Several reviews of this subject are available [27-29]. Maternal complications of hyperthyroidism include miscarriage, placenta abruptio and preterm delivery. Congestive heart failure and thyroid storm may also occur and the risk of pre-eclampsia is significantly higher in women with poorly controlled hyperthyroidism and low birth weight may be up to nine times as common. Neonatal hyperthyroidism, prematurity and intra-uterine growth retardation may be observed. A retrospective review documented a 5.6% incidence of fetal death or stillbirth in 249 pregnancies from hyperthyroid mothers and a further 5% fetal and neonatal abnormalities. Women with thyroid hormone resistance who, despite being euthyroid, had high levels of circulating T4 had a significantly increased miscarriage rate compared to euthyroid unaffected couples . However, a recent study of women with subclinical hyperthyroidism, comprising 1.7% of women, showed no significant adverse pregnancy outcomes suggesting that treatment of this condition in pregnancy is not warranted . Nevertheless, there is no doubt that overt clinical and biochemical hyperthy-roidism should be treated to lessen the rate of complications described above. Gestational amelioration of Graves' disease is often associated with a reduction in titre of TSHR Ab and a change from stimulatory to blocking antibody activity . A variety of TSHR Abs directed against the TSH receptor may occur in pregnant patients with Graves' disease. Zakarija et al. , e.g., reported the presence of high titres of two species of stimulating antibody in a patient who gave birth to 3 children with transient neonatal hyperthyroidism due to transpla-cental passage of the antibodies. A small number of newborns from mothers with Graves' disease develop central hypothyroidism. This is characterised by low FT4 concentrations in combination with suppressed TSH levels and a blunted TSH response after TRH administration. This situation may arise because of passively transferred thyroxine from the mother who is hyperthyroid in the short term or as a result of longer term (1 month) of neonatal hyperthy-roidism due to passively transferred TsAb. There is a suggestion from the clinical description that maternal thyrotoxicosis before 32 weeks of gestation may be an important time point for the development of central hypothyroidism in the baby. The syndrome provides some indication of the effect of excess maternal thyroid hormones on the development of the hypothalamic pituitary thyroid axis as well as the effect of excess neonatal thyroid hormones on the same system .
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