The Effect of Thyrotropin-Releasing Hormone and Antithyroid Drugs on Fetal Thyroid Function.
TRH
antithyroid drugs
feto-maternal interaction
fetus
thyroid
Journal
Children (Basel, Switzerland)
ISSN: 2227-9067
Titre abrégé: Children (Basel)
Pays: Switzerland
ID NLM: 101648936
Informations de publication
Date de publication:
28 May 2021
28 May 2021
Historique:
received:
28
03
2021
revised:
21
05
2021
accepted:
25
05
2021
entrez:
2
6
2021
pubmed:
3
6
2021
medline:
3
6
2021
Statut:
epublish
Résumé
A euthyroid pregnant woman will normally have a fetus that displays normal fetal development. However, studies have long demonstrated the role of T3 (Triiodothyronine), T4 (Thyroxine), and TSH (Thyroid Stimulating Hormone) and their degree of penetrability into the fetal circulation. Maternal thyrotropin-releasing hormone (TRH) crosses the placental site and, from mid-gestation onward, is able to promote fetal TSH secretion. Its origin is not only hypothalamic, as was believed until recently. The maternal pancreas, and other extraneural and extrahypothalamic organs, can produce TRH variants, which are transported through the placenta affecting, to a degree, fetal thyroid function. Antithyroid drugs (ATDs) also cross the placenta and, because of their therapeutic actions, can affect fetal thyroid development, leading in some cases to adverse outcomes. Furthermore, there are a number of TRH analogues that share the same properties as the endogenous hormone. Thus, in this narrative review, we highlight the interaction of all the above with fetal growth in uncomplicated pregnancies.
Identifiants
pubmed: 34071168
pii: children8060454
doi: 10.3390/children8060454
pmc: PMC8228147
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
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