Assessment and treatment of thyroid disorders in pregnancy and the postpartum period

Abstract

Thyroid disorders are prevalent in pregnant women. Furthermore, thyroid hormone has a critical role in fetal development and thyroid dysfunction can adversely affect obstetric outcomes. Thus, the appropriate management of hyperthyroidism, most commonly caused by Graves disease, and hypothyroidism, which in iodine sufficient regions is most commonly caused by Hashimoto thyroiditis, in pregnancy is important for the health of both pregnant women and their offspring. Gestational transient thyrotoxicosis can also occur during pregnancy and should be differentiated from Graves disease. Effects of thyroid autoimmunity and subclinical hypothyroidism in pregnancy remain controversial. Iodine deficiency is the leading cause of hypothyroidism worldwide. Despite global efforts to eradicate iodine deficiency disorders, pregnant women remain at risk of iodine deficiency due to increased iodine requirements during gestation. The incidence of thyroid cancer is increasing worldwide, including in young adults. As such, the diagnosis of thyroid nodules or thyroid cancer during pregnancy is becoming more frequent. The evaluation and management of thyroid nodules and thyroid cancer in pregnancy pose a particular challenge. Postpartum thyroiditis can occur up to 1 year after delivery and must be differentiated from other forms of thyroid dysfunction, as treatment differs. This Review provides current evidence and recommendations for the evaluation and management of thyroid disorders in pregnancy and in the postpartum period.

Fig. 1 |. Factors increasing maternal dietary iodine requirement in pregnancy.

Maternal and fetal factors leading to increased iodine requirements in pregnancy are described. During pregnancy, there is a ~50% increase in demand for thyroid hormone, which requires an additional 50–100 μg daily dietary iodine intake. Maternal thyroid hormone production is in part increased by the thyrotropic action of human chorionic gonadotropin (hCG), a hormone produced by the placenta. Oestrogen mediates a twofold increase in circulating levels of thyroxine-binding globulin (TBG), which binds thyroid hormones in the maternal circulation, leading to a relative decrease in levels of active free T₄, which further promotes an increase in thyroid hormone production. Furthermore, placental type 3 iodothyronine deiodinase deactivates T₄ in the circulation to reverse T₃. Increased maternal renal clearance of iodine (by 30–50%) also occurs due to the increase in maternal blood volume. Finally, iodine is transferred from the maternal systemic circulation (red box) to the fetus for fetal thyroid hormone production.

Fig. 2 |. Time course of postpartum thyroiditis.

Typical time course in changes in serum levels of thyroid stimulating hormone (TSH), T₄ and radioactive iodine uptake in postpartum thyroiditis up to 12 months after delivery is depicted. Transient thyrotoxicosis is generally followed by transient hypothyroidism, before full recovery to euthyroidism. However, about 20% of women with postpartum thyroiditis might develop permanent hypothyroidism (as indicated by the dashed lines).