Graves’ hyperthyroidism in pregnancy: a clinical review

Abstract

BackgroundGraves’ hyperthyroidism affects 0.2% of pregnant women. Establishing the correct diagnosis and effectively managing Graves’ hyperthyroidism in pregnancy remains a challenge for physicians.MainThe goal of this paper is to review the diagnosis and management of Graves’ hyperthyroidism in pregnancy. The paper will discuss preconception counseling, etiologies of hyperthyroidism, thyroid function testing, pregnancy-related complications, maternal management, including thyroid storm, anti-thyroid drugs and the complications for mother and fetus, fetal and neonatal thyroid function, neonatal management, and maternal post-partum management.ConclusionEstablishing the diagnosis of Graves’ hyperthyroidism early, maintaining euthyroidism, and achieving a serum total T4 in the upper limit of normal throughout pregnancy is key to reducing the risk of maternal, fetal, and newborn complications. The key to a successful pregnancy begins with preconception counseling.

Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth

“…This is of significant importance because hyperthyroidism in pregnancy is associated with a range of adverse pregnancy outcomes, including low birth weight, intra‐uterine growth restriction (IUGR), pregnancy‐induced hypertension and pregnancy loss (Carroll & Matfin, ; Ross, 2017; Nguyen et al . ). A number of recent clinical trials have demonstrated that selenium supplementation can reduce thyroid autoimmunity (Mantovani et al .…”

“…current animal model, we aimed to investigate possible mechanisms linking selenium deficiency to increased thyroid hormone levels. This is of significant importance because hyperthyroidism in pregnancy is associated with a range of adverse pregnancy outcomes, including low birth weight, intra-uterine growth restriction (IUGR), pregnancy-induced hypertension and pregnancy loss (Carroll & Matfin, 2010;Ross, 2017;Nguyen et al 2018).…”

Hyperthyroid Fetal Goiter: A Case Report

“…These immunoglobulins, IgG type, have two types of possible action: some stimulate the synthesis of Cyclic Adenosine Monophosphate by these cells, these are the thyroid stimulating immunoglobulins (TSI) while other antibodies will block the binding of TSH with its receptor, these are the thyroid binding inhibiting Immunoglobulins (TBII). Among pregnant women with Graves' disease, 0.2% develops clinical hyperthyroidism and, among them, 1 to 5% of their newborns will present a neonatal hyperthyroidism due to transplacental passage of TRAb [2,6]. Indeed, the fetal thyroid starts its synthesis of thyroid hormone from the 12th week of gestation.…”

“…This explains why fetal hyperthyroidism doesn't appear until the second half of pregnancy, and also in patients with a rate of higher autoantibodies (TRAb) [2,5,[7][8]. The fetal risk concerns both the fetuses of mothers with the past or current Graves' disease and includes: intrauterine growth retardation, prematurity, intrauterine fetal death (15-25% if untreated), fetal Graves' disease [2][3]6]. Moreover the presence of autoantibodies can encourage the development of fetal goiter, responsible in rare cases to a compression of the trachea or fetal esophageal [6].…”

“…The fetal risk concerns both the fetuses of mothers with the past or current Graves' disease and includes: intrauterine growth retardation, prematurity, intrauterine fetal death (15-25% if untreated), fetal Graves' disease [2][3]6]. Moreover the presence of autoantibodies can encourage the development of fetal goiter, responsible in rare cases to a compression of the trachea or fetal esophageal [6]. Fetal hypothyroidism induced due to synthetic antithyroid drugs by transplacental passage may be accompanied by goiter but inconstantly [9].…”