Intrauterine Growth Restriction (IUGR)
Hyperthyroidism can result in IUGR, where the fetus does not grow at the expected rate. This often occurs due to placental insufficiency, which limits the supply of oxygen and nutrients to the fetus. IUGR increases the risks of stillbirth, preterm delivery, and long-term developmental issues in the child.
Neonatal Thyrotoxicosis
If maternal thyroid antibodies (TRAbs) cross the placenta, they can stimulate the fetal thyroid, leading to neonatal thyrotoxicosis. This condition can cause fetal tachycardia, goiter, and IUGR. After birth, affected newborns may experience symptoms like irritability, a rapid heart rate, and poor weight gain. In severe cases, untreated neonatal hyperthyroidism can cause heart failure, developmental delays, or even death. It occurs in about 1% to 5% of infants of mothers with Graves' disease, including mothers previously treated with surgery or radioiodine whose TRAb persists. The ATA (2017) recommends measuring TRAb early in pregnancy in any woman with current or past Graves' disease, repeating it at 18 to 22 weeks if elevated and again at 30 to 34 weeks; a level above three times the upper limit of normal prompts fetal surveillance (heart rate, growth, and goiter on ultrasound) and alerts the neonatal team. Because maternal antithyroid drugs also cross the placenta, the newborn may look euthyroid at first and become thyrotoxic at several days of age as the drug clears while the antibodies, with a half-life of about two weeks, persist.
Preterm Birth
In addition to preterm labor, preterm birth can result in underdeveloped lungs, difficulty with body temperature regulation, and feeding problems in the newborn. Premature infants also face a higher risk of neurodevelopmental disorders and long-term health challenges.
Congenital Malformations
Although hyperthyroidism itself is not directly associated with specific birth defects, antithyroid medications like methimazole, especially when used in the first trimester, have been linked to rare congenital malformations such as aplasia cutis (absence of skin) and choanal atresia (nasal airway blockage); the methimazole embryopathy also includes esophageal atresia, omphalocele, and facial dysmorphism, and the vulnerable window is about weeks 6 to 10 of gestation. PTU carries a smaller risk of milder defects (face and neck cysts, urinary tract anomalies) but a rare risk of severe maternal hepatotoxicity, so the ATA (2017) advises PTU through the first trimester (about 16 weeks) and considering a switch to methimazole afterward, converting at a methimazole-to-PTU dose ratio of about 1:20 (for example, methimazole 5 mg daily for PTU 50 mg twice daily). Both drugs cross the placenta and in excess cause fetal hypothyroidism and goiter, so the lowest dose that keeps maternal free T4 at or just above the upper reference limit is used. Managing hyperthyroidism with appropriate medications while minimizing risks to the fetus is essential.
Fetal Demise
Severe, uncontrolled hyperthyroidism can increase the risk of fetal demise, often due to placental insufficiency, fetal growth restriction, or thyroid storm. Careful management of hyperthyroidism during pregnancy is vital to mitigate these risks and ensure the well-being of both mother and baby.
