Familial Nongoitrous Cretinism Apparently Due to Maternal Antithyroid Antibody

Sutherland, James M.; Esselborn, Virginia M.; Burket, Robert L.; Skillman, Thomas B.; Benson, Joanne T.

doi:10.1056/nejm196008182630703

Cited by 65 publications

(21 citation statements)

References 8 publications

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“…[5][6][7][8][9] Antithyroid antibodies may also have an influence on the fetal brain and subsequent pediatric neurodevelopment. [10][11][12] Obstetric factors may be responsible for some of the differences in neurologic outcomes seen in the offspring of women with maternal thyroid hypofunction compared with their euthyroid counterparts. 4,13 The purpose of this study was to estimate if maternal thyroid hypofunction, diagnosed during the first or second trimesters, affects obstetric outcomes in a subset of patients from the First And Second Trimester Evaluation of Risk (FASTER) Trial.…”

Section: Conclusion-maternal Thyroid Hypofunction Is Not Associated Wmentioning

confidence: 99%

Maternal Thyroid Hypofunction and Pregnancy Outcome

Goldman

Malone

2008

Obstetrics &Amp; Gynecology

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OBJECTIVE-To estimate whether maternal thyroid hypofunction is associated with complications.METHODS-A total of 10,990 patients had first-and second-trimester serum assayed for thyroid-stimulating hormone (TSH), free thyroxine (freeT4), and antithyroglobulin and antithyroid peroxidase antibodies. Thyroid hypofunction was defined as 1) subclinical hypothyroidism: TSH levels above the 97.5th percentile and free T4 between the 2.5th and 97.5th percentiles or 2) hypothyroxinemia: TSH between the 2.5th and 97.5th percentiles and free T4 below the 2.5th percentile. Adverse outcomes were evaluated. Patients with thyroid hypofunction were compared with euthyroid patients (TSH and free T4 between the 2.5th and 97.5th percentiles). Patients with and without antibodies were compared. Multivariable logistic regression analysis adjusted for confounders was used.RESULTS-Subclinical hypothyroidism was documented in 2.2% (240 of 10,990) in the first and 2.2% (243 of 10,990) in the second trimester. Hypothyroxinemia was documented in 2.1% (232 of 10,990) in the first and 2.3% (247 of 10,990) in the second trimester. Subclinical hypothyroidism was not associated with adverse outcomes. In the first trimester, hypothyroxinemia was associated with preterm labor (adjusted odds ratio [aOR] 1.62; 95% confidence interval [CI] 1.00-2.62) and macrosomia (aOR 1.97; 95% CI 1.37-2.83). In the second trimester, it was associated with gestational diabetes (aOR 1.7; 95% CI 1.02-2.84). Fifteen percent (1,585 of 10,990) in the first and 14% (1,491 of 10,990) in the second trimester had antithyroid antibodies. When both antibodies were positive in either trimester, there was an increased risk for preterm premature rupture of membranes (P = .002 and P<.001, respectively). Although it is established that overt hypothyroidism in pregnancy is detrimental to the developing fetal brain, the effect of asymptomatic thyroid hypofunction on pediatric neurodevelopment is controversial. 1-4 Since 1999, several provocative studies have proposed that mild thyroid hypofunction during pregnancy affects brain development in utero and seems to be associated with abnormal pediatric neurologic outcome. 5-9 Antithyroid antibodies may also have an influence on the fetal brain and subsequent pediatric neurodevelopment. [10][11][12] Obstetric factors may be responsible for some of the differences in neurologic outcomes seen in the offspring of women with maternal thyroid hypofunction compared with their euthyroid counterparts. 4,13 The purpose of this study was to estimate if maternal thyroid hypofunction, diagnosed during the first or second trimesters, affects obstetric outcomes in a subset of patients from the First And Second Trimester Evaluation of Risk (FASTER) Trial. The relationship between antithyroid antibodies in the first and second trimesters and obstetric outcomes was also explored. HHS Public Access MATERIALS AND METHODSThe FASTER Trial, a National Institute of Child Health and Human Developmentsponsored study, was a prospective multicenter invest...

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Section: Conclusion-maternal Thyroid Hypofunction Is Not Associated Wmentioning

confidence: 99%

Maternal Thyroid Hypofunction and Pregnancy Outcome

Goldman

Malone

2008

Obstetrics &Amp; Gynecology

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“…In the past several years it has become evident that some patients may have serum anti-TSH receptor antibodies that inhibit or block TSH stimulated events (359)(360)(361)(362)(363)(364)(365)(366)(367)(368)(369). In 1960 Sutherland et al (369) described children who were hypothyroid and who had familial nongoitrous disease.…”

Section: Tsh Receptor Blocking Antibodiesmentioning

confidence: 99%

“…In 1960 Sutherland et al (369) described children who were hypothyroid and who had familial nongoitrous disease. A report in 1973 by Goldsmith et al (359) apparently updated the information on some of the patients in Sutherland's report and observed congenital hypothyroidism in all six offspring of one female family member who had autoimmune thyroiditis.…”

Section: Tsh Receptor Blocking Antibodiesmentioning

confidence: 99%

Immune Mechanisms In Graves' Disease

1985

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“…S UTHERLAND et al (1) in 1960 reported several hypothyroid children born of a mother with Hashimoto's thyroiditis who had nongoitrous hypothyroidism. Transplacental transfer of thyrosuppressive factors later was postulated as the cause of the hypothyroidism in such infants (2).…”

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confidence: 99%

Transient Neonatal Hypothyroidism Due to Maternal Immunoglobulins that Inhibit Thyrotropin-Binding and Post-Receptor Processes

Takasu

Mori

Koizumi

et al. 1984

The Journal of Clinical Endocrinology & Metabolism

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Transient neonatal hypothyroidism was found in a daughter of a 25-yr-old mother, who was receiving treatment for primary hypothyroidism due to Hashimoto's thyroiditis. During the neonatal period the infant had antithyroid microsomal and antithyroglobulin antibodies and TSH-receptor antibodies. The daughter recovered spontaneously from the hypothyroid state and the antithyroid antibodies disappeared from her serum. The mother's serum contained the same antibodies, and immunoglobulin G (IgG) from maternal serum blocked TSH binding to its receptors, TSH-stimulated cAMP responses, and cAMP-stimulated iodine uptake and organification in cultured thyroid cells. The latter finding suggests that the IgG had a postreceptor locus of action as well as inhibiting TSH binding to its receptor. The presence of such IgGs might have induced hypothyroidism both in the mother and in the daughter.

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Familial Nongoitrous Cretinism Apparently Due to Maternal Antithyroid Antibody

Cited by 65 publications

References 8 publications

Maternal Thyroid Hypofunction and Pregnancy Outcome

Maternal Thyroid Hypofunction and Pregnancy Outcome

Immune Mechanisms In Graves' Disease

Transient Neonatal Hypothyroidism Due to Maternal Immunoglobulins that Inhibit Thyrotropin-Binding and Post-Receptor Processes

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