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Review

Important considerations in the management of Graves’ disease in pregnant women

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Abstract

Graves’ disease is an autoimmune disorder in which autoantibodies to the thyroid-stimulating hormone receptor cause hyperthyroidism through unregulated stimulation of the thyroid-stimulating hormone receptor. Effective management of Graves’ disease in pregnancy must address the competing fetal and maternal priorities of controlling hyperthyroidism in the mother on the one hand, and on the other, minimizing the impact of maternal disease and antithyroid drugs on the well-being of the fetus. Optimal strategies for achieving this intricate balance are currently a source of continued debate among thyroid experts and studies in recent decades are now providing greater clarity into the risk posed to the unborn baby by the combination of biochemical, immunological and pharmacological hazards arising from Graves’ disease and its therapy. This review summarizes the current best practice and highlights important considerations and areas of uncertainty in the management of Graves’ disease in pregnant women.

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.

Key issues
  • Poorly treated hyperthyroidism is associated with adverse fetal and maternal outcomes including an increased risk of fetal loss, pre-term delivery and maternal hypertension.

  • Preconception planning and effective management of Graves’ disease in women of reproductive age is essential in preventing morbidity from Graves’ disease in pregnancy.

  • Pregnant women with high concentrations of thyroid-stimulating hormone receptor antibodies should undergo fetal surveillance with ultrasonography due to the risk of fetal thyroid dysfunction and goiter from transplacental transfer of maternal antibodies.

  • Carbimazole and methimazole are associated with a small risk of fetal anomalies including esophageal atresia, omphalocele and aplasia cutis.

  • Emerging evidence suggests that propylthiouracil exposure in early pregnancy also carries a risk of fetal anomalies mostly urinary tract and face and neck lesions.

  • Further research is needed to understand the extent and severity of the risks posed by antithyroid drugs on fetal well-being.

Notes

CMZ: Carbimazole; MMI: Methimazol; PTU: Propylthiouracil.

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