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Thyroid Disease in Pregnancy


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Title: Thyroid Disease in Pregnancy

Thyroid Disease in Pregnancy
  • Chantarojanasiri T. ,MD.

  • Normal physiology changes during pregnancy
  • Hyperthyroid
  • Hypothyroid
  • Postpartum thyroid disease
  • Thyroid cancer
  • Euthyroid with autoimmune thyroid disease
  • Practice guidelines

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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 a and ß subunitß subunit confers
  • TSH secretion regulated by negative feedback from
    circulating thyroid hormone, dopamine, and
  • 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

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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
  • 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
    cross-reactivity of the a 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

  • 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
  • increased maternal glomerular filtration rate--
    increased renal clearance of iodide throughout
  • transplacental passage of T4 and iodide and
    placental metabolism of iodothyronines
  • stimulate the maternal thyroid depleting the
    maternal circulation of thyroid hormone and its

  • Hypothyroid25 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

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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 lt0.01 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
  • 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
  • higher serum hCG and estradiol concentrations
  • 60 have a subnormal serum TSH level (lt 0.4
    mU/L),50 have an elevated serum free T4
  • 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
  • The thyroid gland usually is not enlarged
  • resolution of symptoms parallels the decline in
    hCG levels
  • usually resolves spontaneously by 20 weeks
  • beyond 20 weeks,repeat evaluation for other causes

Trophoblastic hyperthyroidism
  • hydatidiform mole (molar pregnancy)
  • high serum hCG concentrations and abnormal hCG
  • 55 to 60 percent had clinically evident
  • normal thyroid gland and few symptoms of thyroid
    hormone excess.
  • some findings of hyperthyroidism and a diffuse
  • 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
  • thyroid examination goiter (with or without
  • 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
  • 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

Guidelines for clinical management of
maternalhyperthyroidism 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
  • Monitoring serum TSH may become useful later.

Shane O. LeBeau, Endocrinol Metab Clin N Am 35
(2006) 117136
Guidelines for clinical management of
maternalhyperthyroidism during pregnancy
  • 3. Measure TSH receptor antibodies
    (thyroid-stimulating immunoglobulins or TSH
    receptor binding inhibitory immunoglobulins) at
    2628 weeks to assess risk of fetal/neonatal
  • 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
maternalhyperthyroidism during pregnancy
  • 5. Consider thyroidectomy if persistently high
    doses of thionamide (PTU gt 600 mg/d or MMI gt 40
    mg/d) are required,or if the patient cannot
    tolerate thionamide therapy.
  • 6. ß-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

  • Thionamides
  • propylthiouracil (PTU) and methimazole(MMI)
  • Both cross the placenta with equal transfer
  • Both can cause fetal goiter and hypothyroidism,
    usually mild and transient dose-dependent
  • median time to normalization of maternal thyroid
  • 7 weeks with PTU and 8 weeks with MMI
  • PTU more highly bound to albumin
  • theorize that MMI crosses the placenta in higher

  • Thionamides
  • maternal rash
  • rare birth defects in MMI aplasia cutis, choanal
    atresia,esophageal atresia, and minor dysmorphic
  • Low thyroid function at birth ½ neonates whose
    mothers received PTU or MMI and had serum T4
    concentrations within the normal (non-pregnant)
  • normal IQ scores
  • Graves disease may ameliorate
  • thionamide discontinued in 30 during the final
  • 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.

  • ß-Adrenergic blockers
  • weaned as soon as the hyperthyroidism is
  • occasional cases of neonatal growth restriction,
    hypoglycemia, respiratory depression, and
  • increased frequency of first-trimester
  • 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.

  • Surgery
  • Subtotal thyroidectomy
  • persistently high dosages of thionamides (PTU gt
    600 mg/d, MMI gt 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 ß-adrenergic blocking agent and a
    10- to 14-day course of potassium iodide

  • 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
  • Thyroid function in newborn infants is unaffected
  • PTU is preferred because it is less concentrated
    in breast milk

Hypothyroidism in pregnancy
  • elevated serum TSH concentration2.5 of
  • 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
  • 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
  • mellitus and women who have type I diabetes have
    a 25 risk of developing postpartum thyroid

Causes of hypothyroidism
  • Worldwide, the most common is iodine deficiency.
  • impaired neurologic development severe mental
    retardation, deafness,
  • muteness, and pyramidal or extrapyramidal
  • Hashimotos thyroiditis
  • Idiopathic hypothyroidism atrophic thyroid gland
  • and absent antithyroid antibodies.
  • 131I treatment for Graves disease and
  • Drugs interfere with the metabolism of thyroid

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
  • 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
maternalhypothyroidism during pregnancy
  • 1. Check serum TSH level as soon as pregnancy is
  • 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 lt 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
  • 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
  • adjusting levothyroxine
  • 1. TSH lt 10 mU/L, increase 0.05 mg/d.
  • 2. TSH 1020 mU/L, increase 0.075 mg/d.
  • 3. TSH gt 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
  • 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
  • many eventually become hypothyroid or have a
  • 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
  • Recommendmaintain 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

Thyroid cancer
  • Thyroid tumors most common endocrine neoplasms.
  • thyroid cancer accounts for 1 of all cancers. ¾
    women 1/2 reproductive years.
  • biopsy ,Serum TSH and free T4 levels,ultrasonograp
    hy 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

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Euthyroidism with autoimmune thyroid disease
  • increased risk for spontaneous miscarriage,
    subclinical hypothyroidism, and postpartum
  • 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
  • maintain the TSH concentration at 2.5 mU/L or

Dysfunction during Pregnancyand Postpartum An
Endocrine Society ClinicalPractice Guideline
  • 1.1.1. maternal hypothyroidism should be
    avoided.Targeted case finding is recommended at
    the first prenatalvisit or at diagnosis of
  • 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
  • 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
  • 1.1.6. Subclinical hypothyroidism associated
    with an
  • adverse outcome for both the mother and
  • 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

  • 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
  • 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
  • 2.1.a.5. no evidence that treatment of
    subclinical hyperthyroidism improves pregnancy
  • 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
  • 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
  • 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

  • 3.1. 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
  • 4.1. universal screening for antithyroid
    antibodies and possible treatment cannot be
    recommended at this time.

  • 5.1. Fine-needle aspiration (FNA) cytology should
    be performed for thyroid nodules larger than 1
  • Ultrasound-guided FNA minimizing inadequate
  • 5.2. When nodules are discovered in the first or
    early second trimester to be malignant on
    cytopathological analysis or exhibit rapid
  • 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
  • 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

  • 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.

  • 7.1. 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
  • 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

  • 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

  • 1. Women with a history of hyperthyroid or
    hypothyroid disease, PPT, or thyroid lobectomy.
  • 2. Women with a family history of thyroid
  • 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
  • 9. Women with previous therapeutic head or neck
  • 10. Women with a history of miscarriage or
    preterm delivery.

  • 1. LeBeau Mandel.Thyroid Disorders During
    Pregnancy.Endocrinol Metab Clin N Am 35 (2006)
  • 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)
  • 4. Kronenber Williams Textbook of Endocrinology,
    11th ed.
  • 5. Up To Date ver.15.1
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