Gestational hypothyroxinemia

A Novel Iodine Deficiency Disorder Gestational Hypothyroxinemia How Safe is it for Progeny ... 

It occurs in very specific environmental and/or physiological circumstances, namely ID and pregnancy. The coexistence of both of these conditions, i.e. pregnancy in women whose iodine intake is inadequate, results in the highest risk of gestational hypothyroxinemia in the mothers. 

Universal thyroxine supplementation in extreme preterm infants does not improve neurodevelopmental outcome (van Wassenaer et al., 1997a). However, subgroup analysis of the developmental scores of infants <27 weeks gestation in the thyroxine group, compared to placebo, were increased by 18 points, but decreased by 10 points in infants of 27—29 weeks. Thyroxine supplementation may be detrimental in some infants and there are no indications, apart from gestation, why this should be so. With this uncertainty, we believe that the correction of iodine deficiency is the first and safest approach to the correction of hypothyroxinemia. 

Previous studies have used various combinations of T4, T3 and TSH levels at various postnatal days to define hypothyroxinemia. None of these definitions use serum levels adjusted for gestational age this is crucial, as there are major developmental changes in cord and postnatal serum levels from 23 to 30 weeks gestation (Williams... 

A wide range of serum thyroid hormones (T4, FT4, T3, reverse triiodothyronine (rT3), thyroxine sulfate (T4S)), TSH and thyroid binding globulin (TBG) were analyzed in our studies T4, but not FT4 levels were indicative of hypothyroxinemia (Williams et at, 2004 Simpson et at, 2005). In 23—27 week gestation infants, T4 serum levels decrease to a nadir at 7 postnatal days and fail to increase in 28—30 week infants. This is in marked contrast to 31—34 and 37—42 week term infants, who show an increase in serum T4 levels at day 7 (Williams et al., 2004 Simpson et at, 2005). 

Iodine deficiency at any degree of severity causes maternal and fetal hypothyroxinemia. As thyroid hormones of the mother and the fetus must be kept at optimal levels, iodine prophylaxis should be provided, especially in iodine deficient areas. To establish normal fetal brain development, iodine supplementation must be started before pregnancy and should be continued during the gestational period. 

The growing concern that hypothyroxinemia during early gestation could be harmful to the fetus (Morreale de Escobar et al., 2000 Pop et al., 1999b Utiger, 1999) has also been reinforced by the first experimental evidence of a permanent alteration of cortical cytoarchitecture in the progeny of ID-induced hypothyroxinemic dams (Lavado-Autric et al, 2003). 

The ADHD prevalence of almost 90% in children born to hypothyroxinemic mothers seems to point to a strong association of this neuropsychological disorder with ID-related early gestational maternal hypothyroxinemia. 

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