Optimal Use of Laboratory Tests in Pediatric

Endocrine Practice
Michael J. Bourgeois

Department of Pediatrics, Texas Tech University School of Medicine, Lubbock, Texas

Abstract. Optimal use of the laboratory in the practice of pediatric endocrinology begins with careful consideration of
the patient's history and physical findings. After a review of the differential diagnosis, an orderly plan of laboratory
investigation can be devised. This paper outlines some of the more common laboratory tests used to evaluate some
common pediatric endocrine disorders. The intent is to provide a concise, logical approach to choose the most efficient
approach. [Indian J Pediatr 2000; 67 (3) : 203-209]

Key words : Pediatric endocrinology; Laboratory tests; Diagnosis.

The use and interpretation of laboratory data in the
practice of pediatric endocrinology must be done in
the context of the individual patient's problems. The
evaluation of a patient should always start with a
thorough history and physical examination and
proceed to a problem list and differential diagnosis.
Only then will the physician be able to choose the
proper laboratory studies in the proper sequence.
While laboratory studies can be used to "screen"
patients with vague symptoms and signs, they are
best used to confirm a suspected diagnosis a n d / o r to
monitor the progress of a disease and its treatment.
This paper summarizes some of the commonly used
lab tests in these three areas by hormonal disorder.
Diabetes Mellitus
Insulin dependent diabetes mellitus (IDDM), the
most common hormonal disorder seen in children,
requires very little laboratory testing for diagnosis. A
child presenting with a history of polyuria,
polydypsia and weight loss, rarely requires more
than a serum blood glucose and urinalysis (to confirm
glucosuria and ketonuria) to make the diagnosis. At
the initial presentation, measurement of serum
ketones and electrolytes (Na, K, C1 and CO2) may be
indicated to check for ketosis, acidosis or electrolyte
imbalance.
With the increasing number of adolescents
Reprint requests : Michael J. Bourgeois, Department of
Pediatrics, Texas Tech University School of Medicine, 3601 4th
Street, Lubbock, Texas 7940. E-mail : pedmjb@ttuhsc.edu.
presenting with what appears to be Type 2, or non-
insulin dependent diabetes mellitus (NIDDM), and
other forms of glucose intolerance, the diagnosis is
not always clear. Still, the basic laboratory tests listed
above suffice in most cases. Table 1 lists the criteria
for diagnosing diabetes mellitus as recommended by
the American Diabetes Association 1. While an oral
glucose tolerance test (OGGT) is usually not
necessary to diagnose Type 2 diabetes mellitus, it
may be used to evaluate insulin secretion in relation
to glucose levels. Rarely should a glucose tolerance
test be done in a young person without measuring
insulin. To maximize the usefulness of such testing, it
is important to remember that patients need to be on
a high carbohydrate diet for at least 3 days prior to
the test.
Other laboratory tests that could be done during
the initial diagnosis of a patient with diabetes
mellitus include anti-islet cell antibodies, anti-insulin
auto- antibodies and C-peptide levels. While they
have been valuable research tools, they offer little
benefit in clinical practice.
In established patients with diabetes mellitus,
Types I and 2, routine self-blood glucose monitoring
(SBGM) has become the standard of care of ongoing
monitoring. Routine m e a s u r e m e n t of glycosylated
hemoglobin (GHb), or H g A l c , every 3 to 4 months
provides an independent assessment of ongoing
blood glucose control. Along with the usual clinical
monitoring, patients with diabetes should have
periodic screening for proteinuria. Measurement of

Indian Journal of Pediatrics, 2000; 67 (3) : 203-209

 M.J. 8our0eoi$

TABLE1. Criteria for the Diagnosis of Diabetes Mellitus ~

1. Symptoms of diabetes plus casual plasma glucose concentrations > 200 mg/dl (11.1 mmol/1). Casual is defined as
any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria,
polydipsia and unexplained weight loss.
or

2. Fasting plasma glucose >126 mg/dl (7.0 mmol/1). Fasting is defined as no caloric intake for at least 8 hours.
or

3. 2-hour plasma glucose > 200 mg/dl (11.1 mmol/1) during an oral glucose tolerance test (OGTF). The test should be
performed as described by WHO, using a glucose load containing the equivalent of 75-grams of anhydrous glucose
dissolved in water.
In the absence of unequivocal hyperglycemia with acute metabolic decompensation, these criteria should be confirmed by
repeat testing on a different day. The third measure (OGT1Ois not recommended for routine clinical use.
Reproduced with kind permission of Editor, Diabetes Care 1999; 22 (Suppl-1).

microalbumin on an annual or semi-annual basis is
r e c o m m e n d e d 2. In older patients and those with
family history of lipid abnormalities, periodic
assessment of serum triglyceride and cholesterol
levels is warranted.
Disorders of the Thyroid Gland
Laboratory evaluation of suspected or known-
thyroid disorders is probably the most
straightforward evaluation of endocrine disorders.
Since the vast majority of cases of suspected or
known hypothyroidism and hyperthyroidism are
primary in origin, a TSH (thyroid stimulating
hormone) and a total or free T4 (thyroxine) are
usually adequate to confirm the diagnosis. Until
recently, measurement of total T4 was the most
readily available method of assessing thyroid
hormone levels. Since most of the circulating T4 is
protein bound, alterations in serum proteins can alter
the results. Conditions such as pregnancy and the use
of oral contraceptives can elevate total T4 levels,
while low levels of proteins could give fictitiously
low levels of thyroxine. While more difficult to
perform and standardize, free T4 levels look to the
unbound fraction of circulating thyroid hormone. It is
not significantly affected by alterations in serum
proteins 3. The RT3U (Resin T3 Uptake) has
traditionally been used as an indirect assessment of
thyroid binding globulin (TBG). In recent years, the
availability of assays to directly measure TBG and
free-T4 levels, have reduced the need for the RT3U.
In patients who are clinically hyperthyroid but have
normal or low T4 levels, measuring a total or free T3
level is indicated to confirm the diagnosis of T3
thyrotoxicosis. Table 2 summarizes the more
204
common pattern of thyroid function tests seen and
their interpretation. When a patient is diagnosed with
a thyroid disorder (hyothyroidism or
hyperthyroidism), antibody testing is often done.
This might include antiperoxidase antibodies and
antithyroglobulin antibodies for suspected thyroiditis
and thyroid-stimulating immunoglobulins (TSI) or
long-acting thyroid antibodies (LATS) for suspected
Grave's disease. While these m a y provide some
insight into to the etiology of the patient's problem,
they rarely change the course of treatment.
While laboratory testing in primary
hypothyroidism is fairly straightforward, the
assessment of secondary (pituitary deficiency) or
tertiary (hypothalamic dysfunction) is more subtle.
Both should have a low T4 and TSH, but the results
are usually equivocal. When necessary a thyrotropin
releasing hormone (TRH) stimulation test can be
performed. To do the test the patient is given a dose
of TRFI ( 7 m c g / k g , m a x i m u m dose of 500 mug),
intravenously, and blood is d r a w n at 30-minute
intervals for 11,4to 2 hours to determine the TSH, and
sometimes, prolactin response. No rise in TSH'would
suggest secondary hypothyroidism and a sustained
rise would suggest tertiary hypothyroidism4~.
The same tests (T4 and TSH) are used to monitor
the progress of treatment of hyperthyroidism, as wei1
as hypothyrodism. Obviously, optimal therapy aims
to maintain both tests in the normal range. Because of
the half-life of T4, it is rarely necessary to repeat
thyroid function tests more than every 1 to 3 months.
Even in infants with congenital hypothyroidism,
where early treatment and normalization of T4 and
TSH levels are crucial to maximize outcome, this
interval is reasonable. The American Academy of
Indian Journal of Pediatrics, 2000; 67 (3)
 Optimal Use of Laboratory Tests in Pediatric E n d o c r i n e Practice
TABLE2. Patterns of Thyroid Function Tests & Interpretation
TSH Total T4 Free T4 RT3 U
E L L L
N or L E E E N
NorL Nor L N or L
N L L L
N L N E
N E N L
N = normal, E = elevated, L = low
Pediatrics 6 recommends the following schedule for
laboratory evaluations in children with congenital
hypothyroidism :
1. At 2 and 4 weeks after beginning L-thyroxine
treatment.
2. Every 1 to 2 months during the first year of
life.
3. Every 2 to 3 months during the second to
fourth years of life.
4. Every 3 to 12 months from the age of 3 years
until the completion of growth.
5. At more frequent intervals when compliance is
questioned or abnormal values are obtained.
Vogiatzi and Kirkland 7 support these intervals
during the first two years of life. They showed that
infants started on 0.0375 mg of L-thyroxine, daily,
required fewer dosage changes than infants started
on 0.025 mg daily.
Disorders of the Adrenal Gland
The normal circadian rhythm of ACTH and cortisol
production and age of the patient, as well as the
nature of the suspected disorder, must be kept in
mind as one considers the laboratory evaluation of
adrenal disorders. In children and adults, ACTH and
cortisol levels are higher in the mornir~g than evening.
Infants, especially newborns, w h o have not
established a normal sleep-wake cycle, may not have
the expected pattern.
In hypoadrenalcorticism, one expects to find low
levels of cortisol all through the day. If the condition
is due to primary failure of the gland (i.e., Addison's
disease), ACTH levels will be markedly elevated.
There may also be co-existing electrolyte imbalance
(hyponatremia and hyperkalemia). If the condition is
secondary (pituitary insufficiency) or tertiary
Indian Journal of Pediatrics, 2000; 67 (3)
TBG Total T3 Possible diagnoses
N NorL Primary hypothyroidism
N or E Primary hyperthyroidism
N E T3 thyrotoxicosis
Secondary/tertiary
N hypothyroidism;
Sick thyroid syndrome
L TBG deficiency
E TBG excess; pregnancy;
Oral contraceptives
(hypothalamic dysfunction), ACTH levels will be
low. In either case an ACTH .simulation test will show
a lack of rise in cortisol. This is done by giving 0.25 to
1 mg of synthetic ACTH 1-24 (cortrosyn),
intravenously, over 1 to 2 minutes, and measuring
cortisol levels every 30 minutes for 2 hours s. This test
has also been r e c o m m e n d e d as a w a y to evaluate
adrenal recovery from long-term suppression due to
high dose glucocorticoid therapy.
In evaluating a child for endogenous
glucocorticoid excess, a comparison of a morning and
evening cortisol level has been the traditional
screening method. Normally, the morning level is
expected to be 2 or 3 times higher than the evening
level. A more definitive test is to give the patient
dexamethasone - low dose (1 mg) one day and high
dose (8 rag) the next. Classic Cushing's disease (due
to excess pituitary secretion of ACTH) is indicated
when the cortisol level is suppressed by the high
dose, but not the low dose of dexamethasone. Lack of
suppression, even with high dose dexamethasone is
highly suggestive of an adrenal tumor 9. Any form of
endogenous Cushing's syndrome will usually require
some form of surgical intervention which, if
successful, may result in the need for subsequent
glucocorticoid replacement.
Improvements and refinements of immunoassay
techniques have made the assessment of problems of
adrenal androgen excess (congenital adrenal hyper-
plasia, virilizing tumours, etc.) much easier and more
straightforward than past years. No longer is it neces-
sary to collect 24-hour urine specimen of an infant.
For most patients, measurements of serum or plasma
17-alpha-hydroxyprogesterone, androstenedione, tes-
tosterone, and sometimes, dehydroepiandrostenedi-
one (DHEA) are sufficient in evaluating children for
205
 M.J. Bourgeois
excessive premature virilization. Occasionally, meas-
uring these hormones before and after a dose of
ACTH is more helpful in defining the problem8.
A child with ambiguous genitalia presents the
pediatrician with a social and possibly medical
emergency. Immediate evaluation is needed to
determine the appropriate gender assignment as well
as the need for glucocorticoid replacement. While it is
not a laboratory test, per se, a pelvic ultrasound is an
excellent first step. The demonstration of a uterus,
especially if ovaries are identified, clearly indicates
the appropriate gender assignment and virtually
assures that the child will have congenital adrenal
hyperplasia. Initial laboratory tests would include a
chromosomal analysis (to confirm chromosomal sex)
and serum or plasma 17-alpha-hydroxyprogesterone,
androstenedione and testosterone. In confirmed cases
of CAH on treatment, these same tests are used to
monitor treatment. The goal is to keep them
suppressed while allowing the child to grow
normally and avoiding Cushingoid features.
Disorders of Puberty
Children presenting with abnormalities of puberty,
both early and late, are among the most challenging
problems to assess. This is because random
laboratory testing is often equivocal and difficult to
interpret. As children enter puberty, gonadotropin
levels (LH and FSH) fluctuate dramatically and are
not good discriminators of pubertal stage. Gonadal
hormones (estrogen and progesterone) in girls also
cycle and "normal reference values" are different for
different stages of the menstrual cycle. In boys,
testosterone levels tend to be more stable, but still
show wide ranges of normalcy in early puberty.
Before deciding on any particular laboratory tests
it is helpful to consider what hormones are
responsible for what secondary sex characteristics
and the sequence in which they are expected to occur.
In girls, estrogen is the main pubertal hormone and is
responsible for breast development, fat
redistribution, increased vaginal secretions and
uterine changes, which ultimately led to menarche.
Pubic and axillary hair, seen in girls at puberty time,
are androgen mediated, much of which is produced
by the adrenal gland. While some "normally
developing" girls will have onset of pubic hair before
breast development, girls with precocious puberty
almost always have estrogen effect (breast
development, vaginal secretions or bleeding, etc.)
206
before pubic hair appears. A girl presenting with
early pubic hair development, especially if other
signs of virilization (clitoromegaly, etc.) are seen,
should be evaluated for androgen excess before being
worked up for precocious puberty.
When true central precocious puberty is
suspected, serum or plasma levels of LH, FSH, and
gonadal hormones (estradiol in girls and testosterone
in boys) are often measured. Unfortunately, the
results are usually equivocal. Definitive testing is
usually in the form of a gonadotropin releasing
hormone (GnRH) stimulation test. The patient is
given a dose of a gonadotropin releasing hormone
analog and serial levels of LH and FSH are done. The
higher the response, the further into puberty is the
patient. In confirmed cases of central precocious
puberty, treatment with gonadotropin releasing
hormone analogs (GnRHa) has been shown to be
effective. In treated girls the GnRH stimulation test
should be repeated periodically to confirm that
puberty is being suppressed. In boys, periodic
testosterone levels appear adequate to monitor
treatment.
Disorders of Growth
The laboratory can be a valuable adjunct to the
evaluation of a child with poor, or attenuated growth,
provided the physician performs a thorough history
and physical examination and carefully contemplates
the differential diagnosis. A better approach would
be to consider what, if any, lab tests would be
beneficial based on the patient's history and physical
findings.
The first step is to ensure that the child does
indeed have a growth problem. No laboratory testing
is needed for this step. Just a good history, including
growth records, and b)hysical exam. What is the
child's growth velocity? Does the child have growth
failure (growth velocity less than 2SD below the
mean) or short stature with normal growth velocity?
What is the family history? Are there any clinical
clues that point to a specific endocrine or
nonendocrine disorder (dysmorphic features, specific
signs and symptoms, septo-optic dysplasia, etc.)?
Obviously specific clues should be pursued with
appropriate testing.
The second step would be to decide if tests are
necessary to look for organ system problems. Some
organ system disorders are fairly obvious (cyanotic
heart disease, severe pulmonary problems, severe
Indian Journal of Pediatrics, 2000; 67 (3)
 Optimal Use of Laboratory Tests in Pediatric Endocrine Practice

TABLE3 : Commonly Used Provocative Agents for Growth Hormone Testing

Provocative Dose and Blood samples

route of administration (in minutes)

Arginine 0.5 gm/kg, maximum of 40 gm 0, 30, 60, 90

given IV over 30 minutes
Insulin 0.075 to 0.1 U/kg 0, 15, 30, 60
given IV bolus
Clonidine 5 mcg/kg, maximum of 250 mcg 0, 60, 75, 90, 120
L-Dopa 500 mg for weights over 30 kg 0, 40, 60, 90, 120
250 mg for weights 15 to 30 kg
Glucagon 1 rag, given IM or SQ 0, 60, 120, 180, 240

neurological dysfunction, etc.) Others may be less
obvious. Is there reason to suspect renal, hepatic, or
hematological dysfunction? Could the child's poor
growth be an early sign of evolving inflammatory
bowel disease? What is the child's nutritional status
and c o u l d it account for the child's poor growth?
Obviously, the answers to these questions would
determine if there w a s a need to do a complete blood
count, serum electrolytes, liver function studies, or
sedimentation rate.
The third step is the endocrine screening a n d / o r
testing. In children with growth failure in the absence
of significant organ s y s t e m disease, the first
endocrine test probably should be thyroid function
tests (T4 and TSH). While most patients with
hypothyroidism m a y have some signs and
symptoms, others may not. In short, poorly growing
girls, an additional consideration is a chromosomal
analysis to check for the possibility of Turner
syndrome.
Once all of the above considerations have been
exhausted the question about growth hormone is left.
Because of the circadian rhythm of growth hormone
secretion, random measurements of growth hormone
levels are rarely helpful. As a screening test, some
practitioners have used rigorous exercise in children
who are old enough to cooperate m. The child must be
fasting for at least four hours and run, climb stairs, or
ride an exercise bike 11for at least 20 minutes. Growth
hormone levels are d r a w n before and immediately
after the exercise. Depending on the assay, a growth
hormone level greater than 7 or 10 n g / d l is
considered normal.
Insulin-like growth factor-1 (IGF-1), or
s o m a t o m e d i n - C is a commonly used screening test.
However, it is important to recognize that normal
Indian doumal of Pediatrics, 2000; 67 (3)
values vary with age and pubertal status. Even mild
states of undernutrition will lower the level
significantly. Recently, the measurement of insulin-
like growth factor binding protein-3 (IGFBP-3) has
been recommended as a diagnostic too11%
In spite of increasing controversy, there is some
fairly universal agreement that the most definitive
way to diagnose growth hormone deficiency is to
demonstrate poor growth hormone secretion in
response to two provocative agents 13. Table 3 lists
some of the more common provocative agents,
recommended doses, and the commonly
r e c o m m e n d e d blood sampling intervals. There are
differing opinions as to whether or not a priming
agent-estrogen, testosterone, or propranolol-should
be used prior to the stimulation test la. The cutoff
value for growth hormone levels that define
"normal" from growth hormone deficiency has
changed over the years and varies from author to
author. It is important to know the type of assay and
the normative values of the laboratory you will be
using.
Children on growth hormone treatment for growth
hormone deficiency should be monitored carefully.
Routine laboratory testing is not usually needed, but
a child with a waning response to exogenous growth
hormone should have thyroid function tests done. An
occasional IGF-1 level m a y help assess compliance
and adequacy of the dose being used.
The child with accelerated growth presents a
similarly diverse set of considerations. What is the
child's age and family history? Is the child obese and
tall on that basis? Are there sirens of early sexual
development indicating precocious puberty,
excessive androgen production, etc.?
When growth hormone excess is suspected, a
207
 M.J. Bourgeois
serum IGF-I level is a good first step. It is usually
markedly elevated in pituitary gigantism.
Confirmation is obtained by measuring growth
hormone levels during an intravenous or oral glucose
tolerance test. A normal response shows the growth
hormone levels to be suppressed, while growth
hormone excess shows elevated levels13.
Diabetes Insipidus
As discussed earlier, the initial laboratory test of a
child with polyuria and polydypsia should be a
urinalysis and, possibly, a blood glucose to check for
diabetes mellitus. If there is no glucosuria, obviously
the polyuria cannot be explained on the basis of
elevated blood glucose levels. The differential
diagnosis shifts to some form of psychogenic or
compulsive water drinking, renal disease, or diabetes
insipidus (central or nephrogenic). Obviously, a
thorough history is important. Does the increased
drinking and urination occur only during the day, or
day and night? When did it start? Is there a family
history? Is there some pre-existing condition which
predisposes to one of these diagnosis? Is there a
history of hypernatremic dehydration?
There is no simple screening test for diabetes
insipidus. A high random urine specific gravity or
osmolality is good evidence against diabetes
insipidus, but is not always present. Obtaining an
early morning urine specimen may improve the
yield, but must be done with some caution. Children
with true diabetes mellitus are rarely able to tolerate
fluid restriction overnight. Serum electrolytes are
rarely helpful, except in the presence of obvious
dehydration.
The diagnosis of diabetes insipidus requires the
demonstration of a low, or relatively low, urine
osmolality in the face of an elevated or rising serum
osrnolality 14. The distinction between central and
nephrogenic DI is the responsiveness to exogenous
pitressin or DDAVP. Traditionally, this has been
accomplished by doing a water deprivation test.
Under controlled conditions, the patient is deprived
of water and sequential measurements are made of
vital signs, weight, urine output and osmolality, and
serum osmolality and electrolytes. The normal
response would be a decrease in urine output with an
increase in urine osmolality. If this does not happen
the patient is given a dose of aqueous pitressin or
208
DDAVP, at or before the onset of signs of
dehydration (weight loss, rise in serum osmolality
and sodium, etc.). A clear response (decrease in
urine output with a rise in urine osmolality) indicates
the presence of central diabetes insipidus (ADH
deficiency). No response would support the
diagnosis of nephrogenic diabetes insipidus. In recent
years, the availability of direct assays for
antidiurectic hormone have helped in the work up of
these patients. In stable patients on treatment, usually
periodic measurements of urine output and specific
gravity at home are the only lab needed monitoring.
During illnesses and periods of poor control, closer
attention will need to be given to the clinical and
laboratory findings of dehydration and electrolyte
imbalance.
Hypoglycemia
The differential diagnoses and course of evaluation,
of a child with hypoglycemia varies with age and
circumstances of the episode. In the newborn period
potential causes include transient neonatal
hypoglycemia, hyperinsulinism (as in
neisidioblastosis, islet cell hyperplasia etc.), hormone
deficiencies (growth hormone, adrenal etc.), and
metabolic disorders (glycogen storage disease,
galactosemia etc.). In older children, the incidences
of hormonal deficiencies and ketotic hypoglycemia
increase while that of metabolic disorders decrease.
As with other conditions, the laboratory
evaluation of a patient with hypoglycemia should be
decided upon after considering the clinical picture.
For infants, one needs to see if the mother has
diabetes, is there macrosoma, hepatomegaly, etc.?
Did the hypoglycemia start immediately or develop
after feedings started? For an older child, are there
signs suggesting a hormone deficiency, such as poor
growth, weakness, gastrointestinal upset,
hyperpigmentation, etc.?
An episode of spontaneous hypoglycemia offers its
own opportunity for evaluation. Blood samples taken
during such an episode can be assayed for glucose,"
insulin, growth hormone, and cortisol. Elevated
insulin levels in the face of low glucose levels is
suggestive of hyperinsulinemia. Low growth
hormone a n d / o r control levels in the face of
hypoglycemia and low insulin levels would suggest
these hormonal deficiencies. Additional lab studies,
Indian Journal of Pediatrics, 2000; 67 (3)
 Optimal Use of Laboratory Tests in Pediatric E n d o c r i n e Practice
such as urine for ketones, s e r u m lipids and free fatty
acids should be considered.
In o l d e r p a t i e n t s a c o n t r o l l e d fast can be
u n d e r t a k e n . As the fast p r o c e e d s , p e r i o d i c b l o o d
samples are t a k e n to m e a s u r e glucose, insulin, a n d
free fatty acids. As h y p o g l y c e m i a occurs additional
samples for g r o w t h h o r m o n e a n d cortisol can be
done.
REFERENCES
1. The Expert Committee on the Diagnosis and Classifi-
cation of Diabetes Mellitus. Report of the Expert
Committee on the Diagnosis and Classification of Di-
abetes Mellitus. Diabetes Care 1999; 22 (Supp. 1) : $5-
$19.
2. American Diabetes Association. Standards of medi-
cal care for patients with diabetes mellitus. Diabetes
Care 1999; 22 (Supp. 1) : $32-$41.
3. Lee P and Reiter E. Endocrine testing principles and
procedures. In: Kappy MS, Blizzard RM and Migeon
CJ (eds). Wilkins: The Diagnosis and Treatment ot
Endocrine Disorders in Childhood and Adolescence,
Springfield: Charles C. Thomas, 1994; 245-262.
4. Foley T, Matvaux P and Blizzard R. Thyroid disease.
In: Kappy MS, Blizzard RM and Migeon CJ (eds).
Wilkins: The Diagnosis and Treatment of Endocrine Dis-
orders in Childhood and Adolescence, Springfield :
Charles C. Thomas, 1994 : 457-533.
5. Moore WT and Eastman RC. Thyroid diseases. In :
Moore WT and Eastman RC (eds). Diagnostic
Endocrinology, Philadelphia : B.C. Decker Inc., 1990 :
127-165.
6. American Academy of Pediatrics. Newborn screen-
ing for congenital hypothyroidism: recommended
guidelines. Pediatrics 1993; 91 : 1203-1209.
7. Vogiatzi MG and Kirkland JL. Frequency and neces-
sity of thyroid functions tests in neonates and infants
with congenital hypothyroidism. Pediatrics 1997; 100
(3) : E6 (electronic article).
Indian Journal of Pediatrics, 2000; 67 (3)
Conclusion
The laboratory is a useful adjunct to the evaluation of
infants, c h i l d r e n a n d a d o l e s c e n t s w i t h s u s p e c t e d
endocrinological p r o b l e m s . With careful considera-
tion of the patient's history and physical findings, the
a p p r o p r i a t e c o u r s e of e v a l u a t i o n can be d e c i d e d
upon.
8. Migeon CJ and Donohoue PA. Adrenal disorders
In : Kappy MS, Blizzard RM and Migeon CJ (eds)
Wilkins: The Diagnosis and Treatment of Endocrine Dis-
orders in Childhood and Adolescence, Springfield:
Charles C. Thomas, 1994 : 717-856.
9. Kamilaris TC and Chrousos GP. Adrenal diseases.
In : Moore WT and Eastman RC (eds). Diagnostic
Endocrinology, Philadelphia : B.C. Decker Inc. 1990 :
79-109.
10. Johanson AJ and Morris GO. A single growth
hormone determination to rule out growth hormone
deficiency. Pediatrics 1977; 59 : 467.
11. Seip RL, Weltman A, Goodman D et al. Clinical
utility of cycle exercise for the physiological
assessment of growth hormone release in children.
Am l Dzs Child 1990; 144 : 998.
12. Blum WF, Ranke MB, Keitzmann K et al. A specific
radioimmunoassay of the growth hormone
dependent somatomedin binding protein: its use for
diagnosis of growth hormone deficiency. J Clin
Endocrin Metab 1990; 70 : 1292.
13 Blizzard RM and Johanson A. Disorders of growth.
In: Kappy MS, Blizzard RM, and Migeon CJ (eds.)
Wilkins: The Diagnosis and Treatment of Endocrine
Disorders in Childhood and Adolescence, Springfield :
Charles C. Thomas, 1994 : 383-433.
14. Bichet DG. Diabetes insipidus and vasopressin. In :
Moore WT and Eastman RC (eds.) Diagnostic
Endocrinology, Philadelphia : B.C. Decker Inc., 1990 :
111-126.
209