Drug therapy for hyperthyroidism in pregnancy - Safety issues for mother and fetus

Hyperthyroidism (thyrotoxicosis) in pregnancy and the child bearing years i s usually attributable to Graves' disease. This is an autoimmune condition in which thyroid-stimulating immunoglobulins (TSI) cause hyperthyroidism. A s a rule, pregnancy complicates the management of hyperthyroidism, rather t han vice versa. However, patients who remain thyrotoxic during pregnancy ar e at increased risk of maternal and fetal complications, particularly misca rriage and stillbirth. Therefore, bodyweight loss, eye signs and a bruit ov er the thyroid gland in a pregnant woman warrant thyroid investigation. Inv estigations should include measurement of serum free thyroid hormone levels [free thyroxine (T-4) and free triiodothyronine (T-3)] rather than total T -4 and T-3 levels, because total T-4 and T-3 levels may be raised in euthyr oid pregnancies due to the presence of increased levels of thyroxine bindin g globulin (TBG). By 20 weeks' gestational age, the fetal thyroid is fully responsive to TSI and to antithyroid drugs. Maternal T-4 and T-3 and thyrotropin pass across the placenta in small and decreasing amounts as gestation progresses, but t hyrotropin releasing hormone, TSI, antithyroid drugs, iodides and beta-bloc kers are readily transferred to the fetus from the mother. Hyperthyroidism is usually treated throughout pregnancy with an antithyroid drug, preferably propylthiouracil. The smallest dose which controls the di sease is given with careful monitoring of free T-4 and T-3 levels to minimi se the risk of fetal hypothyroidism and goitre. Bilateral subtotal thyroide ctomy may be an option for a small number of patients with hyperthyroidism in pregnancy.