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In NTI serum TSH is usually normal or even suppressed despite lowered
serum T3 and sometimes also T4. The mechanism of this inappropriately low
TSH is not well-known. Everts, Rotterdam, The Netherlands, investigated
if TRIAC was taken up by the pituitary and evaluated its biological effects
with regard to TSH secretion as it is known that free TRIAC concentrations
are markedly elevated in NTI. It was found that TRIAC was taken up in a
carrier-mediated energy dependent fashion by rat anterior pituitary cells
in culture and also that after TRH, TSH secretion was markedly inhibited
by TRIAC. The TSH suppressive effect of TRIAC was higher than that of T3
or T4 (Comment: As low T3 production in NTI is considered as an energy
and protein saving mechanism, the teleological significance of the absence
of TSH increase is to keep T3 low in these patients. It is therefore important
to evaluate the mechanisms that are responsible for continued TSH suppression
under these circumstances and TRIAC might be one of the factors causing
this effect.)
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