Objective: To present an overview of autoimmune thyroid disease (AITD) that can occur in pregnancy.
Methods: The major thyroid antibodies that can traverse the maternal-fetal circulation and affect the fetus are summarized, those women at risk of having affected fetuses are identified, and the diagnosis, course, and treatment of AITD in maternal and neonatal patients are discussed.
Summary: AITD, including Graves' disease and autoimmune thyroiditis, is common in women of childbearing age. Rarely, the fetus can be affected because of transplacental passage of maternal IgG. Of the thyroid autoantibodies found in AITD, only those directed against the thyroid-stimulating hormone (TSH) receptor have been shown to cause fetal thyroid dysfunction. Both transient neonatal hyperthyroidism and hypothyroidism have been described, as has delayed onset of neonatal hyperthyroidism due to the coexistence of stimulating and blocking TSH receptor antibodies. In general, affected infants are those born to mothers with the most potent antibody activity, and the duration of the neonatal thyroid dysfunction is dependent on the antibody titer and the rate of metabolic clearance from the infant's circulation. If fetal hyperthyroidism is suspected, maternal TSH receptor antibodies should be measured during the third trimester of pregnancy. For neonatal hypothyroidism, this measurement in the mother or baby soon after birth will suffice. Screening for the presence of TSH receptor antibodies by radioreceptor assay is the most cost-effective approach. If results are positive, bioassay should be done to determine the nature of the antibody activity. Women at risk of having babies with neonatal hyperthyroidism include those with a history of previous affected infants, with difficult to control thyrotoxicosis, or with a history of Graves' disease and development of hypothyroidism either spontaneously or as a result of thyroid gland ablation. Transient neonatal hypothyroidism due to TSH receptor-blocking antibodies should be suspected in any infant with hypothyroidism born to a mother with AITD (particularly those with previously affected offspring).
Conclusion: Treatment of maternal hyperthyroidism must consider both maternal and fetal thyroid status. In general, the lowest dose of antithyroid medication sufficient to produce maternal euthyroidism or slight hyperthyroidism is used. In pregnant women with hypothyroidism, doses of L-thyroxine should be sufficient to normalize maternal thyroid function without regard to the fetus. Identification and treatment of affected infants soon after birth will ensure a normal outcome. Whether inadequately treated maternal hypothyroidism is associated with a permanent intellectual deficit in the offspring is currently unknown.