Thyroid hormone (TH) is indispensable for normal embryonic and fetal development. Throughout gestation TH is provided by the mother via the placenta, later in pregnancy the fetal thyroid gland makes an increasing contribution. Maternal thyroid dysfunction, resulting in lower or higher than normal (maternal) TH levels and transfer to the embryo/fetus, can disturb normal early development. (Maternal) thyroid dysfunction is mostly caused by autoimmune hypo- or hyperthyroidism, i.e. Hashimoto and Graves disease. Autoimmune hyperthyroidism is caused by stimulating TSH receptor antibodies (TSHR Ab), patients with autoimmune hypothyroidism may have blocking TSHR Ab. Maternal TSHR Ab cross the placenta from mid gestation and may cause fetal and transient neonatal hyper- or hypothyroidism. Anti-thyroid drugs taken for autoimmune hyperthyroidism cross the placenta throughout gestation, and may cause fetal and transient neonatal hypothyroidism. This review focusses on the consequences of maternal hypo- and hyperthyroidism for fetus and neonate, and provides a practical approach to clinical management of neonates born to mothers with thyroid dysfunction.
Copyright © 2020 The Author. Published by Elsevier Ltd.. All rights reserved.

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