex organs and controls
development of male sex characteristics, inhibits pituitary
LH, promotes long-bone growth without closure of
epiphyses, and has many anabolic effects (e.g. retention
of sodium, chloride, water, decrease in gluconeogenesis).
It is required for spermatogenesis. However, it cannot be
taken exogenously for this purpose since it would suppress
FSH and thus prevent this process.
Before puberty, eunuchoidism or cryptorchism. After
puberty, asthenia, loss of beard and potency, atrophy
of sex organs, hot flushes, nervousness, depression and
osteoporosis. Partial deficiency syndromes may occur (e.g.
Masculinization as with adrenocortical tumors, Leydig
cell tumors, testicular teratomas and seminomas.
Administered excess may depress spermatogenesis which
“rebounds” to supranormal level after withdrawal.
Noting pubic and temporal hair, prostate, and testes.
The study of male hypogonadism or sperm deficiencies
involves testicular biopsy, examination of the semen
and spermatozoa count, and such urinary hormone
the pituitary gonadotropins (FSH determination). The
absence of hyaluronidase from semen may indicate an
obstructive lesion of the ducts leading from the testes,
where the enzyme is produced. Urinary testosterone and
plasma testosterone measurements are very helpful.
Hypogonadism originating in the testis is accompanied by
high excretory and serum levels of LH and FSH, whereas
both are low when the defect is in the pituitary. Evidences
of hypogonadism will disappear and 17-ketosteroid
excretion will rise in a patient with hypopituitarism when
The patient should not be receiving endocrine therapy
Chorionic gonadotropin is given intramuscularly in a
daily dose of 2000 IU for 3 weeks. The patient is watched for
abatement of evidences of hypogonadism: in men, sperm
count, testicular biopsy, 17-ketosteroids, testosterone,
secondary sex characteristics, in women, vaginal smear for
estrogenic effects, secondary sex characteristics.
Disappearance of the evidences of hypogonadism
indicates hypogonadism secondary to pituitary failure.
Cord blood 5–22 17.4–76.3 2.0–4.4
Newborn 1.5–31.0 5.2–107.5 0.9–1.7
4 weeks- 3.3–8.0 11.5–62.5 0.4–0.8
3–5 months 0.7–14.0 2.4–48.6 0.4–1.1
5–7 months 0.4–4.8 1.4–16.6 0.4–1.0
6–9 years 0.1–3.2 0.3–11.1 0.9–1.7
10–11 years 0.6–5.7 2.1–19.8 1.0–1.9
12–14 years 1.4–156 4.9–541 1.3–3.0
15–17 years 80–159 278–552 1.8–2.7
Adults 1.0–8.5 3.5–29.5 0.5–1.8
Cord blood 4.0–16.0 13.9–55.5 2.0–3.9
Newborn 0.5–2.5 1.7–8.7 0.8–1.5
4 weeks-3 months 0.1–1.3 0.3–4.5 0.4–1.1
3–5 months 0.3–1.1 1.0–3.8 0.5–1.0
5–7 months 0.2–0.6 0.7–2.1 0.5–0.8
6–9 years 0.1–0.9 0.3–3.1 0.9–1.4
10–11 years 1.0–5.2 3.5–18.0 1.0–1.9
12–14 years 1.0–5.2 3.5–18.0 1.0–1.9
15–17 years 1.0–5.2 3.5–18.0 1.0–1.9
Androgen resistance, hirsutism, polycystic ovary
syndrome, tumor (virilizing) See also testosterone, total,
Hypogonadism, P-450 enzyme deficiency. (See also
Free testosterone is that portion of circulating testosterone
that is not bound to the sex hormone-binding globulin
(SHBG) plasma protein. This test is used to differentiate
true abnormal testosterone levels from those caused by
abnormally low or high amounts of circulating SHBG. (See
also Testosterone, Total, Blood).
Adrenal hyperplasia, adrenal tumor, arrhenoblastoma,
central nervous system lesions, hirsutism (idiopathic),
hyperthyroidism, ovarian tumor (virilizing), testicular
feminization, testicular tumor, virilizing luteoma, and
virilization. In women, idiopathic hirsutism, cystic
acne, polycystic ovary syndrome, adrenogenic alopecia,
abnormal menstruation, anovulation, adrenogenital
anticonvulsants, barbiturates, cimetidine, clomiphene,
estrogens, gonadotropin (males), and oral contraceptives.
Anemia, cirrhosis, cryptoorchidism, Down syndrome,
gynecomastia, hypogonadism (male), hypopituitarism,
impotence, Klinefelter’s syndrome, male climacteric,
obesity, and orchidectomy. Drugs include androgens,
cyproterone, dexamethasone, diethylistilbestrol, digoxin
(males), digitalis, estrogens (males), ethanol, glucose,
glucocorticoids, gonadotropin-releasing hormone analogs,
halothane, ketoconazole, metoprolol, metyrapone, phenothiazines, spironolactone, and tetracyline.
Testosterone is the dominant androgen found
in the adrenal glands, brain, ovary, pituitary, skin, kidney,
and testes. It circulates both freely, and bound to plasma
proteins (sex hormone-binding globulin [SHBG]).
Testosterone promotes the growth and development of
the male sexual organs, and increases body mass and hair
replacement. This test measures total testosterone levels in
clients with normal SHBG levels.
In adult males, an inverse correlation of free testosterone
with age occurs. The upper limit of normal range generally
decreases from the age of 20 to 60 years. The lower range of
free normal does not change significantly with age.
ng/dL SI Units nmol/L ng/dL SI Units mmol/L
Adult 300–1200 10.4–41.6 30–95 1.0–3.3
Cord blood 13–55 0.45–1.91 5–45 0.17–1.56
Premature infant 37–198 1.28–6.87 5–22 0.17–0.76
Newborn 75–400 2.6–13.9 20–64 0.69–2.22
1–5 months 1–177 0.03–6.14 1–5 0.03–0.17
6–11 months 2–7 0.07–0.24 2–5 0.07–0.17
12 months-5 years 2–25 0.07–0.87 2–10 0.07–0.35
6–9 years 3–30 0.10–1.04 2–20 0.07–0.69
1 2–23 0.07–0.80 2–10 0.07–0.35
3 15–280 0.52–9.72 10–30 0.35–1.04
4 105–545 3.64–18.91 15–40 0.52–1.39
5 265–800 9.19–27.76 10–40 0.35–1.39
Estriol Values are Increased in
Feminizing tumors, true precocious puberty, liver cirrhosis
and multiple pregnancy. Drugs include oxytocin.
Estriol Values are Decreased in
Anencephaly, abortion, anemia, choriocarcinoma, diabetes
mellitus, erythroblastosis, fetalis, fetal adrenal aplasia,
fetal Down syndrome, fetal growth retardation, fetal
drugs include betamethasone, cascara, corticosteroids
(large doses), dexamethasone, diuretics, glutethimide,
estrogens, mandelamine, meprobamate, penicillins,
phenazopyridine, phenophthalein, probenecid and senna.
The serum or plasma 17-β-estradiol values are comprised
Women Follicular phase 30–120 pg/mL
evaluation of normal sexual development (menarche),
lowest at menses and into the early follicular phase and
then rise in the late follicular phase to a peak just before
the LH surge, initiating ovulation. If conception occurs,
estradiol levels continue to rise. At menopause, estradiol
Adrenal tumors, cirrhosis, gynecomastia in males,
hyperthyroidism, Klinefelter’s syndrome, liver tumors,
ovarian neoplasm, polycystic ovary syndrome.
Amenorrhea, anorexia nervosa, hypopituitarism, infertility,
menopause, osteoporosis, ovarian hypofunction, pituitary
disease, and polycystic ovary syndrome.
The serum or plasma dehydroepiandrosterone sulfate
values are comprised in the following intervals:
Before puberty 0.25–1.0 0.25–1.0
Adrenal cortex adenoma and carcinoma, Cushing’s
disease, ectopic ACTH-producing tumors, female acne
and hirsutism, oligomenorrhea in female athletes,
polycystic ovarian syndrome, Stein-Levinthal syndrome,
and virilizing congenital hyperplasia.
Primary and secondary adrenal insufficiency. Low levels
in amniotic fluid indicate anencephaly in the fetus.
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