seconds intervals. Maximum effect appears in 2 minutes and lasts for 3-5 minutes. If pheochromocytoma is strongly suspected, a dose of 1 mg should be administered to avoid
This test is useful in detecting primary or secondary
aldosteronism. Patients with primary aldosteronism
characteristically have hypertension, muscular pains and
cramps, weakness, tetany, paralyses and polyuria.
1. Elevated levels occur in primary aldosteronism as in:
a. Aldosterone producing adenoma
b. Adrenal cortical hyperplasia
c. Glucucorticoid 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:
e. Hepatic cirrhosis with ascites
i. Hypovolemia and hemorrhage.
Values are increased in pregnancy and by posture.
Clinical Disorders of Mineralocorticoids
Primary hyperaldosteronism is usually due to
adrenocortical adenoma. The principal manifestations
of excess aldosterone secretion are hypertension and
hypokalemia. Urinary aldosterone levels are high and
plasma-renin activity is reduced or absent.
The most effective screening method is to determine
whether hypertension is due to hyperaldosteronism or not
is the serum potassium measurement. The disease must be
suspected if more than 50 mEq of potassium are excreted in
24 hours and the serum potassium level is below 3 mEq/L.
The patient should be on a high salt intake (2 g of salt with
each meal for 4 days before electrolyte measurements
and ECG are done). The electrocardiographic changes are
those of prolonged hypertension and hypokalemia.
The patient with hyperaldosteronism frequently
complains of severe headache. Potassium depletion
causes weakness, paresthesia, flaccid paralysis, polyuria,
and nocturia. Transient correction of hypokalemia by
administration of spironolactone, 400 mg daily in divided
doses for 3 days, is presumptive evidence of primary
hyperaldosteronism. A diabetic glucose tolerance curve is
present in about half of cases.
Isothenuria which does not respond to vasopressin is
also due to potassium depletion.
Sodium retention causes hypernatremia and dilutional
anemia due to increased plasma volume (low hematocrit).
Autonomic dysfunction is manifested by a postural fall in
blood pressure without changes in pulse rate.
Desoxycorticosterone acetate, 20 mg IM daily in
divided doses for 3 days, causes no change in aldosterone
production, if an aldosterone-producing tumor is present.
The measurement of plasma aldosterone can be used.
Care must be taken because of its increased response
to posture, activity, and salt restriction. The plasma
aldosterone does not normally increase 2-to 3-fold after
4 hours upright in patients with adenoma. While 83% of
patients with the syndrome of primary aldosteronism have
a solitary adenoma, the hypertension seen in patients
with hyperplasia in the remaining 17% usually does not
respond to subtotal or total adrenalectomy.
Excessive secretion of aldosterone is seen in edematous
states, such as cirrhosis with ascites, nephrosis, congestive
heart failure, and toxemia of pregnancy; in non-edematous
states, such as malignant hypertension; in unilateral renal
arterial narrowing, and after diuretic therapy. Useful
differential diagnostic aids are: (i) low serum concentration,
(ii) blood volume, usually reduced in hypertensive patients,
and (iii) normal or elevated plasma-renin activity.
Hyperkalemia unexplained by diminished renal function
can be the presenting finding in patients with reduced
aldosterone levels. All other adrenal steroids are normal,
and the defect resides in the defective release or production
The adrenal medullary hormones are catecholamines:
(i) epinephrine, and (ii) norepinephrine, the parent
compound from which epinephrine is formed by addition
Epinephrine 0–140 pg/mL 0–762 pmol/L
Norepinephrine 200–1700 pg/mL 1088–9256 pmol/L
Dopamine 0–30 pg/mL 0–163 pmol/L
Epinephrine 0–110 pg/mL 0–599 pmol/L
Norepinephrine 70–750 pg/mL 381–4083 pmol/L
Dopamine 0–30 pg/mL 0–163 pmol/L
Total 150–650 pg/mL 886–3843 pmol/L
Total catecholamines 0–18 µg/dL 0–103 nmol/dL
778 Concise Book of Medical Laboratory Technology: Methods and Interpretations Actions
Epinephrine is sympathomimetic, increases cardiac output
and rate, systolic blood pressure, blood glucose, hepatic
glycogenolysis, basal metabolic rate, sweating, and causes
and rise in diastolic blood pressure, and has much less
Hypotension. Idiopathic spontaneous hypoglycemia
(failure of epinephrine response to hypoglycemia).
Paroxysmal or persistent hypertension, headaches,
sweating, tachycardia, elevated blood glucose.
Chemical assay of epinephrine or norepinephrine
in blood or urine, provocative and blocking tests for
pheochromocytoma; glucose tolerance test; X-rays of
Adrenal medullary hyperactivity, as in pheochromocytoma, produces symptoms and signs, including
hypertension, through the release of large amounts of
epinephrine and norepinephrine into the bloodstream.
The most satisfactory single diagnostic procedure is
the discovery of plasma levels of norepinephrine in
excess of 0.5 µg/L. Jaundice, azotemia, and tetracycline
administration also cause high levels.
than 170/110, a provocative test with histamine may cause
a characteristic rise in the blood pressure and in the urine
and plasma catecholamines. Higher levels of basal blood
pressure are best investigated by the phentolamine test.
The levels of urinary catecholamines and their
metabolites (such as Vanillylmandelic acid—VMA
normetanephrine and metanephrine) are greatly increased
(10-100 times) in the presence of pheochromocytoma. The
usual 24 hours excretion of epinephrine is up to 50 mg, of
the metabolite, VMA, 2.5 µg/mg creatinine and less than
1.3 mg/24 hours for 1 ml metanephrine. The ingestion of
tea, coffee, bananas, vanilla, salicylates, phenobarbital,
fruit, morphine, iproniazid, and methocarbamol will
invalidate the VMA measurement. Tetracyclines,
cause a rise in metanephrine and a low VMA. The pressor
amine output at rest is about half that during normal
daily activity. If the urine contains increased amounts of
epinephrine (40% of cases), the tumor is almost always
in one of the adrenal areas or the organ of Zuckerkandl. If
urine contains increased amounts of norepinephrine (60%
of cases), the tumor may still be expected to be in or near
one of the adrenal areas in two-third of cases; and in the
remaining one-third, all possible sites must be considered.
In both, provocative and blocking tests, control blood
pressure must be taken and the pressure must restabilize
after venipuncture before the drug is given. Hypotensive
drugs, e.g. rauwolfia, chlorothiazide, or sedatives, will
confuse the results if given within 24 hours before testing.
No diagnosis of pheochromocytoma should be based on
Keep phentolamine ready for a case where there is a severe
blood pressure rise in a hypertensive patient.
Method: A cold pressure test is first performed by placing
the patient’s forearm in a water-ice bath for 1 minute after
basal blood pressure reading has been taken, and then
recording postimmersion blood pressure readings at 30
seconds intervals for 3 minutes or until the basal state
Total catecholamines 0–135 µg/M2
Age 4–10 0–10 µg/D 0–55 nmol/D
Age 10–15 0.5–20 µg/D 2.7–110 nmol/D
Epinephrine > 50 µg/D > 295 nmol/D panic level
Age 1–4 0–29 µg/D 0–170 nmol/D
Age 4–10 8–65 µg/D 47–380 nmol/D
Age 10–15 15–80 µg/D 89–470 nmol/D
Age 4 years to adult 65–400 µg/D 384–2364 nmol/D
Age 4 years or less 40–260 µg/D 236–1535 nmol/D
is reachieved. At this time, 0.01-0.05 mg of histamine
phosphate in 0.5 mL of isotonic saline is injected rapidly
IV, and the readings are again followed to a basal level at
Interpretation: Normal subjects experience flushing,
headache, and slight blood pressure fall. An elevation in
blood pressure significantly greater than the cold pressure
response within 2 minutes of the injection, or an increase
in the basal levels of plasma catecholamines following
histamine stimulation, may indicate pheochromocytoma.
This test is used for diagnosis of pheochromocytoma in the
hypertensive phase. Barbiturates interfere with the test.
Method: When the resting patient has achieved a basal
blood pressure level, 5 mg of phentolamine are given
rapidly IV and the blood pressure is determined at 30
seconds intervals. Maximum effect appears in 2 minutes
and lasts for 3-5 minutes. If pheochromocytoma is strongly
suspected, a dose of 1 mg should be administered to avoid
profound and prolonged hypotension.
Interpretation: In normal individuals, phentolamine
causes a slight transient fall in blood pressure. In the
presence of pheochromocytoma with hypertension, a fall
in systolic blood pressure of more than 35 mm Hg and a
fall in diastolic blood pressure of more than 25 mm Hg
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