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Hyperthyroidism in Pregnancy

Author: Helen R. Dunnington, MD

Mentor: Laurie S. Swaim, MD
Editor: Brett Worley, MD

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During pregnancy, physiological adaptations of the thyroid include increased thyroid volume (up to 30%) and a 40-100% increase in thyroid hormone production.  Cross-reactivity between human chorionic gonadotropin and thyroid-stimulating hormone (TSH) during the first trimester frequently results in elevated free thyroxine (FT4) and decreased TSH measurements, with subsequent normalization.

Hyperthyroidism occurs in approximately 0.2% of pregnancies, with Graves’ disease accounting for 95% of the cases.  Possible symptoms include nervousness, palpitations, frequent stools, diaphoresis, heat intolerance, weight loss, and insomnia.  Physical exam findings may consist of goiter, tachycardia, hypertension, tremors, ophthalmopathy (lid lag and retraction), and pretibial edema.  Laboratory findings include decreased TSH and increased free T4.  Detection of thyrotropin receptor antibodies is confirmatory.  Pregnancy is a contraindication for radionuclide studies.

Pregnancy outcomes are related to free T4 level, with a therapeutic goal to reduce FT4 to at, or slightly above, the upper limit of normal.  Uncontrolled maternal hyperthyroidism is associated with an increased risk of preeclampsia, heart failure, and first trimester miscarriage.  Postpartum exacerbation of hyperthyroidism or relapse of Graves’ disease can occur.

Hyperthyroidism's potential fetal effects include preterm birth, growth restriction, goiter, tachycardia, hydrops, and stillbirth, and ultrasound should be used to evaluate the fetus for these findings. Fetal thyrotoxicosis is rare but warrants subspecialist referral when detected. 

Most neonates born to mothers with Graves’ disease are euthyroid.  Transient hypothyroidism occurs in 10 to 20% of newborns of treated mothers.  Transplacental passage of TSH receptor antibodies (TRAb's) causes hyperthyroidism in less than 5% of neonates.  Maternal thyroid levels at delivery do not accurately predict neonatal Graves' disease.

Hyperthyroidism may be treated with propylthiouracil (PTU) or methimazole. PTU may cause maternal hepatotoxicity, but methimazole in the first trimester may cause fetal anomalies such as esophageal or choanal atresia and aplasia cutis. For that reason, PTU is recommended only in the first trimester with transition to methimazole beyond the period of organogenesis. Medication dosing is started empirically (PTU 50-150 mg/day; methimazole 10-40 mg/day) and titrated every two to four weeks to achieve desired free T4 levels.  Approximately 10% of pregnant women taking thioamide medications have transient leukopenia, which does not require discontinuation.  However, in <1% of patients, medication-related agranulocytosis can happen suddenly.  While monitoring serial blood counts is not helpful, patients should only discontinue the medication during suspected acute infection episodes and check their blood counts.

Thyroid storm and thyrotoxic heart failure are rare, life-threatening conditions.  Thyroid storm occurs in 1-2% of hyperthyroid pregnancies and presents with abrupt onset of fever, tachycardia, cardiac arrhythmia, and gastrointestinal and CNS dysfunction.  If untreated, it may cause multiorgan decompensation.  Thyrotoxic heart failure occurs in 8% of pregnancies with uncontrolled hyperthyroidism.  Treatment requires an intensive care setting.  Immediate therapeutic goals are inhibiting the release of triiodothyronine (T3) and T4 with PTU and iodine and blocking the peripheral conversion of T4 to T3 with corticosteroids.  Beta-blockers may control tachycardia while monitoring the potential effects on heart failure.  The underlying cause of hyperthyroidism requires treatment.  Delivery should be avoided during thyroid storm as the fetal status may improve with maternal stabilization.

Further Reading:

American College of Obstetricians and Gynecologists' Committee on Practice Bulletins—Obstetrics. Thyroid Disease in Pregnancy: ACOG Practice Bulletin, Number 223. Obstet Gynecol. 2020;135(6):e261-e274. doi:10.1097/AOG.0000000000003893

Initial Approval March 2015; Revised September 2017. Reaffirmed March 2019; Revised September 2020, Minor Revision March 2022; Reaffirmed March 2024


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