Thyroid Disease in Pregnancy

Chantarojanasiri T. ,MD.

OUTLINE

Normal physiology& changes during pregnancy

Hyperthyroid
Hypothyroid
Postpartum thyroid disease
Thyroid cancer
Euthyroid with autoimmune thyroid disease
Practice guidelines

Normal physiology
The hypothalamic pituitary axis
Thyrotropin-releasing hormone (TRH)
Produced in a tonic fashion in the paraventricular
nucleus of the hypothalamus.

TSH has an and subunit; subunit confers

specificity.
TSH secretion regulated by negative feedback
from circulating thyroid hormone, dopamine, and
somatostatin.
TSH then stimulates the thyroid gland to produce,
as well as secrete, thyroxine(T4) and
triiodothyronine (T3).

 The rate-limiting
step is iodide
trapping
mediated by TSH.

nonpregnant
state, 80 mg/d to
100 mg/d of
iodine taken up
20% of the intake
is cleared by the
thyroid gland;
remainder renally

Physiologic adaptation during pregnancy

increase in thyroid-binding globulin
secondary to an estrogenic stimulation of TBG synthesis
and reduced hepatic clearance of TBG ;two to threefold
levels of bound proteins, total thyroxine, and total
triiodothyronine are increased and resin triiodothyronine
uptake (RT3U) is decreased
begins early in the first trimester, plateaus during
midgestation, and persists until shortly after delivery
decrease in its hepatic clearance,estrogen-induced
sialylation
free T4 and T3 increase slightly during the first trimester in
response to elevated hCG. decline to nadir in third
trimester

 human chorionic gonadotropin (hCG)

intrinsic thyrotropic activity
begins shortly after conception, peaks around
gestational week 10,declines to a nadir by about week
20
directly activate the TSH receptor
partial inhibition of the pituitary gland (by crossreactivity of the subunit)
transient decrease in TSH between Weeks 8 and 14
mirrors the peak in hCG concentrations

20% of normal women, TSH levels decrease to less

than the lower limit of normal

TSH

hCG

 A decrease in basal TSH of 0.1 mU/L was

observed for every 10,000 IU/L increment in
hCG
reduction in plasma iodide
fetal :monodeiodinase types II and III in the placenta
increased maternal glomerular filtration rate-increased renal clearance of iodide throughout
pregnancy

transplacental passage of T4 and iodide and

placental metabolism of iodothyronines
stimulate the maternal thyroid ; depleting the maternal
circulation of thyroid hormone and its precursors

 Hypothyroid;25% to 47% average dosage

increase during pregnancy
increased serum thyroid stimulating hormone
(TSH) and thyroglobulin concentrations, relative
hypothyroxinemia, and occasional goiter
formation
Esp. from area with borderline iodine sufficiency

associated with increase in thyroid gland size in

15%

EFFECTS OF PREGNANCY ON THYROID

PHYSIOLOGY
Physiologic Change
Serum thyroxine-binding globulin

Thyroid-Related Consequences
Total T4 and T3; T4 production

Plasma volume

T4 and T3 pool size; T4

production; cardiac output

D3 expression in placenta and (?) uterus

T4 production

First trimester in hCG

Free T4; basal thyrotropin; T4

production

Renal I- clearance

Iodine requirements

T4 production; fetal T4 synthesis during

second and third trimesters
Oxygen consumption by fetoplacental
unit, gravid uterus, and mother

Basal metabolic rate; cardiac

output

Hyperthyroidism and pregnancy

0.2% of pregnancies
prevalence 0.1% to 0.4%, with 85% Graves
disease
Single toxic adenoma, multinodular toxic goiter, and
subacute thyroiditis
gestational trophoblastic disease,viral thyroiditis and
tumors of the pituitary gland or ovary (struma ovarii)

TSH is depressed and fT4 and fTI are increased.

The RT3U that normally is decreased in
pregnancy is increased in hyperthyroidism.

Hyperthyroidism and pregnancy

serum TSH value <0.01 mU/L and also a high
serum free T4 value
may be difficult to determine the cause
thyroid radionuclide imaging is contraindicated in pregnant
women.

Measurement of thyrotropin receptor antibody (thyroid

stimulating immunoglobulins) Graves' disease during
pregnancy
transient hyperthyroidism in hyperemesis gravidarum and
gestational transient thyrotoxicity (GET)

Hyperthyroidism and pregnancy

Severe maternal hyperthyroidism

increased risk of stillbirth

preterm delivery
intrauterine growth restriction
Preeclampsia
heart failure
spontaneous abortion
Fetal thyroid hyperfunction or hypofunction caused by
TSHRAbs
Fetal goiter from excessive antithyroid drug treatment
Neonatal thyrotoxicosis
Increased perinatal and maternal mortality
Decreased IQ of offspring because of excessive use of
antithyroid drugs

Transient hyperthyroidism during pregnancy &

gestational transient thyrotoxicity (GET)
hyperemesis gravidarum
severe nausea and vomiting leading to a 5% loss of body
weight, dehydration, and ketosis.
absence of goiter and ophthalmopathy, and absence of the common
symptoms and signs of hyperthyroidism

higher serum hCG and estradiol concentrations

60% have a subnormal serum TSH level (< 0.4 mU/L),50% have
an elevated serum free T4 concentration
Severity positively correlated with maternal free T4 levels but not
to thyroid function.
12% elevated free T3 index

believed to be related to hCG stimulation of the thyroid gland

Normalization of T4 levels by midgestation.
Treatment is supportive care

 GET
first trimester
related to hCG stimulation of the thyroid gland
symptoms of hyperthyroidism and elevated free T4
levels.
The thyroid gland usually is not enlarged
resolution of symptoms parallels the decline in hCG
levels
usually resolves spontaneously by 20 weeks
gestation
beyond 20 weeks,repeat evaluation for other causes

Trophoblastic hyperthyroidism
hydatidiform mole (molar pregnancy) &
choriocarcinoma.
high serum hCG concentrations and abnormal hCG
isoforms

55 to 60 percent had clinically evident

hyperthyroidism
normal thyroid gland and few symptoms of thyroid
hormone excess.
some :findings of hyperthyroidism and a diffuse goiter
ophthalmopathy is not present

Nausea and vomiting may predominate

subclinical hyperthyroidism
associated with osteoporosis,
cardiovascular morbidity, and progression
to overt thyrotoxicosis and thyroid failure.
not associated with adverse pregnancy
outcomes
does not warrant treatment.

Graves disease
95% of thyrotoxicosis during pregnancy.
activity level fluctuate during gestation, with
exacerbation during the first trimester
gradual improvement during the latter half.
exacerbation shortly after delivery

clinical scenarios.
stable Graves disease receiving thionamide therapy
with exacerbation during early pregnancy.
in remission with a relapse of disease.
without prior history diagnosed with Graves disease
de novo during pregnancy.

Graves disease
Diagnosis
difficult :hypermetabolic symptoms in normal
pregnancy
thyroid examination: goiter (with or without bruit)
suppressed serum TSH level and usually elevated
free and total T4 serum concentrations.
TSH receptor antibodies

complications related to the duration and control

of maternal hyperthyroidism
autoantibodies mimic TSH can cross the
placenta and cause neonatal Graves disease

Graves disease
Pregnancy outcome

preterm labor
untreated (88%)/partially treated(25%) /adequately treated (8%) [

preeclampsia
untreated twice

stillbirth
untreated (50%) /partially treated (16%) /adequately treated (0%)

small for gestational age

congenital malformations unrelated to thionamide therapy
Mother may have thyroid-stimulating hormone-binding inhibitory
immunoglobulin (TBII),
cause transient neonatal hypothyroidism
fetal bradycardia, goiter,and growth restriction

Graves disease
Neonatal thyrotoxicosis :
1% of infants
occur in euthyroid mother or has had surgical or radioactive
131I treatments before pregnancy
fetal ultrasound to exclude evidence of fetal thyrotoxicosis
(eg, an anterior fetal neck mass) or fetal tachycardia.
fetal goiter, advanced bone age, poor growth, and
craniosynostosis, Cardiac failure and hydrops
Fetal blood sampling Fetal blood for thyroid function tests
by percutaneous umbilical vein sampling after 20 weeks of
gestation
High maternal TSH receptor-stimulating antibody levels Fetal signs
suggestive of thyroid disease History of a prior baby with
hyperthyroidism

Thyroid storm

obstetric emergency
extreme metabolic state
10% of pregnant women with hyperthyroidism
high risk of maternal cardiac failure.
fever, change in mental status, seizures, nausea,
diarrhea, and cardiac arrhythmias.
inciting event (eg, infection, surgery, labor/delivery) and a
source of infection
treatment immediately, even if serum free T4, free T3,
and TSH levels are not known.
untreated thyroid storm can be shock, stupor, and coma.

Guidelines for clinical management of maternal

hyperthyroidism during pregnancy
1. Use the lowest dosage of thionamide
(preferably PTU) to maintain maternal total T4
concentrations in the upper one third of normal
to slightly elevated range for pregnancy.
Normal range of total T4 during pregnancy is
estimated to be 1.5 times the nonpregnant state

2. Monitor maternal total T4 serum concentration

every 24 weeks, and titrate thionamide as
necessary.
Monitoring serum TSH may become useful later.
Shane O. LeBeau, Endocrinol Metab Clin N Am
35 (2006) 117136

Guidelines for clinical management of maternal

hyperthyroidism during pregnancy
3. Measure TSH receptor antibodies (thyroidstimulating immunoglobulins or TSH receptor
binding inhibitory immunoglobulins) at 2628
weeks to assess risk of fetal/neonatal
hyperthyroidism.
TSH receptor antibody measurement is crucial in
hypothyroid levothyroxine-treated women with a prior
history of Graves disease, who do not appear
thyrotoxic.

4. Perform fetal ultrasound at weeks 2628 to

assess potential fetal response to thionamide
treatment and effect of TSH receptor antibodies
on fetal thyroid function

Guidelines for clinical management of maternal

hyperthyroidism during pregnancy
5. Consider thyroidectomy if persistently high
doses of thionamide (PTU > 600 mg/d or MMI >
40 mg/d) are required,or if the patient cannot
tolerate thionamide therapy.
6. -Adrenergic blocking agents and low doses
of iodine may be used perioperatively to control
hyperthyroid state.
7. Check fetal cord blood at delivery for TSH and
T4.

Treatment
Thionamides
propylthiouracil (PTU) and methimazole(MMI)
Both cross the placenta with equal transfer kinetics.
Both can cause fetal goiter and hypothyroidism,
usually mild and transient & dose-dependent
median time to normalization of maternal thyroid
function
7 weeks with PTU and 8 weeks with MMI

PTU more highly bound to albumin

theorize that MMI crosses the placenta in higher
concentrations

Treatment
Thionamides
maternal :rash
rare birth defects in MMI: aplasia cutis, choanal
atresia,esophageal atresia, and minor dysmorphic features

Low thyroid function at birth neonates whose mothers received PTU or MMI
and had serum T4 concentrations within the normal (non-pregnant) range
normal IQ scores

Graves disease may ameliorate

thionamide discontinued in 30% during the final weeks
fall in serum TSH receptor-stimulating antibody concentrations and a rise in
TSH receptor-blocking antibodies.

Graves' hyperthyroidism can worsen postpartum

do not recommend the use of T4 with thionamide therapy during
pregnancy.

Treatment
-Adrenergic blockers
weaned as soon as the hyperthyroidism is controlled
occasional cases of neonatal growth restriction,
hypoglycemia, respiratory depression, and bradycardia
increased frequency of first-trimester miscarriages
avoiding in the first trimester

Iodides
past reports of neonatal hypothyroidism after exposure to
iodine
low-dose potassium iodide may be considered
Preparation for thyroidectomy
thionamide-intolerant patients refusing surgery.

Treatment
Surgery

Subtotal thyroidectomy :
persistently high dosages of thionamides (PTU > 600 mg/d, MMI > 40
mg/d) are required to control maternal disease
allergic or intolerant of both thionamides
noncompliant with medical therapy
compressive symptoms

second trimester, before gestational week 24

prepared with a -adrenergic blocking agent and a 10- to 14-day
course of potassium iodide

Treatment
Radioactive iodine therapy
contraindicated
fetal thyroid gland begins to concentrate iodine after
gestational week 10, Fetal thyroid tissue is present by 10 to
12 weeks
predisposing to congenital hypothyroidism

Nursing
Breast feeding in mothers taking PTU or MMI is safe
Thyroid function in newborn infants is unaffected
PTU is preferred because it is less concentrated in breast
milk

Hypothyroidism in pregnancy
elevated serum TSH concentration:2.5%
of pregnancies
In iodine-sufficient environment
Hashimotos thyroiditis
prior radioactive iodine treatment
surgical ablation of Graves disease
less common causes: overtreatment of hyperthyroidism with
thionamides, transient hypothyroidism owing to postpartum
thyroiditis, medications that alter the absorption or metabolism of
levothyroxine, and pituitary/hypothalamic disease)

Hypothyroidism in pregnancy
diagnosis
Symptoms masked by the hypermetabolic state of
pregnancy.
20% to 30% overt hypothyroidism develop symptoms
weight gain, lethargy, decrease in exercise capacity, and
intolerance to cold,constipation, hoarseness, hair loss,
brittle nails, dry skin, goiter, or delay in the relaxation
phase of the deep tendon reflexes
Elevated serum TSH concentration
Central hypothyroidism do not manifest an elevated
serum TSH level

Hypothyroidism in pregnancy
Pregnancy outcome
depends on the severity of disease and adequacy of
treatment
Gestational hypertension in overtly hypothyroid women
(36%) vs subclinical disease (25%) or the general
population (8%)
Overt hypothyroid vs subclinical disease,
increased use of cesarean section because of fetal distress
placental abruption, anemia, andpostpartum hemorrhage
increased rates of miscarriage, preeclampsia,placental
abruption, growth restriction, prematurity and stillbirths

fetuses are at risk for impaired neurologic development

low-birth-weight neonates

Hypothyroidism in pregnancy
TSH can be elevated with or without suppressed levels
of free T4.
antithyroid autoantibodies (eg, antithyroglobulin,
antithyroid
peroxidase) are present
elevated creatine phosphokinase, cholesterol, and liver
function tests
5% to 8% prevalence of hypothyroidism in type I
diabetes
mellitus and women who have type I diabetes have a
25% risk of developing postpartum thyroid dysfunction

Causes of hypothyroidism
Worldwide, the most common is iodine deficiency.
impaired neurologic development; severe mental
retardation, deafness,
muteness, and pyramidal or extrapyramidal syndromes;

Hashimotos thyroiditis
Idiopathic hypothyroidism; atrophic thyroid gland
and absent antithyroid antibodies.
131I treatment for Graves disease and thyroidectomy
Drugs interfere with the metabolism of thyroid hormones

Subclinical hypothyroidism
normal free T4 level
elevated TSH above the upper limit of reference
range (4.510.0mIU/L)
thresholds based on gestational age.

TSH in the first half of pregnancy is 3.0 mIU/L

prevalence of subclinical hypothyroidism 25%
increased risk of placental abruption and
preterm birth
important to monitor TSH and free T4 levels.
25% progress to overt hypothyroidism each
year

Isolated maternal hypothyroxinemia

normal TSH
free T4 below 0.86 ng/dl.
In the first half of pregnancy,
prevalence 1.3%.

not associated with adverse perinatal

outcome

Guidelines for clinical management of maternal

hypothyroidism during pregnancy
1. Check serum TSH level as soon as pregnancy is
confirmed.
2. For newly diagnosed hypothyroid women, initial
levothyroxine dosage is based on severity of hypothyroidism.
For overt hypothyroidism, administer 2 mcg/kg/d. If TSH is <
10 mU/L, initial dose of 0.1 mg/d may be sufficient.
3. For previously diagnosed hypothyroid women, monitor
serum TSH every 34 weeks during first half of pregnancy
and every 6 weeks thereafter.
4. Adjust levothyroxine dosage to maintain serum TSH 2.5
mU/L.
5. Monitor serum TSH and total T4 levels 34 weeks after
every dosage adjustment. When levothyroxine dosage
achieves equilibrium, resume monitoring TSH alone
Shane O. LeBeau, Endocrinol Metab Clin N Am
35 (2006) 117136

Treatment
6. Levothyroxine ingestion should be separated from
prenatal vitamins containing iron, iron and calcium
supplements,and soy products by at least 4 hours to
ensure adequate absorption.
7. After delivery, reduce levothyroxine to prepregnancy
dosage, and check serum TSH in 6 weeks
adjusting levothyroxine
1. TSH < 10 mU/L, increase 0.05 mg/d.
2. TSH =1020 mU/L, increase 0.075 mg/d.
3. TSH > 20 mU/L, increase 0.1 mg/d.

normal range for total T4 concentrations during pregnancy is 1.5 times

the nonpregnant
iodine :prenatal vitamin 220 mg/day

Postpartum thyroid disease

Postpartum thyroiditis
Dx: documenting abnormal TSH (elevated or
suppressed) levels during the first year postpartum in
the absence of positive TSI or a toxic nodule
hypo- or hyperthyroidism
classic presentation :
transient hyperthyroid phase that occurs 6 weeks to 6
months postpartum
followed by a hypothyroid phase that lasts for up to 1
year postpartum

Postpartum thyroiditis
autoimmune disorder with a self-limited hyperthyroid phase
within one year after parturition.

Presentations
Transient hyperthyroidism alone
Transient hypothyroidism alone
Transient hyperthyroidism followed by hypothyroidism
and then recovery.

can also occur after spontaneous or induced

abortion
3 to 16 percent
higher, up to 25 percent, in women with type 1 diabetes mellitus
,and in women with positive antithyroid antibodies (normal thyroid
function)

Postpartum thyroiditis

like painless thyroiditis

variant form of chronic autoimmune thyroiditis (Hashimoto's thyroiditis).

high serum concentrations of anti-peroxidase antibodies

many eventually become hypothyroid or have a goiter
high serum antithyroid antibody concentrations early in pregnancy
decline later (as immunologic tolerance increases during pregnancy)
rise again after delivery

subclinical thyroid autoimmune disease early in pregnancy and soon

after
Progression to permanent hypothyroidism
related to higher TSH concentrations and the antiperoxidase antibody
titer
maternal age and female sex of the infant

Postpartum thyroiditis is likely to recur after subsequent pregnancies

 distinguished from Graves' hyperthyroidism,

hyperthyroidism in postpartum thyroiditis is usually
mild (both clinically and biochemically),
thyroid enlargement is minimal
Graves' ophthalmopathy is absent.
by reevaluation in three to four weeks: postpartum
thyroiditis improved

lymphocytic hypophysitis,
TSH normal or low, low free T4
postpartum thyroiditis, TSH elevated with decreased
FT4.

Postpartum thyroiditis
antithyroids :no role.
Hypothyroid :may require treatment and some
significant rate of residual hypothyroidism
Recommend:maintain thyroxine until childbearing is complete,
with an attempt to wean off medication 1 year after the last
delivery

Postpartum--signs/symptoms of thyroid dysfunction

symptoms mimic normal postpartum changes

TSH, free T4, and antithyroid antibodies levels

postpartum depression and postpartum thyroiditis

Postpartum Graves disease

60% Graves disease in the reproductive
years; postpartum onset
euthyroid patients with Graves disease
with TSI
increased risk of developing recurrent Graves
disease if antithyroid medication was withheld

TSIs differentiate postpartum Graves

disease from postpartum thyroiditis with a
hyperthyroid component.

Thyroid cancer

Thyroid tumors ;most common endocrine neoplasms.

thyroid cancer accounts for 1% of all cancers. women; 1/2
reproductive years.
biopsy ,Serum TSH and free T4 levels,ultrasonography & Fine
needle aspiration
Radionucleotide scanning is contraindicated during pregnancy
malignant or suspicious for papillary cancer, surgery at the earliest
safe period
no evidence that pregnancy causes a reactivation of thyroid cancer
or that exposure to radioactive iodine poses a risk to future
pregnancies
maintained on thyroid replacement therapy with monitoring of TSH
and free T4 levels every 8 weeks.

Euthyroidism with autoimmune

thyroid disease
increased risk for spontaneous
miscarriage, subclinical hypothyroidism,
and postpartum thyroiditis
Increase in serum TSH levels
most normal

presence of antithyroid antibodies

lack of thyroidal reserve in response to the
stimulatory effects of pregnancy.

Euthyroidism with autoimmune

thyroid disease
recommend initiating levothyroxine therapy in
women with antithyroid antibodies
before pregnancy
TSH level greater than 2.5 mU/L.

Serum TSH should be monitored throughout

pregnancy in all antithyroid antibodypositive
women
maintain the TSH concentration at 2.5 mU/L or
less.

CLINICAL PRACTICE GUIDELINE

Management of Thyroid Dysfunction during Pregnancy
and Postpartum: An Endocrine Society Clinical
Practice Guideline

1. HYPOTHYROIDISM AND PREGNANCY: MATERNAL

AND FETAL ASPECTS
1.1.1. maternal hypothyroidism should be avoided.Targeted case
finding is recommended at the first prenatalvisit or at diagnosis of
pregnancy
1.1.2. If hypothyroidism diagnosed before pregnancy, adjust
preconception T4 dose to reach a TSH 2.5 U/ml before pregnancy.
1.1.3. T4 dose incremented by 46 wk gestation and 3050%
increase in dosage.
1.1.4. If overt hypothyroidism is diagnosed during pregnancy, thyroid
function tests should be normalized as rapidly as possible.
The T4 dosage should be titrated to rapidly ,maintain serum TSH 2.5
U/ml in the first trimester (or 3 U/ml in the second and third trimesters)
or to trimester-specific normal TSH ranges.
Thyroid function tests remeasured within 3040 d.
Abalovich et al. Guideline: Thyroid Dysfunction during and after Pregnancy
J Clin Endocrinol Metab, August 2007, 92(8) (Supplement):S1S47

 1.1.5. Women with thyroid autoimmunity who are euthyroid

in the early stages of pregnancy are at risk of developing
hypothyroidism and should be monitored for elevation of
TSH above the normal range
1.1.6. Subclinical hypothyroidism ;associated with an
adverse outcome for both the mother and offspring.
T4 treatment - improve obstetrical outcome but has not been
proved to modify long-term neurological development in the
offspring.
Recommends T4 replacement in women with subclinical
hypothyroidism.

1.1.7. After delivery, most hypothyroid women need a

decrease in the T4 dosage they received during pregnancy

 2. MANAGEMENT OF MATERNAL HYPERTHYROIDISM:

MATERNAL (A) AND FETAL (B) ASPECTS
2.1.a.1. subnormal serum TSH
hyperthyroidism must be distinguished from both normal physiology during
pregnancy and hyperemesis gravidarum
Differentiation of Graves disease from gestational thyrotoxicosis by evidence of
autoimmunity, a goiter, and presence of TRAb.

2.1.a.2. For overt hyperthyroidism due to Graves disease or

hyperfunctioning thyroid nodules,
ATD therapy should be either initiated (for those with new diagnoses) or
adjusted (for those with a prior history)
maintain the maternal thyroid hormone levels for free T4 in the upper
nonpregnant reference range.

2.1.a.3. methimazole may be associated with congenital anomalies,

propylthiouracil should be used as a first-line drug,
especially during first-trimester organogenesis.
Methimazole may be prescribed if propylthiouracil is not available or if a patient
cannot tolerate or has an adverse response to propylthiouracil

 2.1.a.4. Subtotal thyroidectomy for maternal Graves disease if

1) a patient has a severe adverse reaction to ATD therapy,
2)persistently high doses of ATD are required
3) a patient is not adherent to ATD therapy and has uncontrolled
hyperthyroidism.
optimal timing of surgery is in the second trimester.

2.1.a.5. no evidence that treatment of subclinical hyperthyroidism

improves pregnancy outcome
2.1.b.1 TRAb (either TSH receptor-stimulating or binding
antibodies) freely cross the placenta and can stimulate the fetal
thyroid.
These antibodies should be measured before pregnancy or by the end of
the second trimester in mothers with current Graves disease, with a history
of Graves disease and treatment with 131I or thyroidectomy, or with a
previous neonate with Graves disease.
Women who have a negative TRAb and do not require ATD have a very
low risk of fetal or neonatal thyroid dysfunction.

 2.1.b.2. 131I should not be given to a woman who is or

may be pregnant.
radiation danger to the fetus, including thyroid destruction if
treated after the 12th week of gestation.
There are no data for or against recommending termination of
pregnancy after 131I exposure
2.1.b.3. In women with elevated TRAb or in women treated with ATD,
fetal ultrasound should be performed to look for evidence of fetal
thyroid dysfunction
growth restriction, hydrops, presence of goiter, or cardiac failure.

2.1.b.4. Umbilical blood sampling should be considered only if the

diagnosis of fetal thyroid disease is not reasonably certain from the
clinical data and if the information gained would change the
treatment.
2.1.b.5. All newborns of mothers with Graves disease should be
evaluated for thyroid dysfunction and treated if necessary

 3. GESTATIONAL HYPEREMESIS AND

HYPERTHYROIDISM
3.1. Thyroid function tests should be measured in all patients
with hyperemesis gravidarum (5% weight loss, dehydration,
and ketonuria)
3.2. Few women with hyperemesis gravidarum will require
ATD treatment.
Overt hyperthyroidism believed due to coincident Graves
disease should be treated with ATD.
Gestational hyperthyroidism with clearly elevated thyroid
hormone levels (free T4 above the reference range or total T4
150% of top normal pregnancy value and TSH 0.1 U/ml) and
evidence of hyperthyroidism may require treatment as long as
clinically necessary
4. AUTOIMMUNE THYROID DISEASE AND MISCARRIAGE
4.1. universal screening for antithyroid antibodies and
possible treatment cannot be recommended at this time.

 5. THYROID NODULES AND CANCER

5.1. Fine-needle aspiration (FNA) cytology should be
performed for thyroid nodules larger than 1 cm.
Ultrasound-guided FNA minimizing inadequate sampling.

5.2. When nodules are discovered in the first or early second

trimester to be malignant on cytopathological analysis or
exhibit rapid growth,
surgery should be offered in the second trimester before fetal viability.

For papillary cancer or follicular neoplasm without evidence

of advanced disease
prefer to wait until the postpartum period for definitive surgery
reassured that most well differentiated thyroid cancers are slow
growing
surgical treatment soon after delivery is unlikely to adversely affect
prognosis

 5.3. administer thyroid hormone to achieve a suppressed

but detectable TSH in pregnant women with a previously
treated thyroid cancer or an FNA positive for or
suspicious for cancer and those who elect to delay
surgical treatment until postpartum.
High-risk patients benefit from a greater degree of TSH
suppression
free T4 or total T4 levels should ideally not be increased
above the normal range for pregnancy.
5.4. RAI administration with 131I should not be given to
women who are breastfeeding.
pregnancy should be avoided for 6 months to 1 yr in
women with thyroid cancer who receive therapeutic RAI
doses to ensure stability of thyroid function and confirm
remission of thyroid cancer.

6. IODINE NUTRITION DURING PREGNANCY

6.1. Women of childbearing age ; average iodine intake 150 g/d.
pregnancy and breastfeeding women should increase intake to 250 g
6.2. Iodine intake during pregnancy and breastfeeding should not
exceed twice the daily recommended nutritional intake for iodine, i.e.
500 g iodine per day
6.3. To assess the adequacy of the iodine intake during pregnancy in
a population, urinary iodine concentration should be measured in a
cohort of the population.
Urinary iodine concentration should ideally range between 150 and 250
g/liter.

6.4. To reach the daily recommended nutrient intake for iodine,

multiple means must be considered, tailored to the iodine intake level
in a given population.
1) countries with iodine sufficiency and/or with a well established
universal salt iodization (USI) program,
2) countries without a USI program or an established USI program where
the coverage is known to be only partial, and finally
3) remote areas with no accessible USI program and difficult
socioeconomic conditions.

 7. POSTPARTUM THYROIDITIS
7.1. There are insufficient data to recommend screening
of all women for PPT.
7.2. Women known to be thyroid peroxidase antibody
positive should have a TSH performed at 3 and 6 months
postpartum
7.3. The prevalence of PPT in women with type 1
diabetes is 3-fold greater than in the general population.
Postpartum screening (TSH determination) is
recommended for women with type 1 diabetes mellitus at
3 and 6 months postpartum
7.4. Women with a history of PPT have a markedly
increased risk of developing permanent primary
hypothyroidism in the 5- to 10-yr period after the episode
of PPT.
An annual TSH level should be performed in these
women.

 7.5. Asymptomatic women with PPT who have a TSH

above the reference range but less than 10 U/ml and
who are not planning a subsequent pregnancy do not
necessarily require intervention but should be
remonitored in 48 wk.
Symptomatic women and women with a TSH above
normal and who are attempting pregnancy should be
treated with levothyroxine.
7.6. There is insufficient evidence to conclude whether
an association exists between postpartum depression
and either PPT or thyroid antibody positivity (in women
who did not develop PPT).
women with postpartum depression should be screened
for hypothyroidism and appropriately treated.

 8. SCREENING FOR THYROID DYSFUNCTION

DURING PREGNANCY
1. Women with a history of hyperthyroid or
hypothyroid disease, PPT, or thyroid lobectomy.
2. Women with a family history of thyroid
disease.
3. Women with a goiter.
4. Women with thyroid antibodies (when known).
5. Women with symptoms or clinical signs
suggestive of thyroid underfunction or
overfunction, including anemia,elevated
cholesterol, and hyponatremia.

 6. Women with type I diabetes.

7. Women with other autoimmune disorders.
8. Women with infertility who should have
screening with TSH as part of their infertility
work-up.
9. Women with previous therapeutic head or
neck irradiation.
10. Women with a history of miscarriage or
preterm delivery.

References
1. LeBeau& Mandel.Thyroid Disorders During
Pregnancy.Endocrinol Metab Clin N Am 35 (2006) 117
136.
2. Neale et al. Thyroid Disease in Pregnancy.Clin
Perinatol 34 (2007) 543557.
3. Abalovich et al. Guideline: Thyroid Dysfunction
during and after Pregnancy. J Clin Endocrinol Metab,
August 2007, 92(8) (Supplement):S1S47.
4. Kronenber: Williams Textbook of Endocrinology, 11th
ed.
5. Up To Date ver.15.1