Περίληψη:
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.
Συγγραφείς:
Vrachnis, Nikolaos
Tsonis, Orestis
Vrachnis, Dionisios and
Antonakopoulos, Nikolaos
Paltoglou, George
Barbounaki, Stavroula
and Mastorakos, George
Paschopoulos, Minas
Iliodromiti, Zoi
