Abstract

Graves’ disease, an autoimmune disorder caused by an IgG immunoglobulin stimulating the TSH receptor (TSI – thyroid-stimulating immunoglobulin), is the most common form of thyrotoxicosis in pregnancy. During pregnancy, the immune system undergoes a selective immunosuppression resulting in a decline in TSI titer with a concomitant decrease in thyrotoxicosis severity. An immunologic rebound occurs postpartum accompanied by increased TSI titers and an aggravation of thyrotoxicosis. The prevalence of Graves’ disease in pregnancy is 0.5 %. There is an increased prevalence on new-onset Graves’ disease in the postpartum period. Diagnosis of Graves’ disease during pregnancy consists of an elevated thyroxine and/or triioodothyronine and a suppressed TSH in a woman who tests positive for TSI. High maternal titers of TSI at delivery can result in neonatal thyrotoxicosis. Gestational thyrotoxicosis is secondary to the thyrotrophic effect of human chorionic gonadotropin, is self-limiting, and does not require treatment. Management of Graves’ thyrotoxicosis is predominately via antithyroid drugs. Propylthiouracil is recommended in the first trimester and methimazole is preferred during the second and third trimesters. Surgery is indicated in the second trimester in rare circumstances and radioactive iodine is contraindicated during pregnancy. Women with Graves’ disease preconception should be rendered euthyroid prior to conception.

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