**Abstract**

Graves' Disease (GD) is one of the most common autoimmune conditions in women of reproductive age. The disorder is characterized by the presence of pathogenic immunoglobulins that bind the TSH receptors (TRAbs) and stimulate the production of thyroid hormones leading to hyperthyroidism (the occurrence of inhibiting or neutral antibodies being rare). Affected individuals can be treated by radioiodine therapy, surgical removal of the gland or by antithyroid drugs (ATDs). Thyroid stimulating immunoglobulins may persist for years after medical treatment, radioiodine therapy or surgical removal of the gland in those affected by GD and during pregnancy can cross the placenta and can act on the fetal thyroid gland resulting in the development of fetal and neonatal hyperthyroidism and sometimes to goiter. Antithyroid drugs used during pregnancy can also cross the placenta and may be teratogenic and act on the fetal thyroid gland, leading to fetal and neonatal hypothyroidism and goiter. This chapter will discuss specific aspects of GD during pregnancy and postpartum focusing on fetal and neonatal consequences related to this disorder.

**Keywords:** pregnancy, Graves' Disease, TRAb, anti-thyroid drugs, fetal goiter, fetal hypothyroidism, fetal hyperthyroidism

#### **1. Introduction**

Graves' Disease (GD) is one of the most common autoimmune conditions in women of reproductive age. Pathogenic immunoglobulins that bind the TSH receptors (TRAbs) are the hallmark of GD and stimulate the production of thyroid hormones leading to hyperthyroidism (the occurrence of inhibiting or neutral antibodies being exceptional). Treatment for affected individuals is either by radioiodine therapy, surgical removal of the gland or by antithyroid drugs (ATDs). TRAbs may persist for years after medical treatment, radioiodine therapy or surgical removal of the gland in those affected by Graves' Disease and during pregnancy can cross the placenta by hijacking the physiological maternal-fetal antibody transfer pathways [1] and can act on the fetal thyroid gland resulting in the development of fetal hyperthyroidism and sometimes to fetal goiter. Antithyroid drugs used during pregnancy can also cross the placenta and may be teratogenic and act on the fetal thyroid gland, leading to hypothyroidism and fetal goiter.

The maternal thyroid gland undergoes extensive changes during pregnancy and postpartum. These changes are supported by the interaction between the fetalplacental unit and the maternal endocrine system and are reflected in the thyroid

function tests, which differ from outside pregnancy as early as first trimester. Normal fetal development depends on maternally derived thyroid hormones (TH) at least until 16–18 weeks' gestation when the fetal thyroid starts to function [2].

This chapter will discuss specific aspects of Graves' Disease during pregnancy and postpartum with focus on its fetal and neonatal consequences.
