Hyperthyroidism fetal

Pregnancy may be adversely affected by poorly controlled hyperthyroidism, with an increased rate of fetal loss. The goal of treatment during pregnancy is to maintain euthyroidism, using the smallest doses of anti thyroid drugs possible. 

Pregnancy. If a pregnant woman has hyperthyroidism (2/1000 pregnancies) she should be treated with the smallest possible amount of these drugs because they cross the placenta with overtreatment fetal goitre occurs. Surgery in the second trimester may be preferred to continued drug therapy. 

Propylthiouracil crosses the placenta as readily as the thioimidazoles, but the rare and probably real association between thioimidazoles and fetal anomalies makes the thioimidazoles less attractive first-line alternatives (81-83). When propylthiouracil is used cautiously in minimal amounts and with frequent dose adjustments, it is probably the safest form of treatment of hyperthyroidism during pregnancy (SEDA-8,373) (SEDA-11, 357). 

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. 

Momotani N, Noh JY, Ishikawa N, Ito K. Effects of propylthiouracil and methimazole on fetal thyroid status in mothers with Graves hyperthyroidism. J Endocrinol Metab 1997 82 3633-3636. 

Ritodrine is contraindicated in antepartnm hemorrhage, which demands immediate delivery eclampsia and severe preeclampsia intrauterine fetal death chorioamnionitis maternal cardiac disease pulmonary hypertension maternal hyperthyroidism and uncontrolled maternal diabetes mellitus. Overdosage with ritodrine may canse tachycardia (maternal and fetal), palpitations, cardiac arrhythmia, hypotension, dyspnea, nervousness, tremor, nansea, and vomiting. 

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... 

Excess iodine exposure during pregnancy may influence maternal-fetal TH metabolism and result in fetal/neo-natal hypothyroidism or hyperthyroidism therefore,... 

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) ... 

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