Epidemiology and prevention of thyroid disease in pregnancy.

Pregnancy has variable effects on thyroid hormone concentrations throughout pregnancy as well as being associated with goiter. The latter is largely preventable by ensuring optimal iodine intake of at least 200 microg/d. Immunologic changes in pregnancy include a so-called T(H)2 shift that reverts to T(H)1 status around birth or early in the postpartum period. Hyperthyroidism during gestation, usually caused by Graves' disease, is rare (0.2%) and is best managed medically with propylthiouracil; thyroid-stimulating antibodies should be measured. Prevention of the deleterious effects of Graves' disease includes adequate preconception advice, adequate monitoring during pregnancy, and total avoidance of (131)I therapy during pregnancy. Hypothyroidism during pregnancy has an incidence of 2.5% although there is a 10% incidence of thyroid peroxidase (TPO)-antibody positivity in early gestation. There are convincing epidemiologic data to show that suboptimal thyroid function in pregnancy is associated with impaired neurointellectual development (e.g., 19% with IQ < 85 compared to 5% in one study). Therefore, there is a case for screening for thyroid function in early pregnancy with thyroxine (T(4)) intervention therapy. Maintenance of optimal iodine intake is critical to prevent nonautoimmune gestational maternal hypothyroxinaemia. Postpartum thyroid dysfunction (PPTD) occurs in 5%-9% of women and in up to 50% of TPO-antibody positive women (as ascertained in early pregnancy). Prevention of PPTD at this time could only be achieved by pregestational ablation of the thyroid. Another approach is to at least improve the prediction of postpartum thyroid disease (PPT) because the TPO antibody has a sensitivity of only 50%.