Hyperthyroidism detected during pregnancy

A low or suppressed serum TSH concentration in the first trimester is not usually a cause for concern. It is usually caused by the increased human chorionic gonadotrophin (hCG) concentration that occurs in the first trimester—hCG stimulates TSH receptors, increasing triiodothyronine (T₃) and T₄ production, which in turn suppresses TSH via negative feedback.

Gestational hyperthyroidism (also known as gestational transient thyrotoxicosis) can occur if the TSH receptor is hypersensitive to hCG, resulting in excessive production of T₃ and T₄. However, gestational hyperthyroidism is self-limiting, as the hCG concentration declines after approximately week 12 of gestation, and usually does not require treatment.

It is important to differentiate gestational hyperthyroidism from both Graves disease and pre-existing toxic multinodular goitre, which usually do require treatment. Serum hCG elevation is not differential. Gestational hyperthyroidism is often associated with hyperemesis gravidarum, but also occurs in the absence of vomiting; in addition, thyroid function tests usually normalise with declining hCG concentrations. Graves disease is usually associated with positive TSH-receptor antibody and commonly also positive thyroid peroxidase antibody or thyroglobulin antibody. If available, preconception thyroid function tests can be helpful. If in doubt, particularly if the hyperthyroidism is more than mild, seek expert advice.

Radionuclide thyroid scans are contraindicated in pregnancy.