Vrachnis Nikolaos, Tsonis Orestis, Vrachnis Dionisios, Antonakopoulos Nikolaos, Paltoglou George, Barbounaki Stavroula, Mastorakos George, Paschopoulos Minas, Iliodromiti Zoi
Third Department of Obstetrics and Gynecology, National and Kapodistrian University of Athens Medical School, Attikon Hospital, 157 72 Athens, Greece.
Vascular Biology, Molecular and Clinical Sciences Research Institute, St George's University of London, London SW17 0RE, UK.
Children (Basel). 2021 May 28;8(6):454. doi: 10.3390/children8060454.
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.
甲状腺功能正常的孕妇通常会有一个胎儿发育正常的胎儿。然而,长期以来的研究已经证明了三碘甲状腺原氨酸(T3)、甲状腺素(T4)和促甲状腺激素(TSH)的作用以及它们进入胎儿循环的渗透程度。母体促甲状腺激素释放激素(TRH)穿过胎盘部位,从中期妊娠开始,能够促进胎儿TSH分泌。它的来源并不像直到最近人们所认为的那样仅仅是下丘脑。母体胰腺以及其他神经外和下丘脑外器官可以产生TRH变体,这些变体通过胎盘运输,在一定程度上影响胎儿甲状腺功能。抗甲状腺药物(ATD)也会穿过胎盘,由于其治疗作用,会影响胎儿甲状腺发育,在某些情况下会导致不良后果。此外,有许多TRH类似物与内源性激素具有相同的特性。因此,在这篇叙述性综述中,我们强调了上述所有因素与正常妊娠中胎儿生长的相互作用。