Fetal Thyrotoxicosis due to Maternal TSH Receptor Stimulating Antibodies Causes Infant Central Hypothyroidism

Introduction: Women with a current diagnosis or past history of Graves’ disease (GD) are at risk of developing fetal thyrotoxicosis (FT) during pregnancy when they are inadequately treated, or because of placental passage of TSH receptor antibodies (TRAb). It is known that FT induced by high materna...

Full description

Saved in:
Bibliographic Details
Published inHormone research in paediatrics Vol. 97; no. 2; pp. 180 - 186
Main Authors van Hulsteijn, Leonie T., Prins, Jelmer R., Scheffer-Rath, Mirjam E.A., van Trotsenburg, A.S. Paul, Links, Thera P., Dullaart, Robin P.F.
Format Journal Article
LanguageEnglish
Published Basel, Switzerland 01.04.2024
Subjects
Child
Female
Graves Disease - complications
Humans
Hypothyroidism - therapy
Infant
Infant, Newborn
Novel Insights from Clinical Practice / Case Report
Placenta
Pregnancy
Pregnancy Complications
Receptors, Thyrotropin
Thyroid Hormones
Thyrotoxicosis - diagnosis
Graves’ disease
Fetal thyrotoxicosis
Maternal TSH receptor antibodies
Infant central hypothyroidism
Online AccessGet full text

Cover

More Information
Summary:Introduction: Women with a current diagnosis or past history of Graves’ disease (GD) are at risk of developing fetal thyrotoxicosis (FT) during pregnancy when they are inadequately treated, or because of placental passage of TSH receptor antibodies (TRAb). It is known that FT induced by high maternal thyroid hormone concentrations may result in infant (central) hypothyroidism. Case Presentation: In a euthyroid woman with a history of GD treated with radioactive iodide (I 131 ), persistently high levels of maternal TRAb resulted in recurrent FT during two separate pregnancies, followed by neonatal hyperthyroidism and infant central hypothyroidism. Discussion: This case demonstrates the novel insight that FT due to high fetal thyroid hormone concentrations stimulated by high maternal TRAb levels might also result in (central) hypothyroidism, requiring long-term evaluation of the hypothalamus-pituitary-thyroid axis in these children.
ISSN:1663-2818
1663-2826
DOI:10.1159/000530725