Gestational hypothyroidism

Gestational hypothyroidism has been associated with severe complications, such as hypertension, preterm birth, low birth weight, placental abruption and fetal death by Leung et al, (1993) and Allan et al. (2000). Many studies in children of hypothyroid pregnant women including Mans group (1976, 1991), and many later ones (Liu et al, 1994 Smit et al, 2000 Klein et al, 2001 Mitchell and Klein, 2004), have demonstrated the importance of maternal thyroid function on the neurodevelopmental evolution of the child. 

Early worries about risk of cancer or leukaemia have proven unfounded in prolonged follow-up studies. However radioactive treatment is contraindicated in pregnant woman or nursing mothers. Other risks for the fetus are abortion, intrauterine death, congenital malformation and congenital hypothyroidism (if administered after 12 weeks gestation). It is customary to avoid pregnancy for the first... 

Groppel etal. (1986) found that the mating frequency of goats and sheep fed casein, starch and cellulose diets without additional iodine was similar to that of animals given supplemental iodine (0.4mg.iodine/kg.diet). However, the dietary iodine deficit increased the abortion rate. As with hypothyroid sows, the gestation period was prolonged and the live-born goitrous kids were less viable than controls. 

There has been no support for the role of elemental iodine deficiency from the animal models. The effect of iodine deficiency in early gestation now appears to be due to maternal hypothyroidism, with reduced T4 transfer across the placental barrier. However, an additional direct effect of iodine itself cannot be excluded from the existing data. 

At this point, the thyroid functional status of the pregnant women was significantly poorer than at early gestation p < 0.000). The fT4 level of 38 of them (62%) was below the tenth percentile, and 19 (29%) were hypothyroid (below the third). There was no reaction of TSH (Figure 63.3). Thyroxinemia and UIE followed diverging evolutions at this time the rate of fT4 is not UIE-related. Only four women wereTPO-Ab (+), with a maximum value of 562U/ml, and two were just over the upper level of normality. They had no thyroid function repercussions. 

The mean UIE of the pregnant women, in the first trimester of gestation, was under the critical level of 200 pg/1 (15% of them were in severe deficiency), while 21.4% of their newborns had TSH over 5mU/l. These data, which are worse than that of the last decade (Enguix et al., 1995), describe the researched zone as in area of a moderate deficiency, based on the criteria of the WHO (2001). One quarter of the pregnant women had their fT4 lower than the tenth percentile. Seven of them (11.2%) were hypothyroid, but none showed clinical evidence about their thyroid insufficiency. A similar observation was referred to by... 

In areas of iodine deficiency Karmarkar et al. (1993) found D2 activity in human cerebral cortex at 11—14 weeks gestational age, which did not respond to a decrease in maternal T4 caused by iodine deficiency. To which extent this indicates that a delay in the capacity of D2 to respond to hypothyroidism or the T4 levels in the brain should be much lower to observe increases in D2 activity remains to be studied. 

In that study, NAA, Cho and Cr were measured in frontal white matter (FWM), parietal white mater (PWM) and the thalamus of the eight full-term neonates with hypothyroidism. They were 5-7 days of age, and were born to mothers living in iodine-deficient areas. Their mothers had not received iodine supplementation in the pregestational or gestational period. A repeat MRS examination was performed after 8 weeks of thyroxine therapy. Metabolite levels of these patients were compared to levels obtained from eight full-term age-matched healthy neonates of mothers who had been using iodine-supplemented salt since the pregestational period. 

Behavioral disorders, including hyperactivity and impaited concentration, are known to be associated with hyperthyroidism and hypothyroidism, respectively. This evidence validated the hypothesis that ADHD might be similarly related to thyroid disease. Nonetheless, the vast majority of the studies carried out to address this issue failed to demonstrate a definite association between ADHD and thyroid function abnormalities, and therefore the effective role of thyroid hormones in the pathogenesis of the disorder became a candidate for reassessment. It must be pointed out however, that most of these studies evaluated thyroid function in schoolchildren or adults, without taking into account any previous thyroid dysfunction suffered either by them or their mothers during gestation. 

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