Are detection and treatment of thyroid insufficiency in pregnancy feasible?

A workshop entitled, "The Impact of Maternal Thyroid Diseases on the Developing Fetus: Implications for Diagnosis, Treatment, and Screening," was held in Atlanta, Georgia, January 12-13, 2004. The workshop was sponsored jointly by The National Center on Birth Defects and Developmental Disabilities of The Centers for Disease Control and Prevention (CDC) and The American Thyroid Association. This paper reports on the individual session that examined the ability to detect and treat thyroid dysfunction during pregnancy. For this session, presented papers included: "Laboratory Reference Values in Pregnancy" and "Criteria for Diagnosis and Treatment of Hypothyroidism in Pregnancy." These presentations were formally discussed by invited respondents and by others in attendance. Salient points from this session about which there was agreement include the following: thyrotropin (TSH) can be used as marker for hypothyroidism in pregnancy, except when there is iodine deficiency usually evidenced by elevated serum thyroglobulin (Tg). We need more longitudinal studies of TSH during pregnancy in iodine-sufficient populations without evidence of autoimmune thyroid disease to develop trimester-specific TSH reference ranges. Current free thyroxine (FT4) estimate methods are sensitive to abnormal binding-protein states such as pregnancy. There is no absolute FT4 value that will define hypothyroxinemia across methods. Total thyroxine (TT4) changes in pregnancy are predictable and not method-specific. TT4 below 100 nmol/L (7.8 microg/dL) is a reasonable indicator of hypothyroxinemia in pregnancy. Women with known hypothyroidism and receiving levothyroxine (LT4) before pregnancy should plan to increase their dosage by 30% to 60% early in pregnancy. Women with autoimmune thyroid disease prior to pregnancy are at increased risk for thyroid insufficiency during pregnancy and postpartum thyroiditis and should be monitored with TSH during pregnancy.