How is subclinical hyperthyroidism treated in pregnant women?

Treatment of Subclinical Hyperthyroidism in Pregnancy

Subclinical hyperthyroidism in pregnancy (suppressed TSH with normal free T4) does not require treatment and is not associated with adverse pregnancy outcomes.

Evidence Against Treatment

The available evidence demonstrates that subclinical hyperthyroidism during pregnancy—defined as TSH below the normal reference range with normal free T4 levels—does not warrant intervention:

• Subclinical hyperthyroidism is not associated with adverse pregnancy outcomes, including no increased risk of preterm delivery, pre-eclampsia, low birth weight, or perinatal morbidity or mortality 1
• The 2004 JAMA guidelines explicitly state that no data support treatment to prevent adverse outcomes in subclinical hyperthyroidism, even though TSH <0.1 mIU/L is associated with atrial fibrillation and progression to overt hyperthyroidism in non-pregnant populations 2
• Treatment during pregnancy is unwarranted based on the lack of evidence for benefit 1

When Treatment IS Required: Overt Hyperthyroidism

The distinction between subclinical and overt hyperthyroidism is critical, as overt disease requires immediate intervention:

• Overt hyperthyroidism (suppressed TSH with elevated free T4) requires antithyroid drug therapy to prevent maternal heart failure, spontaneous abortion, preterm birth, stillbirth, and fetal/neonatal hyperthyroidism 3, 4, 5
• Propylthiouracil (PTU) is preferred in the first trimester due to lower risk of congenital malformations compared to methimazole, which has been associated with rare birth defects 3, 5
• Switching from PTU to methimazole in the second and third trimesters may be preferable given PTU's hepatotoxicity risk 3
• Treatment with antithyroid drugs reduces risk of preterm delivery (RR: 0.23), pre-eclampsia (RR: 0.23), and low birthweight (RR: 0.38) in overt hyperthyroidism 5

Monitoring Strategy for Subclinical Hyperthyroidism

While treatment is not indicated, monitoring ensures the condition remains subclinical:

• Recheck TSH and free T4 each trimester to confirm the condition remains subclinical and has not progressed to overt hyperthyroidism 6, 7
• Use pregnancy-specific TSH reference ranges: 0.01-4.00 mU/L in first and second trimesters, with third trimester values likely comparable to second trimester 7
• If TSH remains suppressed but free T4 becomes elevated, initiate antithyroid drug therapy immediately 4, 8

Critical Distinction: Gestational Transient Thyrotoxicosis

• Gestational transient thyrotoxicosis (GTT), caused by hCG-mediated stimulation in early pregnancy, is self-limited and does not require antithyroid drugs 4, 8
• GTT typically resolves by mid-pregnancy without intervention 8
• Distinguish GTT from Graves' disease by absence of thyroid autoantibodies and resolution by 14-18 weeks gestation 4

Common Pitfalls to Avoid

• Do not treat subclinical hyperthyroidism based solely on suppressed TSH—confirm free T4 is normal before withholding treatment 1
• Do not use radioactive iodine therapy during pregnancy—it is absolutely contraindicated 4
• Avoid undertreating overt hyperthyroidism, as inadequate control increases risk of maternal and fetal complications including thyroid storm 3, 8
• Do not overlook the need for postpartum monitoring, as 83% of women with Graves' disease relapse postpartum at median 3 months 8