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.
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.
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.