Hypothyroxinemia consequences

Neonates, and especially preterm infants, are a population at risk of suffering the consequences of iodine deficiency because of the impact of neonatal hypothyroxinemia on brain development. We evaluate the possible association between mental development scores at different ages and iodine intake during the neonatal period. Sixty-seven preterm infants were subdivided into GA groups for data analysis. The mental development scores reported here are those of the Brunet-Lezine scale index for children (0-24 months of age). The children were tested at 6, 9, 12, 18 and 24 months of postnatal age, and results were corrected for their GA. The test assesses P, motor abilities and postural... 

Most preterm babies are at high risk of iodine deficiency neonates, and especially preterm infants, are a very important population at risk of suffering the consequences of both iodine deficiency and excess, because of the impact of neonatal hypothyroxinemia on brain development. 

Correction of hypothyroxinemia and its consequences appears, at present, to be an intervention with promising possibilities. 

As discussed elsewhere in more detail (Morreale de Escobar et ai, 2004), it is inaccurate to assume, which has been very frequently done, that inhabitants of areas of ID are chnically hypothyroid individuals. The present experimental model supports the epidemiological findings that inhabitants of areas of ID are not clinically hypothyroid individuals, as their normal circulating T3 ensures euthyroidism of most tissues by extrathyroid adaptive mechanisms known to be operative in man when iodine availability decreases. But, as shown experimentally here, this does not avoid selective hypothyroidism of tissues, such as the brain, that depend mostly on T4 for their intracellular T3 supply. This selective hypothyroidism is aheady present in conditions of mildly decreased iodine availability, and may already negatively affect mental functions (Delange, 2001 Vitti et al., 2003 Vermiglio et ai, 2004). Indeed, inhabitants of areas of ID are often described as dull. Whole populations appear to wake up when their ID — and the consequent hypothyroxinemia — are corrected (Dunn, 1992). 

In conclusion, not only screening, but also monitoring of maternal thyroid function should be encouraged in moderately iodine-deficient areas, in order to correct maternal hypothyroxinemia promptly and consequently prevent irreversible neurological damage in progeny. 

In order to understand the total responsiveness of the brain to hypothyroxinemia one must integrate the consequences of all of the changes which occur under these circumstances. For example, in Table 5 are shown the changes in T3 uptake in two week old hypothyroid rats as demonstrated in the studies of Silva and Matthews (40). The fractional... 

The consequences for the newborn of maternal alterations in thyroid function were also investigated In brief, while mothers displayed relative hypothyroxinemia, this was not the case for the newborns who had significantly higher total T4, free T4, and TBG saturation levels than their respective mothers. Hence, in conditions with only moderate iodine restriction, newborns are protected from hypothyroxinemia. To do so, and presumably because of their low intrathyroidal iodine stores, the newborns need to stimulate at the extreme their own thyroidal machinery and this was reflected by markedly higher neonatal TSH and TG levels, compared to mothers... 

The newborn infants may be more sensitive than adults to iodine deficiency, probably due to the low iodine stores of the thyroid and the enhanced intrathyroidal iodine turnover rate of the neonates. Neonatal hypothyroxinemia related to a suboptimal iodine intake may be responsible for more long-term consequences that we may suspected Indeed, apparently normal schoolchildren may suffer from some degree of mental retardation due to iodine deficiency. ... 

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