steroid levels are not significantly altered. 5. A synthetic 24 amino acid ACTH compound has made possible a rapid intramuscular test. 0.25 mg IM will take more than double normal plasma cortisol in less
The adrenal medulla is actually an extension of
the nervous system. The adrenal medulla produces
norepinephrine and epinepherine (adrenaline) that are
released in response to stress or a fright.
The major mineralocorticoid, which is secreted almost
independently of ACTH from the pituitary, is aldosterone.
Aldosterone secretion is controlled mostly by the levels
of potassium and sodium in serum and a blood pressure
control system called the renin-angiotensin system.
Aldosterone has the opposite effect on serum levels
of potassium as it is lost in the urine in exchange for
sodium in the renal tubules. Salivary and sweat glands
are also influenced by aldosterone to save sodium and the
intestine increases the absorption of sodium in response to
1. Elevated levels occur in primary aldosteronism as in:
• Aldosterone-producing adenoma
• Adrenal cortical hyperplasia
• Glucocorticoid remediable hyperaldosteronism.
2. Elevated levels also occur in secondary aldosteronism
when aldosterone output is elevated due to external
stimuli or because of greater activity in the reninangiotensin system as in:
• Hepatic cirrhosis with ascites
The major glucocorticoid is cortisol. Cortisol has important
actions in the control and metabolism of carbohydrates,
lipids, and proteins and assists in the metabolic reaction
to stress, especially chronic stress. It causes glucose to be
liberated from the liver by increasing glucose production
from fatty acids (by-products of lipid breakdown) and
amino acids. Cortisol causes the tissues to take up less
glucose from the blood and mobilizes fat breakdown. The
net effect is to increase serum glucose concentrations,
which is protective for the brain in that it cannot use any
other fuel source than glucose. It also stimulates protein
breakdown for glucose formation in all tissues except the
liver where it stimulates protein synthesis.
in plasma is 120 ng/mL (range 60–230 ng/mL). Diurnal
variation is striking. In normal humans observing
customary day-night activity, the highest levels occur at
about 8 am and the lowest level shortly after midnight
cortisol plasma or serum norms. Peak occur at about 0800
(8 am) and troughs occur in late afternoon.
Cortisol interpretation: Normal values in ng/mL
Patient treated with ACTH 280–600
Patient treated with dexamethasone 0–50
Cortisol Levels are Increased in
Burns, Cushing’s disease, Cushing’s syndrome, eclampsia,
exercise, hepatic disease (severe), hyperpituitarism,
hypertension, hyperthyroidism, infectious disease, obesity
acute pancreatitis, pregnancy, severe renal disease,
(severe heat, cold, trauma, psychological), surgery, and
virilism. Drugs include corticotropin, estrogens, oral
contraceptives, and vasopressin.
Cortisol Levels are Decreased in
Addison’s disease, adrenal insufficiency adenogenital
necrosis, and Waterhouse-Friderichsen syndrome. Drugs
include dexamethasone, dexamethasone acetate, and
dexamethasone sodium phosphate.
1. Pregnancy will cause an increased value
2. There is no normal diurnal variation in patients under
3. Drugs, such as spironolactone and oral contraceptives
will give falsely elevated results.
Cortisol Suppression (Dexamethasone Suppression)
Morning following administration of dexamethasone:
This is screening test for Cushing’s syndrome and depends
on the fact that ACTH production will be suppressed
in normal persons after a low dose of dexamethasone,
whereas it is not in Cushing’s syndrome.
1. Venous blood sample is obtained at 8 am, 4 pm and
again at 8 am the next day after dexamethasone has
2. At 4 pm, dexamethasone tablets are given orally. The
dosage varies according to weight.
All medications should be discontinued for 24 to 48
hours before the study. Especially important are aldactone,
estrogens, contraceptive pills, cortisol, tetracyclines,
No diurnal variation or suppression will occur in:
2. Conditions causing extreme stress
4. If dilantin has been administered.
Cortisol Stimulation (Cortrosyn Stimulation)
This is a good test to detect adrenal insufficiency.
Cortrosyn is a synthetic subunit of ACTH that exhibits
full corticosteroid-stimulating effect of ACTH in normal
persons. Failure to respond is an indication of adrenal
1. A fasting venous sample is obtained
2. Cortrosyn is administered intramuscularly
3. Additional blood samples are obtained 30 and 60
minutes after administration of cortrosyn.
Absent or diminished response occurs in:
3. Prolonged steroid administration.
Tests for Adrenocortical Insufficiency
Method: The patient fasts overnight. In the morning, he
empties his bladder and drinks 1500 mL of water (about
20 mL/kg body weight) over a period of 15-45 minutes.
A 5 hours urine specimen collected from the beginning
of the test is measured. During the 5 hours period, the
patient reclines or sits except while voiding. The test may
be repeated 2 hours after the oral administration of 50 mg
Normal individuals excrete 1200 mL or more of urine over
the 5 hours collection period. Patients with Addison’s
disease may excrete less than 800 mL of urine. False
positive results may be obtained if the rate of absorption
of water from the gastrointestinal tract or its elimination
by the kidney is decreased, e.g. in patients with nephritis,
cirrhosis, celiac disease, or cardiac failure.
Patients with adrenal insufficiency (primary, or
secondary to hypopituitarism) show substantial increase
in diuresis when retested following cortisone.
Corticotropin (ACTH) Response Test (Thorn test)
If responsive adrenocortical tissue is present, the
administration of potent corticotropin results in an
increased secretion of adrenocortical steroids, and increase
in plasma cortisol, producing eosinopenia and increased
pituitary insufficiency, its daily administration leads to a
stepwise increase in adrenocortical response over a period
Adrenal response to corticotropin is retarded in
myxedema as well as in hypopituitarism. Allergic
eosinophilia may mask a fall in eosinophils. The patient
should be free of the effects of large doses of androgens,
cortisone, and corticotropin before urinary steroids are
measured before 25 USP units of corticotropin are
administered in a 4 hours infusion. Four hours later,
another eosinophil count is done or plasma cortisol
2. Eight hours intravenous corticotropin test. 2–5 USP
units of corticotropin in 500 mL of normal saline are
administered IV as a continuous 8 hours infusion.
An eosinophils count or plasma cortisol level is
determined at the beginning and at the end of the
8 hours period. 24 hours urine collections are made
on a control day prior to the test and on the day of
corticotrophin administration. Urinary excretion
levels of 17-ketosteroids, 17-hydroxycorticosteroids,
ketogenic steroids, or urinary-free cortisol on each
specimen are compared with the control value.
3. As an alternative to the intravenous test, 40-80 USP units
of corticotropin gel (repository corticotropin injection)
or corticotropin zinc may be given intramuscularly
twice daily over the testing period. Corticotropin gel
should not be used in suspected adrenal insufficiency.
4. The patient with Addison’s disease may be protected
from an untoward reaction to ACTH by the administration of 0.1-0.25 mg of fludrocortisone, urinary
steroid levels are not significantly altered.
5. A synthetic 24 amino acid ACTH compound has made
possible a rapid intramuscular test. 0.25 mg IM will
take more than double normal plasma cortisol in less
The 4 hours corticotropin screening test normally
decreases circulating eosinophils by more than half. In
test (2) or (3) above, normal subjects respond with an 80-
100% fall in eosinophil levels, a 2-fold to 5-fold increase
in 17-hydroxycorticosteroids, and 2-fold increase in
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