Article endocrinology

Neonatal Thyroid Function

Shiri B. Feingold, MD,*
Rosalind S. Brown, MD, Abstract
CM* Postnatal changes in thyroid hormone economy reflect the adjustment of the fetus to
the extrauterine environment. Thyroid-stimulating hormone (TSH) surges soon after
birth, resulting in thyroxine (T4) concentrations that are higher in the first postnatal
Author Disclosure week than at any other time of life and in circulating triiodothyronine (T3) concen-
trations that are three to four times higher than in the fetus. In preterm infants born
Drs Feingold and
after 31 weeks’ gestation, the pattern is similar, although less pronounced; in younger
Brown have disclosed
infants, a decrease in TSH may be seen, accompanied by a low T4 concentration.
no financial Usually the free T4 concentration is less affected than the total T4. Thyroid hormone
relationships relevant synthesis is critically dependent on an adequate prenatal and postnatal supply of
to this article. This iodine, which can paradoxically suppress T4 secretion when present in excess, espe-
commentary does not cially in preterm infants and in the presence of iodine deficiency. Maternal T4 is a
critical source of thyroid hormone when the fetus is hypothyroid. Postnatal thyroid
contain a discussion
function also can be affected by maternally or postnatally administered drugs, mater-
of an unapproved/
nal TSH receptor antibodies (Abs), and acute illness. Because of the vital role of
investigative use of a thyroid hormone in brain development and the importance of early, adequate therapy
commercial product/ when thyroid function is impaired, knowledge of normal thyroid function in the
device. neonatal period and factors affecting it are critical for physicians caring for newborns.

Objectives After completing this article, readers should be able to:

1. Describe normal postnatal thyroid function in term, preterm, and

small-for-gestational-age neonates.
2. Describe the role of maternal T4 in the fetus and newborn.
3. Explain the importance of iodine in thyroid function.
4. Describe the role of maternal TSH receptor Abs in affecting neonatal thyroid function.
5. Delineate how drugs and critical illness affect neonatal thyroid function.

Introduction
Thyroid hormone is essential for the maturation of many
tissues, including the brain, skeleton, lungs, heart, and intes-
Abbreviations tine, as well as for the development of nonshivering thermo-
Ab: antibody genesis in the neonatal period. Thyroid hormone-dependent
D1: type 1 iodothyronine deiodinase tissue maturation occurs in a highly regulated, temporal
D2: type 2 iodothyronine deiodinase sequence in which the ontogeny of the hypothalamic-
D3: type 3 iodothyronine deiodinase pituitary-thyroid axis is tightly linked to the tissue-specific
MMI: methimazole expression of the thyroid hormone receptor and the local
PTU: propylthiouracil maturation of the deiodinase system that generates T3 from
rT3: reverse triiodothyronine T4. As noted in detail in previous articles in NeoReviews,
SGA: small for gestational age during fetal life, circulating concentrations of T4 and the
T3: triiodothyronine active metabolite T3 are low, and the inactive metabolites
T4: thyroxine reverse T3 (rT3) and T3 sulfate are high. This pattern is a
TBG: thyroxine-binding globulin consequence of both immaturity of the hypothalamic-
TSH: thyroid-stimulating hormone pituitary-thyroid axis and coordinated adjustments in the
deiodinase system that result in high concentrations of the

*Division of Endocrinology, Department of Medicine, Children’s Hospital Boston; Department of Pediatrics, Harvard Medical
School, Boston, Mass.

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inactivating deiodinase, D3 (Fig. 1), and low concentra-
tions of the activating deiodinase, D1. Despite the low
circulating T3 concentration, the amount of T3 in the
fetal brain is 60% to 80% of the adult values as early as
20 to 26 weeks’ gestation, reflecting the importance of
local generation of T3 from T4 (under the influence of a
third deiodinase, D2). The physiologic rationale for the
maintenance of reduced circulating T3 concentrations
throughout fetal life is still unknown, but it has been
suggested that its function may be to avoid tissue ther-
mogenesis and potentiate the anabolic state of the rapidly
growing fetus while, at the same time, permitting highly
regulated, tissue-specific maturation in an orderly, tem-
poral sequence.
Dynamic changes in thyroid hormone secretion and
metabolism occur postnatally that permit the neonate to
adapt to the changing demands of postnatal life. In this
article, we review the changes in circulating thyroid
hormone concentrations that occur in the neonatal pe-
riod and the factors that can affect postnatal thyroid
function.
Normal Postnatal Thyroid Function
The Term Neonate
Significant changes occur in thyroid physiology at the
time of birth in the term newborn (Fig. 2). A surge in the
serum TSH is seen at 30 minutes after delivery, with peak
concentrations as high as 60 to 70 mcU/L. The eleva-
tion in TSH, believed to be a consequence of cold
exposure in the ambient atmosphere, causes marked
stimulation of the thyroid and an increase in the concen-
trations of both serum T4 and T3. In the first postnatal
week, the serum T4 increases to concentrations that are
higher than at any other time of life, decreasing thereaf-
ter. The T3 concentration rises strikingly at postnatal day
7 and continues to rise for the first 28 days. Opposite
effects are noted in values for rT3 and T4 sulfate (not
pictured). The increase in T3 is due not only to a direct
action of TSH but to increased expression of the activat-
ing deiodinase D1 postnatally, coupled with loss of pla-
cental D3. Like T4, serum concentrations of free T4 and
T4-binding globulin (TBG) remain elevated over cord
values at 7 days of postnatal life, decreasing thereafter.
Normal cord and postnatal values of T4 and its
metabolites, TBG and TSH, in a large cohort of babies
have been published recently. Although specific values
obtained in different clinical laboratories vary some-
what, depending on the assay used, serum TSH values
more than 20 mcU/mL after 24 hours and more than
10 mcU/mL after the first postnatal week generally are
consistent with primary hypothyroidism. The serum
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endocrinology neonatal thyroid
Figure 1. Metabolism of thyroid hormone in the fetus, the
newborn, and in critical illness. In the fetus, the circulating
concentration of reverse triiodothyronine (rT3), an inactive
metabolite, is elevated and the concentration of T3, the active
thyroid hormone isomer, is diminished. This is due primarily to
the high concentration of the inactivating deiodinase (D3) in
the placenta and fetal tissues as well as the low concentration
of D1, the major activating deiodinase in adult life. Despite
the low serum T3 concentration, brain T3 is preserved due to
the local action of intracellular D2. After delivery, increased
thyroid-stimulating hormone (TSH) secretion leads to in-
creased thyroidal thyroxine (T4) secretion. D1 is activated and
placental D3 is lost, leading to increased conversion of T4 to
metabolically active T3 and a reduction in reverse T3. Findings
analogous to those in the fetus are observed in the presence of
acute illness.
T4 and free T4 concentrations usually are decreased as
well but may be normal initially or in mild cases. A serum
TSH value of more than 40 mcU/mL suggests the
possibility of permanent congenital hypothyroidism, a
medical emergency. Usually babies who have transient
hypothyroidism have serum TSH concentrations in the
20 to 40 mcU/mL range, but exceptions can occur. Of
note, a serum T4 concentration of less than 6.5 mcg/dL,
although normal in adults, is less than the 3rd percentile
in the first postnatal week, demonstrating the importance
of always using gestational- and postnatal-appropriate
normative values.
Preterm Infants
Thyroid function in the preterm infant reflects, in part,
the relative immaturity of the hypothalamic-pituitary-
thyroid axis. Following delivery, a surge in T4 and TSH
occurs that is analogous to that observed in term infants,
but the magnitude of the increase is less (Fig. 1). In
infants born before 31 weeks’ gestation, the circulating
T4 concentration may not increase and even may fall in
the first 1 to 2 postnatal weeks. This decrease in the T4
concentration is particularly significant in very preterm
infants, in whom the serum T4 occasionally may be
undetectable. It is important to appreciate that in most
cases, the total T4 is more affected than the free T4, a
NeoReviews Vol.11 No.11 November 2010 e641
endocrinology neonatal thyroid

sensitivity to the thyroid suppres-

sive effects of excess iodide found
in certain skin antiseptics and drugs
to which these babies frequently are
exposed. Despite the reduced total
T4 observed in some preterm ba-
bies, the TSH concentration is not
significantly elevated in most. In
other babies, an elevated TSH may
reflect recovery from acute illness and
be difficult to distinguish from true
hypothyroidism. Thyroid function in
preterm infants has been discussed in
detail in several previous NeoReviews
articles.

Small-for-gestational-age
(SGA) Infants
SGA infants have significantly
higher TSH and lower total and
free T4 values than do infants of
normal weight. This can be related
Figure 2. Postnatal changes in thyroxine (T4), free T4 (FT4), thyroid-binding globulin to the severity of the malnutrition
(TBG), triiodothyronine (T3), reverse T3 (rT3), and thyroid-stimulating hormone (TSH) in these infants as well as to fetal
according to gestational age. Note the increase in T4, FT4, and TBG in the term infant in
hypoxemia and acidemia. Impaired
the first postnatal week. T3 also rises strikingly, while rT3 and TSH decline. The increase
in T4 and free T4 is blunted in infants <31 weeks’ gestation and is not seen at all in very
placental perfusion and chronic
preterm infants in whom thyroid hormone concentrations actually may decline. Graphs starvation also may play roles. This
based on data in Williams et al, 2004. pattern of reduced T4 and elevated
TSH differs from the response to
starvation in older individuals and
consequence of abnormal protein binding or the de- healthy adults in whom TSH is reduced. The explanation
creased TBG in these babies, who have immature liver for the relatively higher TSH in SGA infants is not
function. In contrast to the low circulating T4 concen- known.
tration, serum concentrations of thyroglobulin, the stor-
age form of T4, are higher in the preterm than in the Factors Affecting Postnatal Thyroid Function
term infant, particularly in those who are sick. In view of (Table)
the attenuated postnatal TSH rise in the latter babies, it is Maternal T4
likely that impaired clearance or degradation of this Under normal circumstances, passage of maternal T4
glycoprotein from the circulation rather than increased to the fetus is limited because of the high D3 concentra-
secretion plays an important role. tions in the maternal uterus and placenta that inactivate
The causes of the decrease in T4 observed postnatally most maternal T4. The generated rT3 contributes to
in preterm infants are complex. In addition to the clear- the high rT3 concentration observed in the fetal circula-
ance of maternal T4 from the neonatal circulation, pre- tion, and the iodide can be reused for fetal thyroid
term babies have decreased thyroidal iodide stores hormone synthesis. Maternal T4 disappears rapidly from
(a problem of particular significance in borderline iodine- the newborn circulation, with a half-life of approximately
deficient areas of the world), they are frequently sicker 3 to 4 days.
than their more mature counterparts, they are less able to When the fetus has hypothyroidism, significant ma-
regulate iodide balance, and they may be treated with ternal T4 transfer occurs both because of the increased
drugs that affect neonatal thyroid function. In addition, maternal-fetal gradient and downregulation of placental
because the capacity of the immature thyroid to adapt to D3. Even when the fetus is completely unable to synthe-
exogenous iodide is reduced, there is an increase in size any T4, the cord serum concentration of T4 is of the

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Factors Affecting
Table.
Neonatal Thyroid Function
Maternal Thyroxine
Elements
● Iodine (eg, topical antiseptic solutions, contrast
media, drugs)
● Selenium
● Thiocyanate
● Perchlorate?
Drugs
● Maternal antithyroid drugs (propylthiouracil,
methimazole)
● Dopamine
● Steroids
● Aminophylline
● Caffeine
● Diamorphine
● Lithium
Thyroid-stimulating Hormone Receptor Antibodies
● Stimulating
● Blocking
Nonthyroidal acute illness
order of 3 to 4 mcg/dL, ie, 25% to 50% of normal. The
maternal T4 transfer, coupled with coordinate adjust-
ments in deiodinase, is critical in preserving brain T3
concentrations and probably accounts for the excellent
cognitive outcome, even in babies who have severe hy-
pothyroidism and receive adequate postnatal treatment.
These mechanisms also may provide a partial explanation
for the relatively normal clinical appearance at birth of
more than 90% of infants who have congenital hypo-
thyroidism.
In contrast, in situations in which both the mother
and fetus exhibit hypothyroidism, maternal T4 is unable
to compensate for the fetal hypothyroidism, and the cord
serum concentration of T4 is markedly reduced or un-
detectable. Not surprisingly, the clinical features at birth
of babies born after maternal-fetal hypothyroidism are
more severe than after fetal hypothyroidism alone, and
affected babies may have permanent cognitive delay,
despite early postnatal therapy. The most common cause
of maternal-fetal hypothyroidism worldwide is iodine defi-
ciency. Other models include TSH receptor-blocking
Ab-induced congenital hypothyroidism and maternal-
fetal POU1F1 deficiency.
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endocrinology neonatal thyroid
Iodine
Iodine is an essential element for thyroid hormone synthe-
sis, comprising 65% of T4 and 59% of T3 by weight. Both
iodine deficiency and excess can have adverse effects on
neonatal thyroid function, particularly in preterm infants.
Worldwide, iodine deficiency continues to be an im-
portant cause of congenital hypothyroidism and is the
most common treatable cause of intellectual disability.
Preterm infants are unusually susceptible to the effects of
iodine deficiency, not only because of decreased thyroi-
dal iodine stores accumulated in utero, but because of
immaturity in the capacity for thyroid hormonogenesis,
the hypothalamic-pituitary-thyroid axis, and the ability
to convert T4 to the more metabolically active T3.
Furthermore, preterm infants are in negative iodine bal-
ance for the first 1 or 2 weeks of postnatal life, particularly
when they are sick.
The recommended daily intake of iodine is
15 mcg/kg per day for term neonates and 30 mcg/kg
per day for preterm infants. In a recent study in Spain,
the iodine intake of 67 preterm infants born before
30 weeks’ gestation was recorded. Due to the small
amounts of formula ingested, preterm neonates did not
achieve the recommended intake of 30 mcg/kg per day.
Furthermore, infants receiving parenteral nutrition had
an intake of only 3 mcg/kg per day. By 31 to 36 weeks’
gestation, healthy infants were in positive iodine balance.
Similar studies have not been performed in North America.
Fetal and neonatal iodine stores are critically depen-
dent on maternal iodine status in utero and on the iodine
content of formula or human milk postnatally. Although
North America is usually considered to be an iodine-
sufficient area, several years ago, 6.7% of pregnant women
in the United States were found to have moderate-to-severe
iodine deficiency, as reflected by a urinary iodine concen-
tration of 50 mcg/L (394 nmol/L) or less (normal range,
100 to 199 mcg/L [788 to 1,568 nmol/L]).
In addition to iodine deficiency, both the fetus and
newborn are sensitive to the thyroid-suppressive effects
of excess iodine, whether administered to the mother
during pregnancy or lactation or directly to the baby.
This occurs, in part, because recovery from the thyroid-
inhibitory effect of iodine (the Wolff-Chaikoff effect)
does not mature before 36 weeks’ gestation, although
other factors, including increased skin absorption, are
likely to play roles. Reported sources of iodine have
included drugs (eg, potassium iodide, amiodarone), io-
dinated contrast agents, and topical antiseptic solutions
(eg, povidone-iodine) used for skin cleansing. Even vag-
inal douches used by the mother prenatally have been
implicated. Iodine-induced transient hypothyroidism ap-
NeoReviews Vol.11 No.11 November 2010 e643
endocrinology neonatal thyroid
pears to be less frequent in North America and other
iodine-sufficient areas than in Europe, and it is found
primarily in preterm infants and in infants in whom the
exposure is great. Maternal exposure to iodinated con-
trast material used in computed tomography scan during
pregnancy does not appear to affect fetal thyroid func-
tion, although limited data are available.
Other Elements
The iodothyronine deiodinases, D1, D2, and D3, are
selenoproteins, and selenium deficiency has been re-
ported to worsen endemic hypothyroidism due to iodine
deficiency. Thiocyanate, whether derived from cigarette
smoking or ingestion of thiocyanate-containing foods
such as cassava, also can worsen endemic hypothyroid-
ism, but a role for either selenium deficiency or thio-
cyanate excess in iodine-sufficient babies has not been
established. Similarly, a role for perchlorate in neonatal
hypothyroidism remains controversial at present.
Antithyroid Medication
Maternal administration of antithyroid medication (ei-
ther propylthiouracil [PTU] or methimazole [MMI]) for
the treatment of Graves disease is an important cause of
transient congenital hypothyroidism. Antithyroid drugs
inhibit thyroid hormonogenesis by interfering with the
action of the key thyroid enzyme, thyroid peroxidase.
Even maternal PTU doses of 200 mg or less have been
associated with an effect on neonatal thyroid function,
illustrating the increased fetal sensitivity to these drugs.
Babies who have PTU- or MMI-induced hypothyroid-
ism characteristically develop enlarged thyroid glands,
which may cause respiratory embarrassment in severe
cases. Both the hypothyroidism and goiter resolve spon-
taneously with clearance of the drug from the baby’s
circulation.
Other Medications
Both steroids and dopamine, commonly used in the
treatment of sick preterm infants, inhibit TSH secretion
and are relatively common causes of the depressed T4
concentration observed in many sick preterm infants.
Alternative therapies, therefore, should be sought wher-
ever possible, although these may not be as effective.
Aminophylline, caffeine, and diamorphine also have been
implicated in the hypothyroxinemia of prematurity. Ma-
ternal administration of lithium has been reported to
cause goitrous congenital hypothyroidism.
Maternal Thyrotropin Receptor Antibodies
Maternal TSH receptor Abs are immunoglobulins of the
G class and readily cross the placenta by active transfer.
When present in a sufficiently high titer, they can have a
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significant effect on the fetal thyroid economy. Both
stimulating and blocking TSH receptor Abs have been
described.
Transplacental passage of TSH receptor-stimulating
Abs are the cause of neonatal Graves disease (see Her-
nandez and Lee. NeoReviews. 2008;9:e305– e309), but
most babies born to mothers who have Graves disease
have normal thyroid function. TSH receptor Ab potency,
severity and duration of the in utero hyperthyroidism,
and maternal antithyroid medication all contribute to
neonatal thyroid status. Hyperthyroidism develops only
in babies born to the 1% to 2% of mothers who have the
most potent stimulatory activity in serum, corresponding
to approximately 1 in 50,000 newborns. By contrast,
overt or subclinical hypothyroidism due to transpla-
cental passage of maternal antithyroid drugs is threefold
more common. Rarely, babies born to mothers who had
hyperthyroidism during pregnancy develop transient
hypothalamic-pituitary suppression. Such hypothyrox-
inemia is usually self-limited, but in some cases it may last
for years and require replacement therapy. In general, the
titer of TSH receptor-stimulating Abs in this population
of infants is lower than in those who develop transient
neonatal hyperthyroidism.
Unlike TSH receptor-stimulating Abs that mimic the
action of TSH, TSH receptor-blocking Abs inhibit both
the binding and action of TSH. Because TSH-induced
growth is blocked, affected babies do not have a goiter.
Similarly, inhibition of TSH-induced radioactive iodine
uptake may result in a misdiagnosis of thyroid agenesis.
TSH receptor-blocking Ab-induced congenital hypothy-
roidism is much less common than neonatal Graves
disease (approximately 1 in 180,000). Babies who have
TSH receptor-blocking Ab-induced hypothyroidism are
difficult to distinguish at birth from those who have
thyroid dysgenesis, the most common cause of perma-
nent congenital hypothyroidism, but they differ from the
latter in a number of important ways. They do not
require lifelong therapy, and there is a high recurrence
rate in subsequent offspring due to the tendency of the
Abs to persist for many years in the maternal circulation.
Unlike babies who have thyroid dysgenesis, in whom a
normal cognitive outcome is found if postnatal therapy is
early and adequate, babies who have maternal-blocking
Ab-induced hypothyroidism may have a permanent def-
icit in intellectual development if fetomaternal hypothy-
roidism was present in utero. TSH receptor-blocking
Abs most often are found in mothers who have been
treated previously for Graves disease or who have the
nongoitrous form of chronic lymphocytic thyroiditis
(“primary myxedema”). Occasionally, such mothers are

not aware that they have hypothyroidism, and the diag-
nosis is made only after congenital hypothyroidism has
been recognized in their infants. Usually, the hypo-
thyroidism resolves in 3 or 4 months.
Nonthyroidal Critical Illness
Critical illness is a frequent contributor to the thyroid
abnormalities commonly observed in preterm infants. In
one multicenter collaborative study, infants who had
bacteremia, persistent ductus arteriosus, necrotizing en-
terocolitis, cerebral ultrasonography changes, and oxy-
gen dependence at 28 days of age were affected most
commonly, but critically ill infants in the cardiac surgery
intensive care unit constitute another high risk group. In
critical illness, thyroidal secretion of T4 is decreased and
activity of D3 is decreased, resulting in increased conver-
sion of T4 to rT3 (Fig. 1). Steroids, increased free fatty
acids, decreased caloric intake, and cytokines probably
contribute to decreased D1 activity.
Summary
Dynamic changes in thyroid hormone secretion occur
postnatally. Thyroid function differs according to gesta-
tional and postnatal age and can be influenced adversely
by a number of maternal and environmental agents as
well as illness and drugs. In view of the critical impor-
tance of thyroid hormone for brain development, physi-
cians caring for newborns should be able to distinguish
normal from abnormal thyroid function and to identify
the most common causes of these abnormalities. Adult
normal ranges provided by many general hospital labo-
ratories should not be used. Only gestational and post-
natal age-specific normative values are appropriate for
determining thyroid status in the neonatal period.
American Board of Pediatrics Neonatal-Perinatal
Medicine Content Specifications
• Know the relationship between fetal
and maternal thyroid physiology.
• Know the embryology and normal
physiological function of the thyroid
gland.
• Know the proper use of laboratory tests (including screening
tests) in the diagnosis of thyroid dysfunction.
Suggested Reading
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and thyroid dysfunction in premature newborns. Semin Peri-
natol. 2008;32:407– 412
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Boyages SC. Clinical review 49: iodine deficiency disorders. J Clin
Endocrinol Metab. 1993;77:587–591
Brown RS. Autoimmune thyroid disease in pregnant women and
their offspring. Endocr Pract. 1996;2:53– 61
Brown RS. Disorders of the thyroid gland in infancy, childhood and
adolescence. In: Thyroid Disease Manager. 2009. Accessed Au-
gust 2010 at: http://thyroidmanager.org.
Brown RS, Bellisario RL, Botero D, et al. Incidence of transient
congenital hypothyroidism due to maternal thyrotropin
receptor-blocking Abs in over one million babies. J Clin Endo-
crinol Metab. 1996;81:1147–1151
Cao XY, Jiang XM, Dou ZH, et al. Timing of vulnerability of the
brain to iodine deficiency in endemic cretinism. N Engl J Med.
1994;331:1739 –1744
De Nayer P, Cornette C, Vanderschueren M, et al. Serum thyro-
globulin levels in preterm neonates. Clin Endocrinol (Oxf).
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de Zegher F, Pernasetti F, Vanhole C, et al. The prenatal role of
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to lithium in utero. Ann Pharmacother. 2002;36:1745–1748
Hernandez MI, Lee K-W. Neonatal Graves disease caused by
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birth weight infants. Clin Endocrinol (Oxf). 1997;47:411– 417
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endocrinology neonatal thyroid

NeoReviews Quiz
9. A surge in the serum concentration of thyroid-stimulating hormone (TSH) occurs within 30 minutes of
birth in term neonates. This surge is believed to be a consequence of cold exposure in the ambient
atmosphere. The serum concentration of TSH falls thereafter to normal values by 7 days of age. The serum
concentration of TSH remains elevated in cases of primary hypothyroidism. Of the following, the serum
TSH concentration at 7 days of age most suggestive of permanent congenital hypothyroidism is greater
than:
A. 5 mcU/mL.
B. 10 mcU/mL.
C. 20 mcU/mL.
D. 30 mcU/mL.
E. 40 mcU/mL.

10. Thyroid function in the preterm neonate, in contrast to the term neonate, reflects immaturity of the
hypothalamic-pituitary-thyroid axis. Of the following, the thyroid enzyme/hormone most likely to show a
higher serum concentration in the preterm neonate than in the term neonate is:
A. Tetraiodothyronine.
B. Thyroglobulin.
C. Thyroid peroxidase.
D. Thyroxine-binding globulin.
E. Triiodothyronine.

11. Maternal administration of antithyroid drugs (propylthiouracil or methimazole) for the treatment of
Graves disease is an important cause of transient hypothyroidism in the neonate. Of the following, the key
thyroid enzyme/hormone in the neonate inhibited by maternal antithyroid drugs is:
A. Thyroid-coupling enzyme.
B. Thyroid peroxidase.
C. Thyroid-stimulating hormone.
D. Thyroxine-binding globulin.
E. Type 3 iodothyronine deiodinase.

12. Critical illness in preterm infants is a frequent contributor to thyroid dysfunction, referred to as euthyroid
sick syndrome. Of the following, the thyroid dysfunction characteristic of euthyroid sick syndrome is most
likely the result of inhibition of:
A. Thyroid-coupling enzyme.
B. Thyroid peroxidase.
C. Thyroid-stimulating hormone.
D. Thyroxine-binding globulin.
E. Type 3 iodothyronine deiodinase.

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 Neonatal Thyroid Function
Shiri B. Feingold and Rosalind S. Brown
NeoReviews 2010;11;e640
DOI: 10.1542/neo.11-11-e640

Updated Information & including high resolution figures, can be found at:
Services http://neoreviews.aappublications.org/content/11/11/e640
References This article cites 21 articles, 4 of which you can access for free at:
http://neoreviews.aappublications.org/content/11/11/e640#BIBL
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 Neonatal Thyroid Function
Shiri B. Feingold and Rosalind S. Brown
NeoReviews 2010;11;e640
DOI: 10.1542/neo.11-11-e640

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