hroughout pregnancy, maternal thyroxine is transferred to the fetus (American College of Obstetricians and Gynecologists, 2017). Maternal thyroxine is important for normal fetal brain development, especially before the onset of fetal thyroid gland function (Bernal, 2007; Korevaar, 2016). And, even though the fetal gland begins concentrating iodine and synthesizing thyroid hormone after 12 weeks' gestation, maternal thyroxine contribution remains important. In fact, maternal sources account for 30 percent of thyroxine in fetal serum at term (horpe-Beeston, 1991). Still, developmental risks associated with maternal hypothyroidism after midpregnancy remain poorly understood (Morreale de Escobar, 2004; Sarkhail, 2016).
Most thyroid disorders are inextricably linked to autoantibodies against nearly 200 thyrocyte components. These antibodies variably stimulate thyroid function, block function, or cause thyroid inlammation that may lead to follicular cell destruction. Often, these efects overlap or even coexist.
Thyroid-stimulating autoantibodies, also called thyroidstimulating immunoglobulins (TSls), bind to the TSH receptor and activate it, causing thyroid hyperfunction and growth. Although these antibodies are identiied in most patients with classic Graves disease, simultaneous production of thyroidstimulating blocking antibodies may blunt this efect Qameson, ;C ..EJ,50 w)0:J::0 w ...•30 ..•5 -..,20
FIGURE 58-2 Incidence in percent of antithyroid peroxidase anti bodies in 16,407 women who are normal or euthyroid, in 233 with isolated maternal hypothyroxinemia (1M H), in 598 with subclinical hypothyroidism (SCH), and in 134 with overt hypothyroidism.
(Data from Casey, 2007).
2015). Thyroidperoxidase (TPO) is a thyroid gland enzyme that normally functions in the production of thyroid hormones. Thyroid peroxidase antibodies, previously called thyroid microsomal autoantibodies, are directed against TPO and, as shown in Figure 58-2, have been identiied in 5 to 15 percent of all pregnant women (Abbassi-Ghanavati, 2010; Sarkhail, 2016). These antibodies have been associated in some studies with early pregnancy loss and preterm birth (Negro, 2006; Korevaar, 2013; Plowden, 2017; Thangaratinam, 201l). In another study with more than 1000 TPO antibody-positive pregnant women, the risk for preterm birth was not elevated, however, the risk for placental abruption was greater (Abbassi-Ghanavati, 2010). These women are also at high risk for postpartum thyroid dysfunction and at lifelong risk for permanent thyroid failure (Andersen, 2016; Jameson, 2015).