Pregnancy has profound effects on the regulation of thyroid function in healthy women and patients with thyroid disorders. These effects need to be recognized, precisely assessed, clearly interpreted, and correctly managed. For healthy pregnant women who reside in areas with a restricted iodine intake, relative hypothyroxinemia & goitrogenesis occur frequently, indicating that pregnancy constitutes a challenge for the thyroidal economy.

Overt thyroid dysfunction occurs in 2-3% of pregnancies, but subclinical thyroid dysfunction (both hyper- & hypothyroidism) is probably more prevalent and frequently remains undiagnosed, unless specific screening programs are initiated to disclose thyroid function abnormalities in early gestation. Maternal alterations of thyroid function due to iodine deficiency, hypothyroidism and hyperthyroidism have important implications for fetal/neonatal outcome. In recent years, particular attention has been focused on potential developmental risks for the fetuses of women with hypothyroxinemia during early gestation.

Pregnancy increases the metabolic rate, blood flow, heart rate, and cardiac output, and various subjective sensations such as fatigue and heat intolerance that may suggest the possibility of coexistent thyrotoxicosis. Other metabolic changes which also impact the hypothalamic pituitary thyroid system are the potential direct stimulation of the maternal thyroid by hCG, as well as the accelerated metabolism of thyroxine, presumably due to increased placental deiodination enzymes.

In patients with hypothyroidism, it is important to recognize that therapeutic requirements for exogenous thyroxine are increased by 50% on average during pregnancy. This should be taken into account in the management of such patients.

Main causes of thyrotoxicosis in pregnancy include Graves' disease (uncommon, but potentially pregnancy-threatening) and gestational non autoimmune transient hyperthyroidism (more common, but remaining mild usually). The natural history of Graves' disease is altered during pregnancy, with a tendency for exacerbation in 1st trimester, amelioration during 2nd & 3rd trimesters, and typically a rebound during the postpartum period. These changes are the consequences of partial immune suppression during gestation with a rebound during the postpartum period. This must be kept in mind when treating thyrotoxic patients, since all ATD cross the placenta and may affect fetal thyroid function.

Fetal and neonatal hyperthyroidism is due to the transplacental transfer of maternal stimulating TSH-receptor antibodies (TRAb). The diagnosis of fetal (and neonatal) hyperthyroidism is usually made on the basis of fetal tachycardia, accelerated bone age, and intrauterine growth retardation. It may occur in infants born to women with active Graves' disease, but also to women who have had prior definitive cure of their disease by surgery or radioactive iodine, but maintain high titers of TRAb. The proper management of pregnant patients with Graves' disease remains a difficult challenge in clinical endocrinology.

Thyroid nodules discovered during pregnancy should be aspirated for cytological diagnosis. If a malignancy is diagnosed, surgery should be performed during pregnancy or shortly thereafter. Pregnancy by itself does not adversely affect the natural history of differentiated thyroid carcinoma.

During the postpartum period, particular attention should be given to women with thyroid autoimmunity, in who hypothyroidism and/or hyperthyroidism are frequently exacerbated.