Hyperthyroidism during pregnancy

Pregnancy can lead to physiological changes in the thyroid gland, further affecting thyroid function test results. In the early stages of pregnancy, these results can lead to a report of hyperthyroidism, which is normal and does not require further treatment or correction. In contrast, pathologic hyperthyroidism does cause complications during pregnancy, such as miscarriage, preterm delivery, and further aggravation of the pregnant woman's heart burden, so further examination and evaluation and treatment are required.

Diagnosis of hyperthyroidism during pregnancy focuses on determining the cause and whether treatment is needed and which treatment should be chosen. The most commonly recommended treatment is the use of the anti-thyroid drug MMI (Lica^®) or PTU (Polupi^®), but it should be noted that MMI (Lica^®) will have teratogenicity during the first trimester of pregnancy. Therefore, PTU (Polupi^®) is recommended for the first stage of labor as follows:

Considerations for Antithyroid Drug Use and Fetal Health During Pregnancy

When maternal hyperthyroidism—particularly Graves’ disease—occurs during pregnancy, antithyroid drugs (ATDs) are often required to manage the mother's thyroid function. However, during the course of treatment, careful attention must be paid to the potential impact on the fetus. ATDs, such as propylthiouracil (PTU) and methimazole (MMI), can cross the placenta and may inhibit fetal thyroid hormone synthesis. Excessive doses can lead to fetal hypothyroidism, potentially resulting in fetal goiter and intrauterine growth restriction (IUGR).

Conversely, the TSH receptor antibodies (TRAb) produced in maternal Graves’ disease can also cross the placenta, stimulating the fetal thyroid and potentially causing fetal or neonatal hyperthyroidism. Consequently, fetal thyroid function during pregnancy may be simultaneously influenced by two opposing factors: maternal antibodies and medication.

Furthermore, maternal thyroid hormones (T3 and T4) are largely converted into inactive metabolites by high concentrations of type 3 deiodinase within the placenta; as a result, only minimal amounts reach the fetal circulation. This limited placental transfer makes it difficult for the fetus to receive adequate thyroid hormone supplementation from the mother. Therefore, if the inhibitory effect of ATDs is too strong, fetal hypothyroidism is more likely to occur.

Clinically, it is recommended to use the lowest effective dose of ATDs during pregnancy. The goal is to maintain the maternal free T4 (FT4) at or slightly above the upper limit of the normal range to avoid over-suppressing fetal thyroid function. Regular monitoring of maternal thyroid function and TRAb concentrations is essential. When necessary, fetal ultrasound should be performed to evaluate fetal thyroid size, heart rate, and growth patterns to ensure the safety of both the mother and the fetus.

Surgical Treatment During Pregnancy

In pregnancy, a thyroidectomy (surgical removal of the thyroid) is considered a last resort. It is typically only recommended when antithyroid medications are ineffective or lead to severe side effects.

• Optimal Timing: If surgery is required, it is ideally scheduled during the second trimester.
• Risk Considerations: Procedures in the first trimester carry potential teratogenic risks (risks of fetal malformation), while surgery in the third trimester increases the risk of preterm labor.
• Postoperative Follow-up: Maternal TSH receptor antibodies (TRAb) decrease gradually after surgery. Until they are fully cleared, these antibodies can still cross the placenta and stimulate the fetal thyroid. Consequently, physicians recommend enhanced fetal ultrasound monitoring to closely observe fetal cardiovascular and skeletal development.