Thyrotoxicosis in Pregnancy: Results of Treatment by Antithyroid Drugs Combined With T4

Ramsay, Ian; Kaur, Simrat; Krassas, Gerasimos E

doi:10.1111/j.1365-2265.1983.tb03188.x

Cited by 44 publications

(13 citation statements)

References 33 publications

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“…One should not rely on l-T 4 administration to the mother to maintain euthyroidism in the fetus, since the transplacental passage of ATD is high, while it is negligible for thyroid hormones. Preference is usually given to propylthiouracil over methimazole (or carbimazole), although this choice is not mandatory, as long as the minimal dose rule of ATD is implemented (241)(242)(243)(244)(245). It is recommended that maternal free hormone concentrations be maintained in the upper third of the normal range, since it has been shown that such levels in maternal blood are associated with free hormone concentrations in the fetus that remain in the midrange of normal values (246 -248).…”

Section: Hyperthyroidism and Pregnancymentioning

confidence: 99%

The Regulation of Thyroid Function in Pregnancy: Pathways of Endocrine Adaptation from Physiology to Pathology

1997

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Section: Hyperthyroidism and Pregnancymentioning

confidence: 99%

The Regulation of Thyroid Function in Pregnancy: Pathways of Endocrine Adaptation from Physiology to Pathology

1997

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“…Her serum T4 was 8.3 M-g/dL (5.0-12.5), T3 was 148 ng/dL (83-213) and TSH was <0.75 pXJ/mL (1)(2)(3)(4)(5)(6). During outpatient follow-up visits, thyroid hormone levels were monitored at 4-to 8-month intervals.…”

Section: Case Reportmentioning

confidence: 99%

Congenital Nonautoimmune Hyperthyroidism in a Nonidentical Twin Caused by a Sporadic Germline Mutation in the Thyrotropin Receptor Gene

Kopp¹,

Jameson²,

Roe³

1997

Thyroid

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Congenital hyperthyroidism is usually caused by maternal-to-fetal transfer of thyroid-stimulating antibodies from a mother with autoimmune thyroid disease. Very recently, activating thyrotropin (TSH) receptor germline mutations were detected in a few patients with sporadic nonautoimmune congenital hyperthyroidism, as well as in familial forms of nonautoimmune hyperthyroidism defining a new pathophysiological entity of hyperthyroidism. In this report, we describe a nonidentical twin girl with severe congenital hyperthyroidism. The twin brother and the mother were euthyroid. Skull radiographs revealed premature synostosis of the sagittal sutures. Hyperthyroidism was inadequately controlled with antithyroid drugs and radioiodine therapy. After a near-total thyroidectomy performed at age 3, the patient became hypothyroid and required thyroid hormone replacement. At age 14, hyperthyroidism recurred. A hyperplastic remnant of the right upper lobe was removed surgically, resulting in euthyroidism. Over the following years, thyroid hormone levels increased gradually and at age 19 she was again hyperthyroid. There was no clinical or biochemical evidence of an autoimmune process. The patient's neurologic development was impaired and her intelligence is subnormal. Direct sequencing of the TSH receptor gene revealed a heterozygous mutation resulting in a substitution of threonine632 by isoleucine in the sixth transmembrane segment, an amino acid change known to result in constitutive activation of the cyclic adenosine monophosphate (cAMP) pathway. The mutation was absent in the parents and the twin brother, indicating a de novo germline mutation. Early recognition of this disorder is important because of the resistance to standard treatment, special therapeutic implications, and the possibility of familial transmission.

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“…Autoimmune neonatal hyperthyroidism is 1312 P. Kopp The TSH receptor and its role in thyroid disease rare and occurs in less than 2 % of infants born to a mother with a history of Graves' disease [191], a condition with an estimated incidence of about 2 of every 1000 pregnancies [182]. Antibody-induced neonatal hyperthyroidism typically resolves within the first 3 -7 months as the maternal antibodies are cleared from the circulation.…”

Section: Sporadic Germline Mutations In Congenital Hyperthyroidismmentioning

confidence: 99%

Human Genome and Diseases: Review¶The TSH receptor and its role in thyroid disease

Kopp

2001

CMLS, Cell. Mol. Life Sci.

118

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The thyrotropin (TSH) receptor plays a preeminent role in thyroid physiology and disease. TSH, acting through the TSH receptor, is the major stimulator of thyroid cell growth, differentiation and function. In Graves' disease, the TSH receptor is the target of stimulating antibodies that cause hyperthyroidism. Although still a topic of debate, the TSH receptor has been implicated in the pathogenesis of the endocrine ophthalmopathy associated with Graves' disease. Blocking antibodies against the TSH receptor are involved in the development of hypothyroidism in a subset of patients with autoimmune hypothyroidism. Transplacental passage of stimulating or blocking TSH receptor antibodies from a mother with autoimmune thyroid disease may result in transient hyper- or hypothyroidism in early infancy. During pregnancy, the placental hormone human choriogonadotropin (hCG) can cause gestational hyperthyroidism through cross-reaction with the TSH receptor. Gestational hyperthyroidism may also be involved in the pathogenesis of hyperemesis gravidarum. Trophoblast tumors secreting hCG are a rare cause of hyperthyroidism. Somatic activating mutations of the TSH receptor have been identified as a molecular cause of toxic adenomas, whereas activating mutations in the germline give rise to nonautoimmune familial hyperthyroidism or sporadic congenital hyperthyroidism. These gain-of-function mutations are dominant, and one mutated allele is sufficient to result in disease. Inactivating germline mutations of both TSH receptor alleles lead to variable degrees of resistance to TSH, encompassing a spectrum ranging from euthyroid hyperthyrotropinemia to overt hypothyroidism with thyroid hypoplasia.

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Thyrotoxicosis in Pregnancy: Results of Treatment by Antithyroid Drugs Combined With T4

Cited by 44 publications

References 33 publications

The Regulation of Thyroid Function in Pregnancy: Pathways of Endocrine Adaptation from Physiology to Pathology

The Regulation of Thyroid Function in Pregnancy: Pathways of Endocrine Adaptation from Physiology to Pathology

Congenital Nonautoimmune Hyperthyroidism in a Nonidentical Twin Caused by a Sporadic Germline Mutation in the Thyrotropin Receptor Gene

Human Genome and Diseases: Review¶The TSH receptor and its role in thyroid disease

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