Management of Hyperthyroidism in Pregnancy
Use propylthiouracil (PTU) during the first trimester, then switch to methimazole for the second and third trimesters to minimize both birth defects and maternal hepatotoxicity. 1
Medication Selection by Trimester
First Trimester (Weeks 1-13)
- PTU is the preferred antithyroid drug during organogenesis because methimazole carries a risk of congenital malformations when used during weeks 6-10 of pregnancy 1, 2, 3
- Methimazole-associated birth defects can be severe, making PTU the safer choice despite its hepatotoxicity risk 1, 2
Second and Third Trimesters (Weeks 14-40)
- Switch from PTU to methimazole after the first trimester to reduce the risk of maternal hepatotoxicity 1
- Continuing PTU beyond the first trimester unnecessarily exposes the mother to liver injury risk 1
- The FDA label acknowledges that switching to methimazole for the second and third trimesters is preferable given PTU's hepatotoxic potential 2
Treatment Goals and Monitoring
Target Thyroid Levels
- Maintain free T4 or Free Thyroxine Index (FTI) in the high-normal range using the lowest possible thioamide dosage 1
- Aim for subclinical hyperthyroidism rather than complete normalization to minimize fetal exposure to antithyroid drugs 4
- Use free T4 and free T3 measurements rather than total hormone levels, as total T4 and T3 are elevated in normal pregnancy due to increased thyroxine-binding globulin 5
Monitoring Frequency
- Check FT4 or FTI every 2-4 weeks to guide dosage adjustments 1
- A rising TSH indicates the need for a lower maintenance dose 2
- Both maternal and fetal thyroid function require careful monitoring since antithyroid drugs, thyroid-stimulating antibodies, and thyroid hormones all cross the placenta 5, 3
Symptomatic Management
- Initiate beta-adrenergic blockers (such as propranolol) for symptomatic relief while awaiting thyroid control 6
- Beta-blockers readily cross the placenta, so use the lowest effective dose 5
- Dose reduction of beta-blockers may be needed as the patient becomes euthyroid due to decreased clearance 2
Risks of Untreated Hyperthyroidism
- Untreated maternal hyperthyroidism significantly increases risks including severe preeclampsia, preterm delivery, heart failure, miscarriage, stillbirth, and low birth weight 1, 2, 7
- Maternal thyrotoxicosis poses greater risks than the side effects of antithyroid drugs, making treatment essential 7, 5
Critical Monitoring for Drug Toxicity
- Immediately discontinue the thioamide if sore throat and fever develop, as this may indicate agranulocytosis 6
- Monitor for hepatitis, vasculitis, and thrombocytopenia 6
- Check prothrombin time before surgical procedures, as methimazole may cause hypoprothrombinemia 2
Fetal and Neonatal Considerations
- Inform the newborn's physician about maternal thyroid disease due to risk of neonatal thyroid dysfunction from transplacental passage of thyroid-stimulating antibodies or excessive antithyroid drug exposure 1, 7
- The fetal thyroid becomes fully responsive to both thyroid-stimulating antibodies and antithyroid drugs by 20 weeks' gestation 5
- Fetal/neonatal hyperthyroidism can occur in offspring of mothers with Graves' disease, requiring collaboration between endocrinologists, obstetricians, and neonatologists 7, 8
Postpartum Management
- Women treated with PTU or methimazole can safely breastfeed, as studies of 139 thyrotoxic lactating mothers found no toxicity in nursing infants 1, 2
- Monitor thyroid function at frequent (weekly or biweekly) intervals in breastfeeding mothers 2
- Thyroid dysfunction often diminishes as pregnancy progresses, and dose reduction or discontinuation may be possible weeks to months before delivery 2, 8
Common Pitfalls to Avoid
- Failing to switch from PTU to methimazole after the first trimester increases unnecessary hepatotoxicity risk 1
- Inadequate monitoring of thyroid function during pregnancy results in suboptimal treatment 1
- Over-treatment with antithyroid drugs can cause fetal hypothyroidism and goiter, so use the minimum effective dose 5, 3