Iodine deficiency fetus

C03-0144. The thyroid gland produces hormones that help regulate body temperature, metabolic rate, reproduction, the synthesis of red blod cells, and more. Iodine must be present in the diet for these thyroid hormones to be produced. Iodine deficiency leads to sluggishness and weight gain, and can cause severe problems in the development of a fetus. One thyroid hormone is thyroxine, whose chemical formula is... 

Iodine deficiency of the fetus is the result of iodine deficiency in the mother (Manz et al. 1993). The spectrum of iodine deficiency disorders comprises ... 

Pharoah POD, Butteield IH and Hetzel BS (1971) Neurological damage to the fetus resulting from severe iodine deficiency during pregnancy. Lancet 1 308-310. 

Iodine-deficient piglets and calves are partially or totally hairless (Hart and Steenbock, 1918 Andrews et al., 1948 Kursa et al., 1998). The newborn babies of hypothyroid sheep were immature and had reduced vitality. This manifested as retarded growth of the heart, brain and skeleton of the fetuses (Hetzel et al, 1990). There was also evidence of histopathological changes, mainly in the nervous system Potter et al., 1982). 

Thyroid NIS expression has been reported to be increased in fetuses in iodine-deficient rats (Schroder-van der Elst et al.y 2001), but no studies concerning the expression and regulation of gastric NIS during development have so far been performed. 

Pregnant and lactating women are vulnerable to iodine deficiency if specialized enteral preparations are their sole source of nutrition. Only 9 out of 44 specialized enteral preparations for adults provide the current requirement of 200 pg/day. If the WHO technical consultation presently under review is accepted, then only two preparations will meet the proposed allowance of 250 pg/day. This has particular consequences for the brain development of the fetus and infant if the mother has an iodine deficiency during pregnancy and if she breast-feeds. Generally, standard infant formula are recommended for use by the manufacturers for up to 1 year, but as infants are weaned from approximately 6 months, estimation of iodine intakes can only be approximate as the mixed diet progresses. 

Iodine deficiency is still a major pubfic health problem worldwide, although substantial progress has been made towards its eradication in many countries. It is of particular importance in the pregnant woman, because of the sequelae that may be observed in the fetus and the neonate (Table 49.1). Epidemiological demonstration of the association... 

Figure 62.4 The effect of severe iodine deficiency during pregnancy on iamb deveiopment in a 140 day oid iamb fetus (a) subjected to severe iodine deficiency by feeding the mother an iodine-deficient diet for 6 months prior to and during pregnancy (fuii-term 150 days), compared to a controi iamb, (b) of the same age fed the same diet but with the addition of an iodine suppie-ment. The iodine-deficient iamb showed an absence of a wooiiy coat, disiocation of the ieg joints and a smaiier brain. The figure iiiustrates that iodine is essentiai for animai deveiopment and so is important to the animai industry. Reproduced with permission from Hetzei (1989).

This is quantitatively probably the most frequent component of the IDD spectrum. Cerebral hypothyroidism refers to the effect of hypothyroidism on the brain in childhood and adult life, in contrast to the effect on the fetus and in early infancy. There is a more striking effect of hypothyroidism on the brain than on other organs. This produces the characteristic mental torpor and apathy characteristic of the iodine-deficient subjects - it can be reversed at the population level by correction of iodine deficiency, just as it can be reversed in an individual patient by treatment with thyroid hormones (Hetzei, 2004). In a severe endemic, 30-70% of the population may be suffering from cerebral hypothyroidism, as indicated by a low serum thyroxine level (T4) (Buttfield and Hetzei, 1967 Kochupillai ft (S /., 1973). 

After birth, plasma T4 increases in the newborn, mainly due to a new source of iodine provided by the mother through the milk (Escobar del Rey et al, 1987). Iodine is actively concentrated in the milk, which acts as a vehicle to improve the thyroidal status of the newborn. There are small increases in the plasma T4, as well as in brain T4 (Obregon et al, 1991), which together with a large increase in D2 activity in the brain are able to increase T3 in the brain of neonates up to normal levels (Figure 64.3). Therefore, the fetus is able to respond to iodine deficiency the same as the adult rat, but it is more sensitive to iodine deficiency due to its dependence on maternal T4. 

Figure 64.3 Concentrations of T4, T3 and D2 activity in the brain of rat fetuses (left side) between the onset of fetal thyroid function (18dg) and birth (B) and in litters from pups until 4 weeks of postnatal age (right side) born from mothers on an iodine-deficient (LID) and iodine-supplemented (LID -H I) diet. Data (mean SEM) are from Obregon etal., (1991).

Countries where iodine deficiency has been recognized have introduced national programs of iodine supplementation. In places where iodine sufficiency is assumed, and a supplementation program is not carried out, pregnant women and their fetuses may be at risk. 

After the initiation of fetal thyroxine synthesis, transfer of thyroid hormones from the mother to the fetus does not stop, but continues until birth. During that period, 20—50% of cord serum thyroxine is composed from maternal supply (de Escobar et aL, 1990 Vulsma et ai, 1989). Several clinical syndromes attributable to iodine deficiency vary according to the timing and the severity of the deficiency. It has been shown that neurodevelopmental disorders in... 

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. 

Notes-. The results indioated that cretins had disappeared from the offspring of mothers who had received iodized oil injection, but continued to reappear in those who received saline. Six cretins were born following iodized oil injection in all cases, except one in which the mother was pregnant at the time of injection of iodized oil. From the study it was ooncluded that an iodized oil injection before pregnancy could prevent cretinism. In addition, infant deaths were reduced in the iodized-oil-administered group, whioh indicated an effect of iodine deficiency on survival of the fetus. Pregnancies were already established when mothers were injected with iodized oil (six oases) or with saline (five cases). 

The fetus and neonate are both at risk of developing iodine-induced hypothyroidism (Table 96.3). Many cases of such hypothyroidism in fetuses and neonates have been reported, especially in iodine-deficient regions of Europe, but also in iodine-sufficient areas. Iodide goiter in neonates is usually a transient problem. However, tracheal obstruction due to such goiter can be fatal (Markou et al, 2001 Wolff, 1969). Transient hypothyroidism without elevation of thyroid-stimulating hormone (TSH) in extremely... 

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