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Santini et al., Pisa, Italy, and Los Angeles, CA, USA, measured
circulating iodothyronines in newborns (n = 274) and concluded from their
results that maturation of type I-iodothyronine monodeiodinase (MD) that
converts T4 to T3, rT3 to T2 and T3S
to T2S, accelerates starting at 32 weeks of post-conceptional age. Furthermore,
high levels of type III-MD activity (converting T3 to T2 and
T4 to rT3) in fetal tissues prevented the raise of
serum T3 while maintaining high levels of rT3 during
intrauterine life. They conclude that the main mechanism leading to the
transition of the fetal to the post-natal thyroid hormone balance i.e.
an increase in serum T3 and a drop in serum rT3,
is a sudden decrease of type III-MD activity. They suggest that, because
of the fact that the placenta contains a high amount of type III-MD, it
may play a role in regulating serum levels of iodothyronines during fetal
life and that its dissociation from the neonate at birth is responsible
for most changes in iodothyronine serum levels, occurring afterwards.
Snyder et al., Portland, OR, USA, analyzed causes of elevated total T4 values detected in a newborn screening program of neonates. Out of 33,033 babies, 109 newborns with T4 >3 S.D. were detected. 36/109 were further analyzed. 33/36 were false positives and of the remaining 3 babies, 2 had thyroid hormone resistance and 1 TBG excess. |
