Synopsis
Interpret pregnancy-specific thyroid physiology, treat maternal hypo- and hyperthyroidism safely, and coordinate fetal, obstetric, postpartum and neonatal follow-up without therapeutic delay.
- Pregnancy raises thyroxine-binding globulin and changes total hormone concentrations; interpret TSH and free T4 using gestation- and assay-appropriate reference ranges whenever the laboratory supplies them.
- Human chorionic gonadotrophin can suppress TSH in early pregnancy. A low TSH alone is not Graves' disease: examine the clinical picture, free hormones, TSH-receptor antibodies and trajectory.
- Established hypothyroidism usually needs an early levothyroxine increase. The patient should contact the maternity/endocrine team promptly after a positive test rather than wait for routine booking.
- Levothyroxine is safe and should not be stopped in pregnancy. Separate it from iron, calcium and pregnancy multivitamins because these can reduce absorption.
- For Graves' hyperthyroidism, use the lowest effective antithyroid medicine exposure that controls maternal disease while avoiding fetal hypothyroidism; drug choice can change across gestation under specialist supervision.
- Carbimazole is associated with congenital malformations, particularly in the first trimester, while propylthiouracil carries important hepatic toxicity. Pre-conception counselling permits a planned, individualised strategy.
- Radioiodine is contraindicated during pregnancy and breastfeeding. If surgery is essential, timing and preparation are agreed jointly by obstetric, endocrine, anaesthetic and thyroid surgical teams.
- TSH-receptor antibodies cross the placenta and can affect the fetus even after maternal thyroidectomy or radioiodine. A past Graves' history remains obstetrically relevant.
- Postpartum immune rebound may trigger Graves' disease or a transient destructive thyroiditis. The hyperthyroid phase of postpartum thyroiditis is not treated with antithyroid medicines because hormone synthesis is not increased.
Key red flags
Persistent biochemical thyrotoxicosis with goitre, bruit, orbitopathy, prior Graves' disease or positive TSH-receptor antibodies favours Graves' disease over transient hCG-mediated suppression. Maternal tachycardia, weight loss and heart failure indicate severity.
Persistent fetal tachycardia, growth restriction, fetal goitre, hydrops or abnormal bone maturation can reflect fetal hyper- or hypothyroidism. Maternal antibodies and antithyroid exposure guide specialist interpretation.
Investigation priorities
Define maternal thyroid status using pregnancy-appropriate laboratory interpretation.
Management branches
Known levothyroxine-treated disease, or new raised TSH with biochemical hypothyroidism in pregnancy.
- At pregnancy confirmation, contact the endocrine/maternity team promptly and implement the pre-agreed levothyroxine increase or urgent clinician-directed adjustment; check TSH and free T4 without waiting for routine booking.
- Titrate using pregnancy-specific targets and repeat tests regularly through gestation. Check administration, missed doses and separation from iron or calcium before assuming pharmacological failure.
- After delivery, reduce toward the pre-pregnancy dose when appropriate and recheck thyroid function around the locally specified postpartum interval; do not abandon follow-up when treatment began only during pregnancy.