Hyperthyroidism in the pregnant woman: Maternal and fetal aspects

Abstract

Hyperthyroidism during pregnancy is uncommon. Nonetheless, prompt identification and adequate management of hyperthyroidism in a pregnant woman is essential, because uncontrolled thyrotoxicosis significantly increases the risk of maternal and fetal complications. Also, fetal prognosis may be affected by the transplacental passage of maternal thyroid stimulating antibodies or thyrostatic agents, both of which may disrupt fetal thyroid function. Birth defects have been reported in association with the use of antithyroid drugs during early pregnancy. Although rarely, offspring of mothers with Graves’ disease may develop fetal/neonatal hyperthyroidism, the management of which requires a close collaboration between endocrinologists, obstetricians, and neonatologists. Because of the above considerations, the management of pregnant and lactating women with hyperthyroidism requires special care, bearing in mind that both maternal thyroid excess per se and related treatments may adversely affect the newborn’s health. In this review we discuss the diagnosis and management of hyperthyroidism in pregnancy, along with the impact of thyrotoxicosis and medications on fetal outcome.

Stress-Triggered Graves’ Disease with Multiple Exacerbations in a Pregnant Woman with High Levels of Thyrotropin Receptor Antibodies and No Complicated Delivery: a Case Report

“…At physical examination, resting tachycardia, hyperreflexia, warm and moist skin, diffuse goiter, and absence of ophthalmopathy were apparent. Confirming the clinical diagnosis, laboratory investigations showed overt hyperthyroidism (TSH = 0.001 mU/L [normal values 0.27-4.2], FT4 = 69.4 pmol/L [normal values [12][13][14][15][16][17][18][19][20][21][22], FT3 = 42.2 pmol/L [normal values 3.1-6.8]). Thyroglobulin antibodies (TgAb) and thyroperoxidase autoantibodies (TPOAb) tested negative, and TRAb levels were high (30.4 U/L, normal values < 1.5).…”

“…Maternal and fetal adverse outcomes are directly related to a poor control of thyrotoxicosis, consisting in elevated thyroid hormones and TRAb levels. Particularly, exposure to excessive levels of thyroid hormones during pregnancy can lead to maternal hypertension, preeclampsia, thyroid storm, congestive heart failure, pregnancy loss, prematurity, intrauterine growth restriction, and stillbirth [14]. Nevertheless, both TRAb and ATD cross the placenta affecting the fetal thyroid.…”

“…Nevertheless, both TRAb and ATD cross the placenta affecting the fetal thyroid. As ATD is more potent in the fetus than in the mother, fetal hypothyroidism may occur in the face of maternal euthyroidism [14]. Therefore, pregnant women with GD requiring ATD should be treated with the smallest possible dose whenever is possible [11].…”

“…In the first trimester, TRAb measurement is important for either diagnosing GD in women presenting with thyrotoxicosis or for deciding whether to stop ATD in those already taking these drugs from before conception [11]. As TRAb cross the placental barrier (see above), they can stimulate the fetal thyroid leading to hyperthyroidism, which typically develops at week 20 or later [14]. Ultrasonographic signs of fetal hyperthyroidism include tachycardia (> 160 bpm for > 10 min), intrauterine growth retardation, fetal hydrops, centrally hypervascularized goiter, and accelerated bone maturation (with evident distal femoral ossification core before 32 weeks) [19].…”

Thyroid disorders in subfertility and early pregnancy

“…Untreated thyrotoxicosis can lead to spontaneous abortion, premature delivery, intrauterine growth restriction (IUGR), placental abruption, and maternal cardiac failure. 69 , 75 Foetal outcomes are affected by the TRAb titre and control of hyperthyroidism. TRAbs can cross the placenta and can lead to foetal hyperthyroidism, which may manifest as foetal tachycardia, IUGR, and foetal goitre formation.…”