HYPERTHYROIDISM

IN PREGNANCY
 TABLE OF CONTENTS
Thyroid Pregnancy
Physiology Outcomes
01 04
Fetal and
Autoimmunity
Neonatal Effects
02 05
Hyperthyroidism Complications
03 06
 Thyroid Physiology and
Pregnancy

In women with normal thyroid function:

- Maternal serum concentrations of thyroid binding globulin
are increase concomitantly with total or bound thyroid
hormone levels
- Thyrotropin, also called thyroid-stimulating hormone (TSH),
levels change throughout pregnancy. Notably, TSH
receptors are cross stimulated, by massive quantities of
human chorionic gonadotropin (hCG) secreted by
placental trophoblast.
- Throughout pregnancy, maternal thyroxine is transferred
to the fetus (important for normal fetal brain development,
especially before the onset of fetal thyroid gland function.)

Reference: Williams Obstetrics 26th Edition

Reference: https://www.thelancet.com/journals/landia/article/PIIS2213-8587%2813%2970086-X/
fulltext
 Autoimmunity and Thyroid Disease

- Most thyroid disorders are inextricably linked to autoantibodies against nearly 200
thyrocyte components.
- These antibodies variably stimulate thyroid function, block function, or cause thyroid
inflammation that may lead to follicular cell destruction.
- Thyroid-stimulating autoantibodies, also called thyroid stimulating
immunoglobulins (TSIs), bind and activate the TSH receptor to cause thyroid
hyperfunction and growth. (found in patients with Graves disease)
- Thyroid peroxidase (TPO) is a thyroid gland enzyme that normally functions to
produce thyroid hormones
- Thyroid peroxidase antibodies are directed against TPO (associated with early
pregnancy loss and preterm birth)

Reference: Williams Obstetrics 26th Edition

Hyperthyroidism
 ABOUT THE DISEASE
Laboratory Suggestive
Incidence
Picture Findings
Tachycardia that exceeds
Varies and complicates that usually seen with
between 0.4 and 1.7 percent Laboratory testing is normal pregnancy,
of births confirmatory.
Thyromegaly
TSH levels are markedly
depressed, Exophthalmos

Serum free T4 (FT4) levels failure to gain weight

are elevated despite adequate food
intake.

Reference: Williams Obstetrics 26th Edition

 GRAVE’S DISEASE
- The overwhelming cause of thyrotoxicosis in pregnancy is Graves disease
- An organ-specific autoimmune process associated with thyroid-stimulating
TSH-receptor antibodies
- TRAbs that bind the TSH receptor and impact the production of thyroid
hormones
- affects 0.2% of pregnant women
- The diagnosis of Graves hyperthyroidism should be suspected in a
hyperthyroid pregnant woman who
1) was having symptoms prior to pregnancy
2) had a prior diagnosis of hyperthyroidism
3) had a previous birth to an infant with thyroid dysfunction.

Reference: Williams Obstetrics 26th Edition

 Evaluation
- A definitive diagnosis of hyperthyroidism may be difficult due to normally
fluctuating levels of thyroid hormone in pregnancy.
- If the diagnosis is uncertain, it is appropriate to observe the thyroid level trends
with further laboratory testing rather than immediately starting antithyroid drug
therapy.
- TRAbs are usually measurable in Grave disease and can be used to confirm the
diagnosis and differentiate from gestational transient thyrotoxicosis.

Reference: Williams Obstetrics 26th Edition

 Treatment/ Management
- Hyperthyroidism in pregnancy is treated with medications that inhibit excessive
thyroid hormone synthesis, thionamide drugs.
- Propylthiouracil (PTU) has been historically preferred because it partially
inhibits the conversion of T4 to T3 and crosses the placenta less readily than
methimazole
- associated with hepatotoxicity that can lead to liver failure and subsequent
need for transplantation.
- After the first trimester, when the majority of organogenesis is complete, patients
are then transitioned to methimazole.
- This transition is necessary to decrease the likelihood of hepatotoxicity.
- The goal of treatment is to use the lowest dose of antithyroid medication
possible
- Potassium iodide (KI) is another medication that can be used to treat mild
hyperthyroidism.

Reference: Williams Obstetrics 26th Edition

 Treatment/ Management
- Total or subtotal thyroidectomy can be performed in pregnancy, preferably in
the second trimester
- Surgery is also an option in patients who have a large goiter causing
compression issues.
- Radioiodine ablation (RAI) is a procedure that can be used to destroy active
thyroid tissue.
- absolutely contraindicated in pregnancy due to the ability of radioiodine
to cross the placenta and subsequently ablate the fetal thyroid
- Beta-blockers such as propranolol can be used in pregnancy for symptomatic
control until a euthyroid state is maintained.

Reference: Williams Obstetrics 26th Edition

 Pregnancy Outcomes

Reference: Williams Obstetrics 26th Edition

 Fetal and Neonatal Effects
- Perinate are euthyroid in most of the cases
- Clinical hyperthyroidism develops in up to 1% of neonates born to
women with Graves disease.
- Fetus/Neonate who was exposed to excessive maternal thyroxine may
have:
- Goitrous thyrotoxicosis
- Goitrous hypothyroidism
- Nongoitrous hypothyroidism
- Fetal thyrotoxicosis
- Fetal hyper or hypothyroidism may cause hydrops, growth restriction,
goiter, or tachycardia

Reference: Williams Obstetrics 26th Edition

Thyroid Storm and Thyrotoxic Heart Failure

- Both are acute and life threatening in

pregnancy
- Pulmonary hypertension and heart
failure from cardiomyopathy by
myocardial effects of thyroxine are
common in pregnant women
- Pregnant woman with thyrotoxicosis has
minimal cardiac reserve, and
decompensation is usually precipitated by
preeclampsia, anemia, sepsis, or a
combination.

Reference: Williams Obstetrics 26th Edition

 Hyperemesis Gravidarum
- Transient condition
- Also termed as gestational transient thyrotoxicosis
- Transient hyperthyroidism is due to homology between the beta subunit
of hCG and TSH
- Affects 1% to 3% of pregnancies and thus is encountered more
frequently than Grave disease in pregnancy
- Typically resolves by 14-20 weeks’ gestation as hCG levels decline
- Antithyroid drugs not warranted
- Differentiated from Grave-induced hyperthyroidism by a lack of TRAbs.
- Also lack goiter and ophthalmopathy on physical exam, and thyroid
texture will appear normal on ultrasound

Reference: Williams Obstetrics 26th Edition

 Gestational Trophoblastic Disease
- Hydatidiform molar pregnancies are a type of gestational trophoblastic disease.
- incredibly high hCG levels and thus can have increased activation of TSH
receptors.
- Complete removal of the molar pregnancy by dilation and suction curettage is
required for treatment
- serum free T4 levels usually drop to normal levels rapidly in parallel with
declining hCG concentrations.

Reference: Williams Obstetrics 26th Edition

 Subclinical Hyperthyroidism
- Characterized by an abnormally low serum TSH concentration in concert
with normal T4 hormone levels.
- TSH assays with an analytical sensitivity of 0.002 mU/mL permit
identification of subclinical thyroid disorders.
- Long term effects include: osteoporosis, cardiovascular morbidity, and
progression to overt thyrotoxicosis or thyroid failure.
- Treatment is unwarranted in pregnancy
- Treatment could lead to fetal hypothyroidism and adverse outcomes
- Periodic surveillance needed

Reference: Williams Obstetrics 26th Edition

 Complications
Thyroid storm
- life-threatening complication that can occur when hyperthyroidism is uncontrolled
- is a manifestation of the most decompensated state of disease
- there is usually a precipitating event before a thyroid storm
- Patients may present with severe tachycardia, tachyarrhythmias, mental status changes,
heat intolerance, fever, nausea and vomiting, diarrhea, congestive heart failure, and
multi-organ failure
- Delivery should be avoided if possible since both labor or cesarean section can worsen
thyroid storm

Postpartum Thyroiditis
- typically occurs within six weeks of delivery but may happen up to one year
postpartum due to immune rebound after normal immunosuppression of pregnancy
- Often, there is a period of transient hyperthyroidism caused by autoimmune destruction
of thyroid tissue and subsequent release of thyroid hormone stores
- PPT does not require treatment with ATDs, as hyperthyroidism is transient.
Thank you for
listening.