• Nathan Riley, MD

Obgyno Wino Podcast Episode 52 - Thyroid Disease in Pregnancy

"Dost thou reckon thyself only a puny form when within thee the universe is folded?"

- Baha'i teaching

2016 Cabernet Sauvignon from Embrazen Wine

PB#223 - Published June 2020

Five Pearls

1. Fetal brain development relies on adequate maternal T4 until the fetal thyroid gland takes over at ~12 wga

2. Fetuses who develop in environments deficient in thyroid hormone may suffer from impaired psychoneurological development of the newborn

3. Hyperthyroidism is most commonly due to Graves' disease, which is caused by antibodies that stimulate the thyroid gland

4. Screening for thyroid disease in pregnancy starts w/ TSH. More sensitive than thyroid hormone.

5. Propylthiouracil is generally used to treat hyperthyroidism in the 1st trimester because methimazole is associated w/ rare embryopathies

Thyroid function during pregnancy - mom

- thyroid itself gets bigger (30%!) throughout pregnancy

- during first 12 weeks, high levels of bHCG stimulate TSH receptors, causing an increase in thyroid hormone (T4) and a decrease in TSH release through negative feedback loops

- there's also an increase in thyroid-binding globulin (effect of estrogen on the liver), meaning an increase in total thyroid hormone

- TSH increases in 3rd trimester as the placenta grows along with its production of deiodinase

Recall: deiodinase metabolizes T4 --> T3

- refer to your institution's lab for reference ranges of TSH in 1st trimester, but normal is generally considered 0.5 - 2.5 mu/L

- beyond the 1st trimester, TSH normalizes to nonpregnant levels

- normal ranges for T3/T4 should be increased by 50% after 16 wga (don't even look at T3/T4 levels before 16 wga because they gradually increase with the increase is thyroid-binding globulin)

Thyroid function in pregnancy - baby

- fetal thyroid gland begins synthesizing endogenous hormones by 12 wga

- mom T4 is also transferred across the placenta throughout pregnancy

- mom's T4 is critical for fetal brain development before fetal thyroid takes over

Hyperthyroidism - too much thyroid hormone

- increase in free T4, decrease in TSH

- 95% due to Graves', where antibodies stimulate thyroid gland

- pregnant women with Graves' disease can have thyroid-stimulating antibodies along with TSH-receptor binding antibodies, both of which can cross placenta and cause fetal thyrotoxicosis or transient hypothyroidism, respectively

- if mom is treated with thioamides, these drugs also cross the placenta, but they are cleared more rapidly by the baby than the maternal antibodies, which may lead to late presentations of hyperthyroidism in the neonate

- signs and symptoms:

  • nervousness

  • tremors

  • tachycardia

  • frequent stools

  • excessive sweating

  • heat intolerance

  • weight loss

  • goiter

  • insomnia

  • palpitations

  • hypertension

  • eyelid lag and retraction (buggy eyes)

  • pretibial myxedema

- untreated hyperthyroidism is associated with:

  • severe preeclampsia

  • maternal heart failure and thyroid storm

  • preterm birth

  • miscarriage

  • IUFD

  • fetal tachycardia

  • poor fetal growth

Typical ophthalmopathy seen in Graves' disease

Hypothyroidism - too little thyroid hormone

- decrease in free T4, increase in TSH

- Hashimoto's thyroiditis is the most common cause of hypothyroidism in pregnancy, which is characterized by destruction of the thyroid gland by antithyroid peroxidase antibodies (unlike w/ Grave's, these antibodies don't cross the placenta)

- usually not related to poor iodine intake, at least in the United States

- signs and symptoms:

  • fatigue

  • constipation

  • cold intolerance

  • muscle cramps

  • weight gain

  • edema

  • dry skin

  • hair loss

  • prolonged relaxation phase of deep tendon reflexes

- untreated hypothyroidism is associated with:

  • SAB

  • preeclampsia

  • preterm birth

  • placental abruption

  • IUFD

  • poor fetal growth

  • impaired psychoneurological development of the newborn

Subclinical thyroid disorders

- not associated with poor outcomes for mom or baby

- unlikely to convert to overt thyroid disorder during pregnancy

- treatment is not recommended

- subclinical hyperthyroidism: normal free T4, low TSH

- subclinical hypothyroidism: normal free T4, high TSH

Who should be screened for a thyroid disorder in pregnancy?

- universal screening not recommended

- screen if:

  • personal or family history of thyroid disease

  • type 1 diabetes mellitus

  • clinical suspicion of thyroid disease

Work-up and management

Pearl: TSH is more useful in pregnancy because (1) even small fluctuations in thyroid hormone cause changes to TSH through feedback loops and (2) lab assays generally aren't sensitive enough to reliably detect aberrations of free thyroid hormone as they don't routinely use physical separation tests and therefore depend on quantities of circulating binding hormone as an estimation of total hormone circulating

- if TSH is high, follow-up with free T4 alone

- if TSH is low,, follow-up with total T3 and free T4 (total T3 is more accurate than free T3)

- while treating for hyperthyroidism, dose of thioamide should be adjusted according to free T4 level; aim for high normal range for pregnancy

- if thyrotoxicosis is T3-predominant, use total T3 instead

Medications used to treat hyperthyroidism

- methimazole and propylthiouracil: both thioamides; choice of med depends on response in prior therapy, trimester, and T3 versus T4 thyrotoxicosis predominance

- methimazole is avoided in 1st trimester due to its association with esophageal/choanal atresia and aplasia cutis

- you can transition from propylthiouracil after the 1st trimester to methimazole given the former's association with hepatotoxicity, but the transition may cause an unintended period of poor thyroid control

- if you do transition from propylthiouracil to methimazole, dosage is converted 20:1

- leukopenia is seen in 10% of women treated with either med, but it does not warrant discontinuation (if patient develops a sore throat, tell her to stop the medication and report to the lab for CBC)

- agranulocytosis is seen in 1% of women and does warrant discontinuation

- propanolol 10-40 mg daily can be used to treat bothersome heart palpitations in women w/ hyperthyroidism while you are titrating their thioamide

Should I screen my pregnant patient for anti-thyroperoxidase or anti-thyroglobulin antibodies?

- 20% of women of reproductive age have these antibodies but most remain euthyroid

- anti-thyroperoxidase antibodies are associated w/ preterm birth

- women who have the antibodies are also at higher risk for postpartum thyroiditis

- yet the answer is no, don't routinely screen, as treatment with thyroid hormones for the finding of these antibodies alone has not been shown to improve outcomes.

How should you manage a pregnant woman who is found to have thyroid stimulating antibodies?

- monitor fetus for signs of hyperthyroidism through serial growth ultrasound

True or false: thyroid function can change alongside hyperemesis gravidarum (HG)?

- True! Patient's with HG often have very low TSH and very high T4 levels

- both HG and thyroid dysfunction can be linked to the high levels of bHCG classically found in the 1st trimester

- this is AKA as "gestational transient hyperthyroidism"

- manage expectantly

- TSH levels may remain suppressed long after nausea resolves, so it's not recommended to serially repeat thyroid function testing in HG unless over signs of hyperthyroidism are present

Let's talk a little about the diagnosis and management of thyrotoxicosis and thyroid storm...


- rare but may be life-threatening, can lead to thyrotoxic heart failure if left untreated

- basically high thyroid hormones crank up your cardiovascular system --> preeclampsia, anemia, and/or sepsis may ensue --> decompensation/heart failure --> death

- if suspected, collect thyroid studies to confirm diagnosis but begin treatment immediately

Thyroid storm

- signs/symptoms of thyroid storm: fever, tachycardia, cardiac dysrhythmia, and CNS dysfunction

- usually triggered by infection/trauma

- diagnosis and management is same as thyrotoxicosis (except you also need to find and try to reverse the underlying cause)

Can thyrotoxicosis present in the fetus?

- It most certainly can!

- if maternal hyperthyroidism goes untreated, fetal thyrotoxicosis should be investigated if you can find fetal hydrops, growth restriction, fetal goiter, or persistent fetal tachycardia

- get them over to MFM, stat!

How should I manage a thyroid nodule or thyroid cancer during pregnancy?

- incidence of thyroid nodules for reproductive-aged women is 1-2%

- management decision depends on size of mass and gestational age of pregnancy

- ultrasound is the first step if you palpate a nodule, but it's hard to detect a nodule if <0.5 cm

- good news: 90-95% of solitary thyroid nodules are benign!

- >70% likelihood of malignancy if hypoechoic + irregular margins + microcalcifications

- if any of these features are noted, next step is FNA

- radioiodine screening is not recommended of theoretic risk of fetal irradiation; however, the fetal thyroid gland is not active until 12 wga, so in theory it would be dangerous in the 1st trimester

- if cancer is found, generally best to wait until after birth because thyroid cancers are generally slow-growing

- it's safe to perform thyroidectomy in the 1st and 2nd trimesters, but removal of the parathyroid glands would be no good, so often it's best to delay surgery until postpartum period, especially if the cancer is not aggressive or if it's diagnosed in the 3rd trimester

Final remarks: postpartum thyroiditis

- definition: thyroid dysfunction diagnosed within 12 months of birth

- transient autoimmune thyroiditis is found in 5-10% of women during the first year after childbirth

- generally, it initially presents as an abrupt, destruction-induced thyrotoxicosis, which is often accompanied by a small, painless goiter

- after a few months, the patient will then become hypothyroid w/ all the accoutrements (fatigue, constipation, and depression are common)

- thioamide therapy is generally not warranted, but the patient may benefit from short-course therapy with a b-blocker if palpitations are problematic early on

- usually resolves spontaneously, but 1/3 of women will go on to develop overt hypothyroidism, so periodic thyroid testing is reasonable

- the higher the thyroid autoantibodies, the greater the likelihood of developing overt hypothyroidism

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