Prevalence of Thyrotoxicosis, Antithyroid Medication Use, and Complications Among Pregnant Women in the United States

Korelitz, James; McNally, Diane; Masters, Mary N.; Li, Sue X.; Xu, Yiling; Rivkees, Scott A.

doi:10.1089/thy.2012.0488

Cited by 85 publications

(88 citation statements)

References 17 publications

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“…MMI (CBZ) embryopathy, including dysmorphic facies, aplasia cutis, choanal or esophageal atresia, abdominal wall defects, umbilicocele, and ventricular septal defects, affects 2-4% of children who have been exposed to MMI, especially during gestational weeks 6-10 [137,141]. The prevalence of birth defects is the same with PTU, but the spectrum of defects is less severe, primarily consisting of face and neck cysts and urinary tract abnormalities in males [142].…”

Section: Pregnant Women and Gdmentioning

confidence: 99%

2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

Kahaly¹,

Bartalena²,

Hegedüs³

et al. 2018

Eur Thyroid J

678

650

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Graves’ disease (GD) is a systemic autoimmune disorder characterized by the infiltration of thyroid antigen-specific T cells into thyroid-stimulating hormone receptor (TSH-R)-expressing tissues. Stimulatory autoantibodies (Ab) in GD activate the TSH-R leading to thyroid hyperplasia and unregulated thyroid hormone production and secretion. Diagnosis of GD is straightforward in a patient with biochemically confirmed thyrotoxicosis, positive TSH-R-Ab, a hypervascular and hypoechoic thyroid gland (ultrasound), and associated orbitopathy. In GD, measurement of TSH-R-Ab is recommended for an accurate diagnosis/differential diagnosis, prior to stopping antithyroid drug (ATD) treatment and during pregnancy. Graves’ hyperthyroidism is treated by decreasing thyroid hormone synthesis with the use of ATD, or by reducing the amount of thyroid tissue with radioactive iodine (RAI) treatment or total thyroidectomy. Patients with newly diagnosed Graves’ hyperthyroidism are usually medically treated for 12–18 months with methimazole (MMI) as the preferred drug. In children with GD, a 24- to 36-month course of MMI is recommended. Patients with persistently high TSH-R-Ab at 12–18 months can continue MMI treatment, repeating the TSH-R-Ab measurement after an additional 12 months, or opt for therapy with RAI or thyroidectomy. Women treated with MMI should be switched to propylthiouracil when planning pregnancy and during the first trimester of pregnancy. If a patient relapses after completing a course of ATD, definitive treatment is recommended; however, continued long-term low-dose MMI can be considered. Thyroidectomy should be performed by an experienced high-volume thyroid surgeon. RAI is contraindicated in Graves’ patients with active/severe orbitopathy, and steroid prophylaxis is warranted in Graves’ patients with mild/active orbitopathy receiving RAI.

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Section: Pregnant Women and Gdmentioning

confidence: 99%

2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

Kahaly¹,

Bartalena²,

Hegedüs³

et al. 2018

Eur Thyroid J

678

650

View full text Add to dashboard Cite

show abstract

“…Overall, the defects were less severe than the MMI/CMZassociated defects (60), and they consisted of face and neck malformations (preauricular sinus and cysts), and urinary tract malformations (confined to boys). Some uncertainty has existed in this area of research, because some investigators found no association between ATD use in pregnancy and birth defects (61,62,63,64). As recently reviewed in detail (65), the cause for the negative findings likely resides with the methods used in the studies.…”

Section: Therapy Of Graves' Disease and The Risk Of Birth Defectsmentioning

confidence: 99%

ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease

Laurberg

Andersen

2016

European Journal of Endocrinology

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Thyroid hormones are essential developmental factors, and Graves' disease (GD) may severely complicate a pregnancy. This review describes how pregnancy changes the risk of developing GD, how early pregnancy by several mechanisms leads to considerable changes in the results of the thyroid function tests used to diagnose hyperthyroidism, and how these changes may complicate the diagnosing of GD. Standard therapy of GD in pregnancy is anti-thyroid drugs. However, new studies have shown considerable risk of birth defects if these drugs are used in specific weeks of early pregnancy, and this should be taken into consideration when planning therapy and control of women who may in the future become pregnant. Early pregnancy is a period of major focus in GD, where pregnancy should be diagnosed as soon as possible, and where important and instant change in therapy may be warranted. Such change may be an immediate stop of anti-thyroid drug therapy in patients with a low risk of rapid relapse of hyperthyroidism, or it may be an immediate shift from methimazole/carbimazole (with risk of severe birth defects) to propylthiouracil (with less risk), or maybe to other types of therapy where no risk of birth defects have been observed. In the second half of pregnancy, an important concern is that not only the mother with GD but also her foetus should have normal thyroid function.Thyroid hormones are essential developmental factors as first shown by Gudernatsch when he, in 1912, fed tadpoles thyroid tissue and observed metamorphosis (1). In mammals, thyroid hormones are especially of importance for brain development (2, 3), and even a few months with lack of thyroid hormones in infant life may lead to irreversible brain damage. This is the background for the universal screening for congenital hypothyroidism performed in many countries. However, thyroid hormones are also important for normal pregnancy, and maternal thyroid disease may severely increase the risk of pregnancy complications, including Invited author's profile Peter Laurberg was Clinical Professor of Internal Medicine and Endocrinology, Department of Endocrinology, Aalborg University Hospital, Aalborg, Denmark. His research mainly focused on thyroid disease prevention, epidemiology, diagnosing and therapy, including studies on iodine and thyroid, and pregnancy and thyroid. He had special research interest on the risk from and optimal management of autoimmune hypo-and hyperthyroidism in pregnancy and post-partum, management of Graves' disease in general, and how the burden of thyroid disease can be minimized by adjusting the population's iodine intake. He has coauthored several international guidelines on thyroid disease management, including management of thyrotoxicosis, and thyroid disease in pregnancy. Peter Laurberg died June 20, 2016.

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“…[1][2][3][4] The prevalence of transient GD in infants born to these mothers is uncertain, varying from 1.5% to 2.5% [5][6][7] up to 20.0% in observational cohort studies. [7][8][9] The causative antibodies in GD, thyroid-stimulating hormone (TSH) receptor antibodies (TRAb), belong to the immunoglobulin G class and freely cross the placenta, particularly during the second half of pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Management of Neonates Born to Mothers With Graves’ Disease

2016

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Neonates born to mothers with Graves’ disease are at risk for significant morbidity and mortality and need to be appropriately identified and managed. Because no consensus guidelines regarding the treatment of these newborns exist, we sought to generate a literature-based management algorithm. The suggestions include the following: (1) Base initial risk assessment on maternal thyroid stimulating hormone (TSH) receptor antibodies. If levels are negative, no specific neonatal follow-up is necessary; if unavailable or positive, regard the newborn as “at risk” for the development of hyperthyroidism. (2) Determine levels of TSH-receptor antibodies in cord blood, or as soon as possible thereafter, so that newborns with negative antibodies can be discharged from follow-up. (3) Measurement of cord TSH and fT4 levels is not indicated. (4) Perform fT4 and TSH levels at day 3 to 5 of life, repeat at day 10 to 14 of life and follow clinically until 2 to 3 months of life. (5) Use the same testing schedule in neonates born to mothers with treated or untreated Graves’ disease. (6) When warranted, use methimazole (MMI) as the treatment of choice; β-blockers can be added for sympathetic hyperactivity. In refractory cases, potassium iodide may be used in conjunction with MMI. The need for treatment of asymptomatic infants with biochemical hyperthyroidism is uncertain. (7) Assess the MMI-treated newborn on a weekly basis until stable, then every 1 to 2 weeks, with a decrease of MMI (and other medications) as tolerated. MMI treatment duration is most commonly 1 to 2 months. (8) Be cognizant that central or primary hypothyroidism can occur in these newborns.

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Prevalence of Thyrotoxicosis, Antithyroid Medication Use, and Complications Among Pregnant Women in the United States

Cited by 85 publications

References 17 publications

2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease

Management of Neonates Born to Mothers With Graves’ Disease

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