Abstract
Advances in imaging techniques and in molecular diagnosis have enabled the identification in the fetus of disorders of thyroid and adrenal function that can potentially be treated in utero through the mother. In women with Graves disease, the rare instances of autoimmune fetal hyperthyroidism can generally be treated in a noninvasive way by optimizing treatment of the mother. For fetal hypothyroidism with goiter leading to hydramnios, repeated intra-amniotic injections of thyroxine have been reported to decrease the size of the fetal thyroid, but experience is limited and the risk of premature labor is raised. In women who have previously borne a child with severe congenital adrenal hyperplasia, attempts to prevent virilization of the external genitalia of further affected female fetuses involves treatment with high doses of dexamethasone from week 7 of gestation to term, which includes the crucial period of organogenesis. Only one of every eight fetuses treated will, however, benefit from this therapy, meaning that seven are unnecessarily exposed to this potentially harmful agent. In this article, we review the rationale and evidence for efficacy of these approaches, and discuss their potential adverse effects as well as the ethical problems that they raise.
Key Points
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Iodine intake should be optimized in all pregnant women
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Women with present or past Graves disease should be carefully followed when they become pregnant to detect thyroid dysfunction in their fetus
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Fetal goiters can now be revealed by second-trimester echography and, if associated with fetal hypothyroidism, might require intra-amniotic levothyroxine administration
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Virilization of female fetuses with congenital adrenal hyperplasia can be prevented effectively by treating the mother with dexamethasone from 5 weeks of gestation; however, this strategy might unnecessarily expose unaffected fetuses to this treatment, which could have long-term undesired effects
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Van Vliet, G., Polak, M. & Ritzén, E. Treating fetal thyroid and adrenal disorders through the mother. Nat Rev Endocrinol 4, 675–682 (2008). https://doi.org/10.1038/ncpendmet1005
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DOI: https://doi.org/10.1038/ncpendmet1005
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