Thyroid disorders are common in pregnant patients and effective management is critical for maternal, fetal, and neonatal health. As a group, they represent the second most common endocrine disorder in pregnancy in the United States and worldwide. Hypothyroidism is more common than hyperthyroidism, and occurs in an estimated 2–3 % of pregnancies, affecting pregnant persons in both iodine-rich and iodine-deficient regions alike. Hyperthyroidism occurs in an estimated 0.1–1 % of pregnancies, with Graves’ disease representing the most common etiology.1 Thyroid deficiency or excess, particularly during fetal brain development, is a strong teratogen, emphasizing the need for selective screening, accurate diagnosis and treatment of thyroid dysfunction.2 This review will highlight thyroid physiology and the diagnosis and management of thyroid disorders in pregnancy.

The thyroid gland undergoes significant physiologic change during pregnancy. The thyroid gland increases in size by 10 % and the production of thyroid hormones, thyroxine (T4) and triiodothyronine (T3) increase by nearly 50 %.3 Human chorionic gonadotropin (HCG), a rapidly rising hormone in early pregnancy, and TSH share identical alpha subunits, which allows HCG to weakly bind to TSH receptors on the thyroid gland, further increasing T3 and T4 secretion. This cross-reactivity also decreases TSH levels via negative feedback on the pituitary gland.4

Concomitantly, estrogen increases production of thyroxine binding globulin (TBG) and sialylation, which decreases clearance of TBG.5 Although the overall effect is a significant rise in total levels of T4 and T3, serum free T4 (FT4) only increases marginally in the first trimester and then decreases, remaining overall similar in range to nonpregnant persons.6

The fetus is supplied with thyroid hormone by both the maternal thyroid gland throughout gestation and the developing fetal thyroid gland after 18–20 weeks gestation.7 During the first half of gestation, before fetal thyroid production begins, the fetus is dependent on placental transfer of maternal T4.8 Placental deiodinases regulate the amount of maternal T4 that is transferred to the fetus, and iodothyronine deiodinase (D3) then catalyzes the conversion of T4 to T3 in the fetal brain tissue.6 Generally, iodothyronine deiodinases are responsible for closely regulating the balance of T3 supplied to the developing fetal tissues, preventing the negative effects of excessive thyroid hormone.6,8

Iodine is essential for thyroid hormone production and therefore for normal fetal neurodevelopment. Pregnancy results in a 50 % increase in iodine requirement due to an increase in thyroid hormone production, increase in renal iodine clearance, fetal iodine requirements, and lactation requirements.9 The US population remains overall iodine sufficient due to public health efforts on iodization of salt since the 1920s.10

Today, iodine is primarily derived from the diet and from ingestion of vitamin preparations. According to the World Health Organization (WHO) guidelines, median urinary iodine values for pregnant women between 149 and 249 ug/L are consistent with optimal iodine intake.11 The US Institute of Medicine recommends the following total daily iodine intake: 150 ug/L for women planning a pregnancy, 220 ug/L for pregnant women, and 290 ug/L for women who are breastfeeding.12 In contrast, the WHO recommends 250 ug/L for pregnant and lactating women.3

The American Thyroid Association (ATA) along with the WHO recommend not to exceed a daily iodine intake of >500 ug/L. Certain medications may be a source of excess iodine including amiodarone, iodinated IV radiographic contrast agents, and older expectorant medications such as potassium iodide.3

The Wolf-Chaikoff effect is a protective homeostatic mechanism that leads to a transient inhibition of thyroid hormone synthesis in response to a large iodine load.13 With chronic exposure, escape from the acute effect occurs by a decrease in the active transport of iodine into the thyroid gland. In the fetus, the Wolf-Chaikoff effect doesn't mature until 36 weeks gestation, therefore the fetus remains susceptible to excess iodine.14,3