Clinical Aspects of Hyperthyroidism, Hypothyroidism, and Thyroid Screening in Pregnancy

Roberto Negro, MD, FACE; Alex Stagnaro-Green, MD, MHPE


Endocr Pract. 2014;20(6):597-607. 

In This Article

Abstract and Introduction


Objective: To evaluate the peer-reviewed literature on hypothyroidism, hyperthyroidism, and thyroid autoimmunity in pregnancy.

Methods: We review published studies on thyroid autoimmunity and dysfunction in pregnancy, the impact of thyroid disease on pregnancy, and discuss implications for screening.

Results: Overt hyperthyroidism and hypothyroidism are responsible for adverse obstetric and neonatal events. Several studies of association suggest that either subclinical hypothyroidism or thyroid autoimmunity increase the risk of complications. One randomized controlled trial showed that pregnant women with subclinical hypothyroidism benefit from treatment in terms of obstetric and neonatal complications, whereas another study demonstrated no benefit in the intelligence quotient of babies born to women with subclinical hypothyroidism. Thyroid autoimmunity has been associated with increased rate of pregnancy loss, recurrent miscarriage, and preterm delivery.

Conclusion: Current guidelines agree that overt hyperthyroidism and hypothyroidism need to be promptly treated and that as potential benefits outweigh potential harm, subclinical hypothyroidism also requires substitutive treatment. The chance that women with thyroid autoimmunity may benefit from levothyroxine treatment to improve obstetric outcome is intriguing, but adequately powered randomized controlled trials are needed. The issue of universal thyroid screening at the beginning of pregnancy is still a matter of debate, and aggressive case-finding is supported.


Thyroid physiology changes significantly during pregnancy. The metabolic changes include an increase in iodine renal clearance, the impact of human chorionic gonadotrophin (hCG) on the thyrotrope receptor, an increase in serum thyroxine-binding globulin (TBG), and inner-ring deiodination of triiodothyronine (T3) and thyroxine (T4) by the placenta.[1] In geographic areas with sufficient daily iodine intake, the most significant change in maternal thyroid economy is the thyrotropic stimulatory action exerted by hCG. The inverse relationship of hCG and thyroidstimulating hormone (TSH) levels during early pregnancy has been extensively documented and is particularly evident in the subgroup of women with TSH values in the lower percentiles.[2] The thyrotropic action exerted by hCG is heightened in multiple-gestation pregnancies, in which higher hCG levels induce a greater downward shift in TSH levels than is seen in singleton pregnancies.[3] As a consequence of the first-trimester rise in hCG, a slight and temporary increase in free (F)T4, total T4, and total T3 levels may be observed. The above-mentioned physiologic changes induce variations in maternal TSH (lowered) and FT4 (increased), especially during the first trimester, such that ranges used for the nonpregnant population cannot be applied to the pregnant state.[4]