The Fetal Thyroid

Radioiodine is easily transported across the placenta resulting in fetal exposure from maternal radioiodine. The fetal thyroid gland is functional prior to parturition, so it must be considered an important target for environmental radioiodine. 

The potential dose equivalent rate to the fetal thyroid from foods produced in air containing 1 pCi m can be estimated. As determined above, an assumed 30 percent thyroid uptake, a 100-day biologic half-time and a 17-g thyroid in the mother (ICRP, 1975) would result in a steady-state maternal thyroidal burden of 43 pCi, or 2.5 pCi g thyroid for each pCi ingested daily. Such a burden would lead to a dose equivalent rate of 3 mrem y (7 X 10 mrem d ). If a 3-fold increase in concentration in the fetal thyroid relative to that of the maternal gland is assumed, based upon chronic exposures (Book and Goldman, 1975), then the near-term fetus would contain 

5 pCi g thyroid. From Eq. (4-7) and an assumed effective energy of 0.06 MeV, the dose equivalent rate to the fetus would be 0.02 mrem d when the maternal intake is 1 pCi d Therefore, a pregnant woman ingesting 1.5 nCi d (Table 4.4) would receive a dose equivalent rate of 10 mrem d to her thyroid, while the subsequent peak fetal dose equivalent rate could be as much as 30 mrem d  

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Radioactive iodine passes the placenta and accumulates in the fetal thyroid where the concentration probably exceeds that in the maternal thyroid. Detailed studies show that the fetal dose of iodine is virtually nil before the 90th day of gestation but sharply increases thereafter (29). This alone is sufficient reason to avoid the use of 131I in pregnancy, but there is also some controversial evidence that various congenital deformities have been produced by the isotope (30). 

Both thioamides cross the placental barrier and are concentrated by the fetal thyroid, so that caution must be employed when using these drugs in pregnancy. Of the two, propylthiouracil is preferable in pregnancy because it is more strongly protein-bound and therefore crosses the placenta less readily. In addition, it is not secreted in sufficient quantity in breast milk to preclude breast-feeding. 

At 16-25 weeks, the fetal thyroid is active and susceptible to damage from radioactive iodine exposure. Maternal exposures will concentrate in the fetal thyroid at this stage of development (13). 

The fetal thyroid-pituitary axis functions independently from the mother s axis in most cases. However, if the mother has preexisting Graves disease (see Chapter 52), her autoantibodies can cross the placenta and stimulate the fetal thyroid gland. Thus the fetus can develop hyperthyroidism. Measurement of thyrotropin-binding inhibitory immmioglobu-lins (TBII) is useful for assessing risk of fetal or neonatal Graves disease. 

If a positive screening test is obtained, the mother s thyroid function is usually also assessed. Maternal autoantibodies can cross the placenta and block receptor sites on the fetal thyroid. In this rare situation, after an initial transient hypothyroidism just after birth, the baby s own thyroid function will usually develop normally. 

The effects of deficiency are most pronounced pre- and perinatally due to the rapid rate of growth and the nutritional demands of the embryo and fetus. In the first half of pregnancy thyroid hormones are suppfied to the fetus by the dam. Later in the pregnancy the fetal thyroid is able to produce thyroid hormones (Nathanielsz, 1976), but is... 

The fetal thyroid gland begins its hormonal production after 10 weeks of gestation, when many thyroxin-dependent... 

Six women (10%) were TPO-Ab (-E) with values ranging from 1890 to 607U/ml. No repercussion on their own or the fetal thyroid function was detected. There were no significant differences between UIE or serum fT4 between smokers and nonsmokers. 

Caution is necessary to avoid excess iodine in the fetal thyroid. 

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... 

Therefore, based on the above Hmited evidence, we conclude that excess iodine exposure may influence maternal-fetal TH metabohsm by three mechanisms (1) excess iodine affects the maternal hormone thyroid level by inhibition of thyroid function and/or Dl activity (2) excess iodine has an effect on maternal—fetal TH transfer by affecting placental D2 and D3 activity and (3) excess iodine transferred by the placenta has a direct inhibition on the development and function of the fetal thyroid gland (Figure 88.2). 

Even though TPOAb and antithyroglobulin antibody (TgAb) cross the placenta and are detected in blood from the umbilical cord, these would not exert cytotoxic action on the fetal thyroid. 

Although the fetal thyroid gland would eventually take over the supply of thyroid hormone from 12 weeks onward, the fetus continues to receive thyroid hormone from the mother, even after the onset of thyroxine supply from its own gland. For a fetus with no thyroid gland, this supply ensures normal fetal development. It is therefore important to ensure adequate supply to the pregnant woman. 

An extensive study on the iodine content of the thyroid glands of 95 fetal and newborn calves has been conducted in the United States by Wolff et al. (1949). Measurable amounts of iodine were first detected in the fetal thyroid at 60 days of age (28 mg %). A progressive increase in the iodine concentration was found to occur during the period of gestation, reaching a value of 118 mg % at term. The mean iodine level observed for 4 adult cows, aged 6 years, was 138 mg % (88-189 mg %). 

When the fetal thyroid is impaired (as in congenital hypothyroidism) maternal T4 has a protective effect on the fetal brain and on other fetal tissues . This might mitigate adverse effects of fetal thyroid failure on the developing brain. It appeared important to determine whether, or not, T3... 

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