The diagnosis of
Graves' disease in pregnancy can be complex because of normal gravid physiologic changes in
thyroid hormone metabolism. Mothers with active
Graves' disease should be treated with
antithyroid drugs, which impact both maternal and fetal thyroid function. Optimally, the lowest possible dose should be used to maintain maternal free
thyroxine levels at or just above the upper limit of the normal nonpregnant reference range. Fetal thyroid function depends on the balance between the transplacental passage of thyroid-stimulating maternal
antibodies and thyroid-inhibiting
antithyroid drugs. Elevated levels of serum maternal anti-
TSH-receptor antibodies early in the third trimester are a risk factor for fetal
hyperthyroidism and should prompt evaluation of the fetal thyroid by ultrasound, even in women with previously ablated
Graves' disease. Maternal antithyroid medication can be modulated to treat fetal
hyperthyroidism. Serum TSH and either total or free
thyroxine levels should be measured in fetal cord blood at delivery in women with active
Graves' disease, and those with a history of (131)I-mediated thyroid ablation or
thyroidectomy who have anti-
TSH-receptor antibodies. Neonatal
thyrotoxicosis can occur in the first few days of life after clearance of maternal
antithyroid drug, and can last for several months, until maternal
antibodies are also cleared.