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186 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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hyperthyroidism, including that caused by subacute thyroiditis, which results in an absent or reduced uptake of iodine.
56
A high radioactive iodine uptake is noted with the follow-
ing conditions51:
• yrotoxicosis
• Iodine deciency
• Postthyroiditis
•
Withdrawal rebound aer thyroid hormone or antithyroid
drug therapy
A low test result occurs in the following persons51:
• Individuals with acute thyroiditis
• Euthyroid patients who ingest iodine- containing products
• Patients on exogenous thyroid hormone therapy
•
Patients who are taking antithyroid drugs such as
propylthiouracil
• Individuals with hypothyroidism
e radioactive iodine uptake test is aected by the body’s
store of iodine. erefore, the patient should be carefully questioned about the use of iodine- containing products before the
test. is test is contraindicated during pregnancy.
Antithyroid Antibodies
Normal range: varies with antibody
Antibodies that “attack” various thyroid tissue components can
be detected in the serum of patients with autoimmune disorders such as Hashimoto thyroiditis and Graves disease. yroid
microsomal antibody is found in 95% of patients with Hashimoto thyroiditis, 55% of patients with Graves disease, and 10%
of adults without thyroid disease. In patients who have nodular
goiters, high- antibody titers strongly suggest Hashimoto
thyroiditis as opposed to cancer. In Graves disease, hyperthyroidism is caused by antibodies, which activate TSH receptors.
In chronic autoimmune thyroiditis, hypothyroidism may be
caused by antibodies competitively binding to TSH receptors,
thereby blocking TSH from eliciting a response.
Results are reported as titers. Titers in excess of 1:100are
signicant and usually can be detected even during remission.
Antibodies (>1:10) to thyroglobulin are present in 60% to 70%
of adults with active Hashimoto thyroiditis but typically are not
detected during remission. Titers above 1:1,000are found only
in Hashimoto thyroiditis or Graves disease (25% to 10%, respectively). Lower titers may be seen in 4% of the normal population, although the frequency increases with the age in female
patients. e thyroid microsomal antibody and thyroglobulin
antibody serological tests may be elevated or positive in patients
with nonthyroidal autoimmune disease.
Anti-TSH receptor antibodies are present in virtually all
patients with Graves disease, but the test is usually not necessary for diagnosis. ese antibodies mostly stimulate TSH
receptors (eg, thyroid- stimulating immunoglobulin) but also
may compete with TSH and inhibit TSH stimulation of the thyroid gland. High titers allow a conrmation of Graves disease in
asymptomatic patients, such as those whose only manifestation
is exophthalmos.
66,67
66
Laboratory Diagnosis of HypothalamicPituitary-Thyroid Axis Dysfunction
e laboratory diagnosis of primary hypothyroidism can be made
with a low free T4 index and an elevated TSH concentration. e
presence of a low free T4 index and a normal or low serum TSH
concentration indicates secondary or tertiary hypothyroidism or
nonthyroid illness. In such patients, the T3 resin uptake may dierentiate between hypothyroidism and a low T4 state due to nonthyroid illness. An elevated reverse T3 concentration also suggests
nonthyroid illness. T3 is of limited usefulness in diagnosing hypothyroidism because it may be normal in up to one- third of patients
with hypothyroidism.
55,61
With the availability of ultrasensitive TSH
assays, many clinicians begin their evaluations with this test.
e total serum T4 and free T4 or free T4 indexes are commonly
used and are increased in almost all patients with hyperthyroidism.
Usually, both T3 and T4 are elevated. However, a few (<5%) patients
with hyperthyroidism exhibit normal T4 with elevated T3 (T3 toxicosis). Second- line tests such as antithyroid antibody serologies are
necessary to diagnose autoimmune thyroid disorders.
66
e adrenal glands are located extraperitoneally at the upper
poles of each kidney. e adrenal medulla, which makes up 10%
of the adrenal gland, secretes catecholamines (eg, epinephrine
and norepinephrine). e adrenal cortex, which comprises 90%
of the adrenal gland, is divided into three areas.
1.
e outer layer of the adrenal gland, known as the zona
glomerulosa, makes up 15% of the adrenal gland and is
responsible for production of aldosterone, a mineralocorti-
coid that regulates electrolyte and volume homeostasis.
2.
e zona fasciculata, located in the center of the adrenal
gland, occupies 60% of the gland and is responsible for gluco-
corticoid production. Cortisol, a principal end product of
glucocorticoid production, regulates fat, carbohydrate, and
protein metabolism. Glucocorticoids maintain the body’s
homeostasis by regulating bodily functions involved in stress
as well as normal activities.
3. e zona reticularis makes up 25% of the adrenal gland and
secretes mostly inactive androgen precursors that undergo
peripheral conversion to adrenal androgens, such as dehy-
droepiandrosterone (DHEA), DHEA sulfate (DHEA-S),
and androstenedione (the precursor to testosterone). ese
hormones inuence the development of the reproductive
68,69
system.
Cushing Syndrome
Cushing syndrome, rst described 70 years ago, is the result
of excessive concentrations of cortisol. It is an extremely rare
disease in children, with a peak in adults in the third or fourth
decade. In most cases, hypercortisolism is the result of overproduction of cortisol by the adrenal glands due to an ACTHsecreting pituitary tumor. Long- term use of glucocorticoids, the
most common cause of Cushing’s disease, and adrenal tumors
can result in hypercortisolism.
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Patients with hypercortisolism generally present with facial
plethora (moon face) as a result of atrophy of the skin and
underlying tissue. A common sign of hypercortisolism is fat
accumulation in the dorsocervical area oen referred to as “buffalo hump.” Other cardinal signs and symptoms include hypertension, osteopenia, glucose intolerance, myopathy, bruising,
back pain, proximal muscle weakness, and depression. Hyperpigmentation is present in patients with ACTH- secreting pituitary tumors. Hair loss, acne, and oligomenorrhea are also the
result of superuous cortical secretion.
70
Diagnostic Tests
It is important to rule out iatrogenic Cushing’s syndrome when
there is long- term steroid therapy and assess pretest probability
of Cushing’s syndrome based on relatively specic signs stated
previously (Minicase 5).
MINICASE 5
Steroid-Induced Hypercortisolism
In healthy individuals, the level of serum cortisol reaches a
peak in the morning around 7 a.m. to 9 a.m. (5 to 23 mcg/dL)
and reaches the lowest level between bedtime and 2 a.m. (usually <5 ug/dL).
One of the rst signs of Cushing’s syndrome is the loss of
this diurnal variation. Accordingly, the three rst- line biochemical screening tests recommended for the diagnosis of endogenous hypercortisolism are to prove that the patients has lost
this normal secretion of cortisol, and thus it is recommended
that patients are screened with these tests. e following tests
are used to identify patients with Cushing syndrome: 24- hour
urine- free cortisol (UFC), midnight plasma cortisol, and the
low- dose dexamethasone suppression test (DST) using 1 mg
for the overnight test or 0.5 mg every 6 hours for the 2- day
study. e most frequently used test to identify patients with
hypercortisolism is the 24- hour UFC test, which measures free
Teresa S. is a 35- year- old woman with a past medical history of
type 2 diabetes that was diagnosed in her late 20s. She has been
taking metformin 1,000 mg twice a day regularly since her diagnosis.
TeresaS. was diagnosed with rheumatoid arthritis 6months ago
and started on regular treatment with prednisolone 30 mg daily. She
reports to her primary care provider for general muscle weakness
and low back pain. She has been having low back pain for a little
over 4 months. The general muscle weakness has been getting
progressively worse over the past month and is beginning to concern
her. Teresa S. also reports having trouble making it through her
Zumba class on Tuesdays and Thursdays. She says that lately she
has little interest in her regular activities and has been experiencing
fatigue without physical exertion. Lastly, TeresaS. reports having
irregular menstrual cycles for the past 2 years accompanied by
unexplained weight gain in her abdomen.
Physical exam reveals purple/pink stretch marks on arms, abdomen,
and thighs. The patient has multiple cuts and bruises on her arms and
hands, with an explanation of having thin skin. The patient is obese
with noticeable fatty deposits in the upper back and midsection. Her
BP is 154/76mm Hg, and her heart rate is 74 beats/min.
The patient would like to have little to no back pain. She also would
like to be able to increase her strength and endurance to resume
her normal Zumba classes twice a week. Goals for her blood test
results are as follows:
• Sodium, 142 mEq/L (136 to 142 mEq/L)
• Potassium, 3.3 mEq/L (3.8 to 5 mEq/L)
• Chloride, 99 mEq/L (95 to 103 mEq/L)
• BUN, 28 mg/dL (8 to 23 mg/dL)
• SCr, 1.8 mg/dL (0.6 to 1.2 mg/dL)
• Hct, 40% (36% to 45%)
• WBC count, 6.2 × 10
3
10
cells/mm3)
3
cells/mm3 (4.8 to 10.8 ×
• Calcium, 10 mg/dL (9.2 to 11 mg/dL)
• Glucose, 180 mg/dL (70 to 110 mg/dL)
• Ketones, 0 at 1:8 serum dilution (normal = 0)
• Osmolality, 285 mOsm/kg (280 to 295 mOsm/kg)
• Triglycerides, 207 mg/dL (10 to 150 mg/dL)
• Lipase, 1.0 units/mL (<1.5 units/mL)
• Magnesium, 1.7 mEq/L (1.3 to 2.1 mEq/L)
• Hemoglobin A1c, 6.1 (4% to 5.6%)
• 8 a.m. Cortisol, 33.4 mcg/dL
QUESTION: Based on the subjective and objective data provided,
what is the most likely diagnosis for this patient? What signs and
symptoms support the diagnosis? What could have precipitated
this disorder?
DISCUSSION: The patient complained of unusual fatigue, back pain,
headaches, irregular menstrual cycles, generalized weakness, and
a recent lack of interest in her normal hobbies/activities. TeresaS.’s
reports are accompanied by objective findings of elevated BP,
proximal weakness, purple/pink stretch marks, multiple bruises,
and noticeable fatty deposits.
The diagnosis of hypercortisolism due to the chronic use of
prednisolone is supported by her lab results of an elevated 8 a.m.
serum cortisol of 33.4 mcg/dL, potassium level of 3.3 mmol/L,
elevated fasting blood glucose level 180 mg/dL, and serum
triglyceride levels of 207 mg/dL. Based on subjective and objective
evidence, the patient is diagnosed as having Cushing syndrome
caused by the chronic use of prednisolone. The prednisolone dose
is tapered, alternative treatment options for rheumatoid arthritis are
considered, and the serum cortisol level is measured after 3 months
during a follow- up appointment. BP and cholesterol levels will be
rechecked at the follow- up appointment.
188 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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cortisol levels and creatinine in a urine sample that is collected
over a 24- hour period. Laboratory tests in adults with Cushing
syndrome include the following results:
1. 24- hour UFC at least three times above normal
2. Midnight plasma cortisol 5 mcg/dL (138 mmol/L) or more
3.
Low- dose DST plasma cortisol exceeds 2 mcg/dL (50 nmol/L)
when drawn between 8:00 a.m. and 9:00 a.m.
71
Of the suppression tests, the overnight DST, is the least
laborious test to perform. e patient is given 1 mg of dexamethasone at 11:00 p.m. A plasma cortisol levels is obtained at
8:00 a.m. the next morning. Patients with Cushing syndrome
have high cortisol concentrations (>5 mcg/dL or >138 nmol/L)
because of an inability to suppress the negative- feedback mechanism of the hypothalamic- pituitary- adrenal axis.
63,64
Once hypercortisolism is conrmed, one of the following
tests should be performed to identify the source of hypersecretion, which could include the pituitary gland, adrenal gland, or
production from an ectopic site. Such tests include high- dose
DST; plasma ACTH via immunoradiometric assay (IRMA)
or RIA; adrenal vein catheterization; metyrapone stimulation test; adrenal, chest, or abdominal computed tomography;
corticotropin- releasing hormone (CRH) stimulation test; inferior petrosal sinus sampling; and pituitary magnetic resonance
imaging. Other possible tests and procedures include insulininduced hypoglycemia, somatostatin receptor scintigraphy,
desmopressin stimulation test, naloxone CRH stimulation test,
loperamide test, hexarelin stimulation test, and radionuclide
imaging. Additional tests should be performed to conrm the
diagnosis because other factors (eg, starvation, topical steroid
application, and acute stress) inuence the results of the previously mentioned tests.
69,70
Plasma ACTH concentrations can be measured by RIA procedures. Interpretation of the results is as follows:
•
ACTH levels <10 pg/mL indicate an ACTH- independent
adrenal source, such as an adrenal tumor or long- term use
of steroids
•
ACTH levels between 5 and 10 pg/mL should be followed
by a CRH test
•
ACTH levels >10 pg/mL indicate an ACTH- dependent
syndrome
e CRH test can be employed to determine if the source of
hypercortisolism is pituitary or ectopic (extrapituitary). Baseline
ACTH and CRH levels are obtained. en, ACTH and cortisol levels are measured 15 to 30 and 45 to 60 minutes aer the
administration of a 100- mcg IV dose of CRH. A 50% increase
from baseline in ACTH levels indicates an ACTH- dependent
syndrome.
70
Adrenal Insufficiency (Addison Disease)
Adrenal insuciency (Addison disease or primary adrenal insufciency) is the result of an autoimmune destruction of all regions
of the adrenal cortex. Tuberculosis, fungal infections, acquired
immunodeciency syndrome, metastatic cancer, and lymphomas can also precipitate adrenal insuciency. Adrenal insufciency results in deciencies in cortisol, aldosterone, and
androgens. Patients usually present with weakness, weight loss,
increased pigmentation, hypotension, GI symptoms, postural
dizziness, and vertigo.
Secondary adrenal insuciency can result from the use of
high doses or extended duration of use of exogenous steroids,
which suppress the hypothalamic- pituitary axis, resulting in a
decrease in the release of ACTH. Patients with secondary adrenal insuciency maintain normal aldosterone levels and do not
exhibit signs of hyperpigmentation.
71,72
Diagnostic tests. Measurement and interpretation of plasma
corticotropin (ACTH) levels are recommended to distinguish
between primary adrenal insuciency and secondary adrenal
insuciency. A high normal or elevated ACTH concentration
is consistent with primary adrenal insuciency, whereas a low
normal or undetectable level suggests secondary adrenal insufciency.
e cosyntropin stimulation test is used to diagnose patients
with low cortisol levels. Patients receive 250 mcg of synthetic
ACTH or cosyntropin intravenously or intramuscularly. Serum
cortisol levels are drawn at the time of injection and 30 minutes
and 1 hour aer injection. Cortisol levels >18 to 20 mcg/dL (497
to 552 nmol/L) indicate an adequate response from the adrenal
gland, thus ruling out adrenal insuciency. e cosyntropin
stimulation test results may be normal in patients with secondary adrenal insuciency or mild primary adrenal insuciency
due to the high dose of corticotropin given. erefore, many
endocrinologists recommend that higher cuto values (≥22 to
25 mcg/dL or 607 to 690 nmol/L) be used. To distinguish primary from secondary adrenal insuciency, ACTH, renin, and
aldosterone levels are measured.
71,72
Diabetes insipidus is a syndrome in which the body’s inability to
conserve water manifests as excretion of large volumes of dilute
urine. is section explores related pathophysiology, types of
diabetes insipidus, and interpretation of test results to evaluate
this disorder.
73
Physiology
Normally, serum osmolality is maintained around 285 mOsm/kg
and is determined by the amounts of sodium, chloride, bicarbonate, glucose, and urea in the serum. e excretion of these
solutes along with water is a primary factor in determining
urine volume and concentration. In turn, the amount of water
excreted by the kidneys is determined by renal function and
ADH (vasopressin). ADH reduces renal elimination of water
and produces concentrated urine.
ADH is synthesized in the hypothalamus and stored in the
posterior pituitary gland. is hormone is released into the circulation aer physiologic stimulation, such as an increase in serum
osmolality or blood volume detected by the osmoregulatory centers in the hypothalamus.
osmotic threshold for ADH release, whereas nausea— but not
vomiting— strongly stimulates ADH. In general, α- adrenergic
agonists stimulate ADH release, whereas β- adrenergic agonists inhibit release and acts on the distal renal tubule and the
73,74
Congestive heart failure lowers the
CHAPTER 9 • EndoCRinE disoRdERs 189
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collecting duct to cause water reabsorption. Chlorpropamide
potentiates the eect of ADH on renal concentrating ability.
When ADH is lacking or the renal tubules do not respond to
the hormone, polyuria ensues. If the polyuria is severe enough,
a diagnosis of diabetes insipidus is considered.
73,74
Clinical Diagnosis
Diabetes insipidus should be dierentiated from other causes of
polyuria, such as osmotic diuresis (eg, hyperglycemia, mannitol,
and contrast media), renal tubular acidosis, diuretic therapy,
and psychogenic polydipsia. Patients usually excrete 16 to 24L
of dilute urine in 24 hours. e urine specic gravity is <1.005
and urine osmolality <300 mOsm/kg.73 As long as the thirst
mechanism is intact and a patient can drink, no electrolyte
problems result. However, if a patient is unable to replace uids
lost through excessive urine output, he or she can develop dehydration and hypernatremia.
Although diabetes insipidus is usually caused by a defect in
the pituitary secretion (neurogenic, also called central) or renal
activity (nephrogenic) of ADH, it can also be caused by a defect
in thirst (dipsogenic) or psychological function (psychogenic),
with resultant excessive intake of water. If le untreated, diabetes
insipidus can lead to signicant morbidity and mortality; therefore, the underlying cause should be sought to ensure proper
diagnosis and therapy. e specic type of diabetes insipidus
oen can be identied by the clinical setting. If the diagnosis is
equivocal, a therapeutic trial with an antidiuretic drug or measurement of plasma ADH is necessary (Table9-12).
Central Diabetes Insipidus
Central diabetes insipidus (ADH deciency) may be the result
of any disruption in the pituitary- hypothalamic regulation of
ADH. Patients oen present with a sudden onset of polyuria (in
the absence of hyperglycemia) and preference for iced drinks.
Tumors or metastases in or around the pituitary or hypothalamus, head trauma, neurosurgery, genetic abnormalities,
Guillain-Barré syndrome, meningitis, encephalitis, toxoplasmosis, cytomegalovirus, tuberculosis, and aneurysms are some
of the known causes. In addition, phenytoin and alcohol inhibit
74
ADH release from the pituitary. In response to decient secretion of ADH and subsequent hyperosmolality of the plasma,
thirst is stimulated. e absence of eective ADH results in
polyuria.
73
Nephrogenic Diabetes Insipidus
In nephrogenic diabetes insipidus (ADH resistance), the secre-
tion of ADH is normal, but the renal tubules do not respond
to ADH.75 In the kidney, the actions of ADH on its type-2
receptor (V2R) induce increased water reabsorption in addition
to polyphosphorylation and membrane targeting of the water
channel aquaporin-2. Mutations in the V2R have been found
to be associated with nephrogenic diabetes insipidus. Causes
of nephrogenic diabetes insipidus include chronic renal failure,
pyelonephritis, hypokalemia, hypercalciuria, malnutrition,
genetic defects, and sickle cell disease. Additionally, lithium
toxicity, colchicine, glyburide, demeclocycline, cidofovir, and
methoxyurane occasionally cause this disorder.
74
Diabetes Insipidus of Pregnancy
A transient diabetes insipidus, originally thought to be a form of
nephrogenic diabetes insipidus, may develop during late pregnancy from excessive vasopressinase (ADHase) activity. is
kind of diabetes insipidus is associated with preeclampsia with
liver involvement. Because vasopressinase does not metabolize
desmopressin acetate, this is the treatment of choice.
Laboratory diagnosis. Some clinicians avoid dehydration
testing and rely on measuring plasma ADH concentrations
to distinguish central from nephrogenic diabetes insipidus.
In otherwise healthy adults, the average basal plasma ADH
concentration is 1.3 to 4 pg/mL (1.2 to 3.7 pmol/L). Based on
medical history, symptoms, and signs, an elevated basal plasma
ADH level almost always indicates nephrogenic diabetes insipidus. If the basal plasma ADH concentration is low (<1 pg/mL)
or immeasurable, the result is inconclusive and a dehydration
test should be done.
e theory behind the water deprivation test is that in normal
individuals, dehydration stimulates ADH release and the urine
becomes concentrated. An injection of vasopressin at this point
76
TABLE 9-12. Differential Diagnosis of Diabetes Insipidus Based on Water Deprivation Test
URINE
SPECIFIC
DIAGNOSIS
Normal individuals
Central diabetes
GRAVITY
>1.015
<1.010 <300 <300
insipidus
Nephrogenic
<1.010 <300 <300
diabetes insipidus
Source: Sowers JR, Zieve FJ. Clinical disorders of vasopression. In: Lavin N, ed. Manual of Endocrinology and meta bolism. Boston, MA: Little,
Brown; 1986-65-74. Young DS. Effects of Drugs on Clinical Laboratory Tests. 3rd ed. Washington, DC: American Association for Clinical
Chemistry Press; 1990.
AVERAGE URINE
OSMOLALITY
(mOsm/kg)
300–800
PLATEAU URINE
OSMOLALITY
(mOsm/kg)
<1,600
AVERAGE SERUM
OSMOLALITY
(mOsm/kg)
CHANGE IN URINE
OSMOLALITY AFTER
VASOPRESSIN
280–295 Little change
Normal or increased Increases
Normal or increased Little change
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does not further concentrate the urine. In contrast, the urine of
patients with central diabetes insipidus is not maximally concentrated aer uid deprivation but will be aer vasopressin
injection.
77
To perform the test, patients are deprived of uid intake (up
to 18 hours) until the urine osmolality of three consecutive samples varies by no more than 30 mOsm/kg. Urine osmolality and
specic gravity are measured hourly. At this time, 5 units of
aqueous vasopressin is administered subcutaneously, and urine
osmolality is measured 1 hour later. Plasma osmolality is measured before the test, when urine osmolality has stabilized, and
aer vasopressin has been administered.
In healthy individuals, uid deprivation for 8 to 12 hours
results in normal serum osmolality and a urine osmolality of 800mOsm/kg. e urine osmolality plateaus aer 16
to 18hours. Patients with central diabetes insipidus have an
immediate rise in urine osmolality to 600 mOsm/kg, with a
corresponding decrease in urine output with vasopressin injection. Patients with nephrogenic diabetes insipidus are unable to
increase urine osmolality above 300 mOsm/kg because vasopressin injection has little eect.
77
In addition to being inconvenient and expensive, dehydration
procedures are reliable only if the diabetes insipidus is severe
enough that— even with induced dehydration— the urine still
cannot be concentrated.
Accurate interpretation requires consideration of potential confounding factors. If the laboratory cannot ensure accurate and precise plasma (not serum) osmolality measurements,
plasma sodium should be used. Patients should be observed for
nonosmotic stimuli, such as vasovagal reactions, that may aect
ADH release. Lastly, if the patient has previously received ADH
therapy, ADH antibodies may cause false- positive results suggestive of nephrogenic diabetes insipidus.
74,75
Endocrine disorders typically result from a deciency or excess
of a hormone. Laboratory tests that measure the actual hormone,
precursors, or metabolites can help to elucidate whether and
why a hormonal or metabolic imbalance exists. Tests used to
assess thyroid, adrenal, glucose, and water homeostasis or receptors have been discussed.
e FPG and the 2- hour PPG concentration tests are the
most commonly performed tests for evaluation of glucose
homeostasis. Glycated hemoglobin assesses average glucose
control over the previous 2 to 3 months, whereas fructosamine
assesses average control over the previous 2 to 3 weeks.
DKA and hyperosmolar nonketotic hyperglycemia are the
most severe disorders along the continuum of glucose intolerance. Extreme hyperglycemia (600 to 2,000 mg/dL) with insignicant ketonemia/acidosis is consistent with hyperosmolar
nonketotic hyperglycemia, whereas less severe or even absent
hyperglycemia with ketonemia and acidosis is characteristic of
DKA (350 to 650 mg/dL). Hyperglycemia with ketonemia and
acidosis is characteristic of DKA.
yroid tests can be divided into those that (1) measure the concentration of products secreted by the thyroid gland (T3 and T4);
(2) evaluate the integrity of the hypothalamic- pituitary- thyroid
axis (TSH and TRH); (3) assess intrinsic thyroid gland function (radioactive iodine uptake test); and (4) detect antibodies to thyroid tissue (thyroid microsomal antibody). Although
TSH concentrations are usually undetectable or <0.3 milliunit/L
in patients with hyperthyroidism, T4 concentrations are usually
high in patients with overt hyperthyroidism. e TSH concentrations are low or undetectable in patients with hypothyroidism from hypothalamic or pituitary insuciency and in patients
with nonthyroidal illness. In contrast, TSH concentrations are
high and T4 concentrations are low in patients with primary
hypothyroidism.
Glucocorticoids maintain the body’s homeostasis by regulating bodily functions involved in stress and normal activities.
Sex hormone precursors are all produced in the adrenal glands.
Cushing syndrome is the result of excessive cortisol in the body.
Addison disease occurs when there is a deciency in cortisol
production.
Diabetes insipidus is a syndrome in which the body’s inability to conserve water manifests as excretion of large volumes of
dilute urine. It most oen is caused by a defect in the secretion
(neurogenic, also called central) or renal activity (nephrogenic)
of ADH. Urine and plasma osmolality are key tests. With the
advent of high- performance assays, the use of plasma vasopressin concentrations to distinguish central from nephrogenic types
may obviate the need for provocative iatrogenic dehydration
testing procedures.
LEARNING POINTS
1.
Which patients with diabetes benefit from selfmonitoring of blood glucose and how can different test
results (premeal, postmeal, and fasting) be used in diabetes management?
ANSWER: The ADA recommends self- monitoring of blood glu-
cose for all people with dia betes who use insulin.78 Self- monitoring
provides information that patients can use to adjust insulin doses,
physical activity, and carbohydrate intake in response to high or
low glucose levels. The goal of selfis to prevent hypoglycemia while maintaining blood glucose levels as close to normal as possible. Most people with type 1 DM
must use selfAlthough patients with type 2 DM receiving insulin therapy ben-
monitoring of blood glucose for individuals with type 2 DM who
78 The ADA states that
self- monitoring of blood glucose may be desirable in patients
treated with sulfonylureas or other drugs that increase the risk
of hypoglycemia.78 The frequency and timing of self- monitoring
of blood glucose vary based on several factors, including an individual’s glycemic goals, the current level of glucose control, and
the treatment regimen. The ADA recommends self- monitoring
of blood glucose three or more times per day for most individuals who have type 1 DM and seven- point testing for pregnant
women who use insulin.74 More frequent testing (four to six times
per day) may be needed to monitor pump therapy.
monitoring of blood glucose to achieve this goal.
monitoring of blood glucose
79,80
In patients
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with type 1 DM, self- monitoring of blood glucose is most commonly recommended four times a day: before meals and at bedtime. A periodic 2:00 a.m. test is recommended to monitor for
nighttime hypoglycemia. These measurements are used to adjust
insulin doses and attain the fasting glucose goal. However, there
is evidence that blood glucose measurements taken after lunch,
after dinner, and at bedtime have the highest correlation to A1c
79,80
values.
When premeal or fasting goals are reached but A1c
values are not optimal, self- monitoring of blood glucose 2 hours
after meals can provide guidance for further adjustment of insulin regimens. Postmeal measurements are also used to evaluate the effects of rapid- acting insulins (eg, lispro, aspart), which
are injected just before meals. Patients with type 2 DM who use
multiple daily injections of insulin should generally test as often
as patients with type 1 (at least three times per day). Patients on
testing before meals and at bedtime when therapy is initiated or
if control is poor.
2.
What factors should a pharmacis t consider when helping
81,82
a patient select an SMBG meter?
ANSWER: Meters offer a variety of features that should be con-
sidered in the selection process. The key features are meter size;
the amount of blood required for each test; ease of use; speed
of testing; cleaning and calibration requirements; alternate site
testing capability; meter and test strip cost; language choice;
and the capability to store readings, average readings over time,
and download data. Patient factors to consider include lifestyle (where they will be testing, importance of portability, and
speed), preferences (importance of small sample size or alternate
site capability), dexterity (whether they can they operate the
meter), visual acuity, and insurance coverage.
83
3. What are some of the advantages of CGM?
ANSWER: Continuous glucose monitoring can provide a near-
continuous readout of interstitial glucose concentration, which
identify trends and patterns in glucose control with only a single
needle stick to place the sensor. In addition, in the case of realtime CGM, monitors can be programmed to alarm for either high
or low glucose values, thus allowing the patient to treat for these
abnormal values and potentially reduce the risks associated with
hypoglycemia or hyperglycemia as well as diminish patient fear
of such an occurrence.
23,24
4. What factors may affect the accuracy of an A1c result?
ANSWER: False elevations in A1c may be noted with uremia,
chronic alcohol intake, and hypertriglyceridemia. Patients who
have diseases with chronic or episodic hemolysis (eg, sickle cell
disease and thalassemia) generally have spuriously low A1c concentrations caused by the predominance of young RBCs (which
carry less A1c) in the circulation. In splenectomized patients and
those with polycythemia, A1c is increased. If these disorders are
stable, the test still can be used, but values must be compared
with the patient’s previous results rather than published normal
values. Both falsely elevated and falsely lowered measurements
of A1c may also occur during pregnancy. Therefore, it should not
be used to screen for GDM.
10,12,15
5.
Which laboratory tests are recommended in the initial
evaluation of thyroid disorders?
ANSWER: The principal laboratory tests recommend ed in the ini-
tial evaluation of a suspected thyroid disorder are the sensitive TSH
and the free T4 levels. Free T4rometabolic status. The free T4 is the most reliable diagnostic test
for the evaluation of hypothyroidism and hyperthyroidism when
thyroid hormone–binding abnormalities exist. If a direct measure
of the free T4 level is not available, the estimated free T4 index can
provide comparable information. Total serum T4 is still the standard initial screening test to assess thyroid function because of its
wide availability and quick turnaround time. In most patients, the
total serum T4 level is a sensitive test to evaluate the function of
the thyroid gland. This test measures both bound and free T
is, therefore, less reliable than the free T4 or free T4 index when
alterations in TBG or nonthyroidal illnesses exist. The serum TSH
is the most sensitive test to evaluate decreased thyroid function.
TSH secreted by the pituitary is elevated in early or subclinical
hypothyroidism (when thyroid hormone levels appear normal)
or when thyroid hormone replacement therapy is inadequate.
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194 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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QUICKVIEW | Total Serum T
3
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults and children 80–200 ng/dL Affected by TBG changes
(1.2–3.1 nmol/L)
SI conversion factor = 0.0154 (nmol/L)
Critical value Not established Extremely high or low values should be
reported quickly
Natural substance? Yes Only 0.2% of T
is unbound
3
Inherent activity? Only free portion Total assumed to correlate with
activity
free T
3
Location
Production and storage 20%–25% secreted by thyroid
Bound mostly to thyroglobulin
gland, remainder produced by
conversion of T
to T
4
3
Secretion/excretion From thyroid, liver, and kidneys
to blood
Major causes of…
High results
Hyperthyroidism
and T3 supplements
T
4
Other causes
Associated signs and
symptoms
Signs and symptoms of
hyperthyroidism
Nervousness, weight loss, heat intolerance,
tachycardia, diaphoresis
Low results Hypothyroidism
Other causes
Propranolol
Propylthiouracil
Glucocorticoids
Associated signs and
symptoms
Signs and symptoms of
hypothyroidism
Lethargy, constipation, dry skin, cold
intolerance, slow speech, confusion
After insult, time to…
Initial elevation or depression Weeks to months Increases within hours in acute T
Peak values Weeks to months Increases within hours in acute T
or T3 overdose
4
or T3 overdose
4
Normalization Usually same time as onset Assumes insult removed or effectively treated
Drugs often monitored
T
4
and T
3
Other drugs
with test
Causes of spurious results Increased or decreased TBG leads to
falsely increased or decreased total
serum T
, respectively; nonthyroidal
3
illness leads to falsely increased or
decreased total serum T
3
CHAPTER 9 • EndoCRinE disoRdERs 195
https://t.me/med1917
QUICKVIEW | Total Serum T
4
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults and children 5.5–12.5 mcg/dL (71–161 nmol/L) Affected by TBG changes with nonthyroidal
illness
SI conversion factor = 12.87 (nmol/L)
Newborn/3–5 days 11–23/9–18 mcg/dL Affected by TBG changes with nonthyroidal
illness
Critical value Not established Extremely high or low values should be reported
quickly, especially in newborns
Natural substance? Yes Only 0.02% of T
is unbound
4
Inherent activity? Only free portion Total assumed to correlate with free T4 activity
Location
Production and storage Thyroid gland Bound mostly to thyroglobulin
Secretion/excretion From thyroid to blood About 33% converted to T
outside thyroid
3
Major causes of…
High results
Hyperthyroidism
supplements
T
4
Other causes (Tables
9-6
and 9-8)
Associated signs and
symptoms
Signs and symptoms of
hyperthyroidism
Nervousness, weight loss, heat intolerance,
tachycardia, diaphoresis
Low results Hypothyroidism
Other causes (Tables
9-5
and 9-8)
Signs and symptoms of
hyperthyroidism
Lethargy, constipation, dry skin, cold
intolerance, slow speech, confusion
After insult, time to…
Initial elevation or depression Weeks to months Increases within hours in acute T
Peak values Weeks to months Increases within hours in acute T
overdose
4
overdose
4
Normalization Usually same time as onset Assumes insult removed or effectively treated
Drugs often monitored with
T
4
Other drugs
test
Causes of spurious results Increased or decreased TBG leads
to falsely increased or decreased
total serum T
, respectively;
4
nonthyroidal illness leads to
falsely increased or decreased
total serum T
4
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