Goiter fetal

Myxedema and goiter are the main conditions for which thyroid preparations are indicated. The treatment of cretinism is difficult because it is recognized only at or after birth. Even if this disease could be diagnosed m utero, thyroid hormones do not readily cross the placental barrier. In addition, the fetus, as does a premature infant, rapidly deactivates the thyroid hormones. The halogen-free analogue DlMlT [26384-44-7] (3), which is resistant to fetal deiodinases, may prove useful for fetal hypothyroidism (cretinism). 

Both the thiouracils and thioimidazoles readily cross the placenta and can cause fetal hypothyroidism, resulting in a slight delay in neurological or bone maturation. Various degrees of goiter have also been observed, even to the extent of severe tracheal compression and death. Antithyroid drug dosage should therefore be reduced to the minimum required to maintain a euthyroid state without supplementation of levothyroxine (93). 

Reports of fetal goiter and a variety of other lithium-related adverse events in newborns have been reviewed (488). 

Fetal problems, including abortion, stillbirths, congenital anomalies, neurological cretinism. Goiter, hypothyroidism, impaired mental function, increased susceptibility to radiation. 

A second example of an application of the controlled-release technology developed by Rhone-Poulenc is the Rhodifuse lode system (ref. 6). This system is commercialized by Rhone-Poulenc RORER for the treatment of iodine deficiency. Lack of iodine in the diet can cause serious disorders such as goiter and cretinism in adults, growth disorders in children, and fetal death in pregnant women. This... 

When iodine requirements are not met, TH synthesis is reduced, resulting in enlargement of the thyroid gland to compensate for this reduction. In adults, mild iodine deficiency (ID) is associated with nontoxic nodular goiter and, less often, with toxic nodular goiter, due to increases in the constitutive (thyrotropin-independent) growth and functional potential of some clones of thyroid cells. In pregnancy, this can result in fetal neurodevelopmental deficits and mental retardation. 

Women in iodine-deficient areas face increased demands for iodine during both pregnancy and lactation, which results in exaggerated iodine loss over years and consequently causes goiter. Most often, goiter continues after pregnancies cease, and in later years it may become multinodular. Iodine deficiency may also make the mother hypothyroid, with associated complications of anovulation, infertility, gestational hypertension, increased first-trimester abortion, abnormal fetal positions and still births. Further, hypothyroidism, infertility and fetal loss... 

Fetal TH must come from the maternal circulation before the fetal thyroid gland and pituitary—thyroid axis become functional (gestation day (GD) 17—18 in rats and 90 in humans). Maternal transfer of thyroxine (T4) constitutes a major fraction of fetal TH even after the onset of fetal thyroid secretion, they may contribute to the maintenance of fetal development (Burrow et ai, 1994). Therefore, changes in maternal TH levels have an affirmative effect on fetal TH metabolism. Depending on the dose of iodine, the susceptibility of individuals, and previous conditions of the gland, iodine excess can induce maternal hypothyroidism or hyperthyroidism. In a case reported by Serreaul et al. (2004), an obvious thyroid goiter was found in the fetus after excessive maternal iodine... 

Thyroid hormones, T3 and T4, have been i cwn to play significant but poorly understood roles in development and differentiation of rodent and human brain (1-7). In the human, disorders of maternal and fetal thyroid function include maternal and secondary fetal iodine deficiency, maternal hypothyroidism or hyperthyroidism, as well eis disorders related to deficient fetal autcxiomous thyroid hormcaie secretion, i.e., goiter or i radic oongenitel hypothyroidism. These disorders are identifiable causes of mental retardation (4, 8, 9, 10), cer ral peilsy (11, 12), and other significant neurological abnormalities (5, 6, 11) ... 

Goiter was evident from 70 days in the iodine-deficient fetuses and thyroid histology revealed evidence of hyperplasia from 56 days gestation. The increase in thyroid weight was associated with a reduction in fetal thyroid iodine content and greatly reduced plasma T values associated with greatly reduced plasma T levels in the mother (Table 3). 

The LID fetuses developed goiter, and their thyroidal total iodine was 4.7 % of that of LID + I fetuses. The concentrations of T4 and T3 in different embryonic and fetal samples are shown in Figs. 8 and 9, where they are compared to data from age-paired samples obtained from C and T dams. Before onset of fetal thyroid function (11-day-old embryotrophoblasts and 17-day old fetuses) T4 concentrations are decreased by LID to a degree comparable to that of concepta taken from T mothers. T3 concentrations did not differ initially from those of the LID + I group. By 17 gd, however, T3 concentrations were lower both in the fetus, and placenta (not shown). Once fetal thyroid function starts, important differences become apparent between fetuses from T and LID dams. The activated secretion of T4 and T3 by the thyroid in fetuses from T mothers is able to compensate for previous differences related to maternal hypothyroidism, at least as far as the brain is concerned. But this is not possible for fetuses faced with a very low iodine supply, and cerebral T3 is quite low. Similar results were later obtained in another experimental series ... 

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