Abstract
Graves’ disease is the most common cause of thyrotoxicosis in women of childbearing age. Approximately 1% of pregnant women been treated before, or are being treated during pregnancy for Graves’ hyperthyroidism. In pregnancy, as in not pregnant state, thyroid-stimulating hormone (TSH) receptor (TSHR) antibodies (TRAbs) are the pathogenetic hallmark of Graves’ disease. TRAbs are heterogeneous for molecular and functional properties and are subdivided into activating (TSAbs), blocking (TBAbs), or neutral (N-TRAbs) depending on their effect on TSHR. The typical clinical features of Graves’ disease (goiter, hyperthyroidism, ophthalmopathy, dermopathy) occur when TSAbs predominate. Graves’ disease shows some peculiarities in pregnancy. The TRAbs disturb the maternal as well as the fetal thyroid function given their ability to cross the placental barrier. The pregnancy-related immunosuppression reduces the levels of TRAbs in most cases although they persist in women with active disease as well as in women who received definitive therapy (radioiodine or surgery) before pregnancy. Changes of functional properties from stimulating to blocking the TSHR could occur during gestation. Drug therapy is the treatment of choice for hyperthyroidism during gestation. Antithyroid drugs also cross the placenta and therefore decrease both the maternal and the fetal thyroid hormone production. The management of Graves’ disease in pregnancy should be aimed at maintaining euthyroidism in the mother as well as in the fetus. Maternal and fetal thyroid dysfunction (hyperthyroidism as well as hypothyroidism) are in fact associated with several morbidities. Monitoring of the maternal thyroid function, TRAbs measurement, and fetal surveillance are the mainstay for the management of Graves’ disease in pregnancy. This review summarizes the biochemical, immunological, and therapeutic aspects of Graves’ disease in pregnancy focusing on the role of the TRAbs in maternal and fetal function.
Highlights
Pregnancy represents a challenge to the maternal thyroid gland: the various hormonal variations and the increased metabolic demands occurring during gestation deeply affect thyroid function
In the same study TSAbs were assayed in 20 mothers, 4 of them, having high TSAbs values ranging from 412 to 1,584%, gave birth to infants with hyperthyroidism; this was not observed in newborns born to mothers whose TSAbs were below 400%, regardless of the TSHbinding inhibiting immunoglobulins (TBII) value [46]
Fetal/neonatal hyperthyroidism has been described in two consecutive pregnancies in a woman treated with surgery 10 years before the first pregnancy [71] and in up to 11% of women treated with radioiodine whose levels of TSH receptor antibodies (TRAbs) did not decrease during gestation regardless of the time from the radioiodine treatment to conception [72]
Summary
Pregnancy represents a challenge to the maternal thyroid gland: the various hormonal variations and the increased metabolic demands occurring during gestation deeply affect thyroid function. In a population-based study in Denmark, which included 403,958 women, the incidence of hyperthyroidism (defined by redeemed prescription of antithyroid drugs (ATDs) and assumed to be Graves’ disease) was high early in pregnancy, declined during gestation and significantly increased at 7–9 months PP. Such a pattern was not observed for other autoimmune diseases [16]. Different clinical scenarios can be observed in pregnant women: [1] stable active diseases receiving ATDs, [2] relapse in pregnancy after a ATDs course-induced remission, [3] de novo onset early in pregnancy, and [4] previous surgery or radioiodine treatment with persistence of TRAbs (Table 1). In most cases due to the pregnancy-induced amelioration of Graves’ disease, the dose can be gradually reduced and ATDs even discontinued in third trimester especially in women with negative or decreasing TRAbs
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