The fetus or neonate who was exposed to excessive maternal thyroxine may have any of several clinical presentations. First, goitrous thyrotoxicosis is caused by placental transfer of thyroidstimulating immunoglobulins. Nonimmune hydrops and fetal demise have been reported with fetal thyrotoxicosis (Nachum, 2003; Stulberg, 2000). The best predictor of perinatal thyrotoxicosis is presence of thyroid-stimulating TSH-receptor antibodies in women with Graves disease (Nathan, 2014). This is especially true if their levels are more than threefold higher than the upper normal limit (Barbesino, 2013). In a study of 72 pregnant women with Graves disease, Luton and associates (2005) reported that none of the fetuses in 31 low-risk mothers had a goiter, and all were euthyroid at delivery. Low risk was defined as no requirement for antithyroid medications during the third trimester or an absence of antithyroid antibodies. Conversely, in a group of 41 women who either were taking antithyroid medication at delivery or had thyroid receptor antibodies, 11 fetuses-27 percent-had sonographic evidence of a goiter at 32 weeks' gestation. Seven of these 11 fetuses were determined to be hypothyroid, and the remaining fetuses were hyperthyroid. In response to these results, the merican Thyroid Association and American Association of Clinical Endocrinologists (201r1) recommend routine evaluation of TSH-receptor antibodies between 22 and 26 weeks' gestation in women with Graves disease. he American College of Obstetricians and Gynecologists (2017), however, does not recommend such testing. If the fetus is thyrotoxic, maternal thionamide drugs are adjusted even though maternal thyroid function may be within the targeted range (Mestman, 2012). lthough usually short-lived, neonatal thyrotoxicosis may require short-course antithyroid drug treatment (Levy-Shraga, 2014; Nathan, 2014).
A second presentation is goitrous hypothyroidism caused by fetal exposure to maternally administered thionamides (see Fig. 58-3). Although there are theoretical neurological implications, reports of adverse fetal efects seem to have been exaggerated. Available data indicate that thionamides carry an extremely small risk for causing neonatal hypothyroidism (Momotani, 1997; O'Doherty, 1999). For example, in at least 239 treated thyrotoxic women shown in Table 58-1, evidence of hypothyroidism was found in only four newborns. Furthermore, at least four long-term studies report no abnormal intellectual and physical development of these children (Mestman, 1998). If maternal hypothyroidism developed, the fetus can be treated by a reduced maternal antithyroid medication dose and injections of intraamnionic thyroxine if necessary.
A third presentation, nongoitrous hypothyroidism, may develop from transplacental passage of maternal TSH-receptor blocking antibodies (Fitzpatrick, 2010; Gallagher, 2001). And finally,etal thyrotoxicosis after maternal thyroid gland ablation, usually with 1 radioiodine, may result from transplacental thyroid-stimulating antibodies. In one report of early fetal exposure to radioiodine, neonatal thyroid studies indicated transient hyperthyroidism from maternal transfer of stimulating antibodies (Tran, 2010).