Journal ArticleDOI
Prediction and therapy of intrauterine and late-onset neonatal hyperthyroidism.
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TLDR
The effects of multiple antibodies directed against the TSH receptor that influenced thyroid function in the fetus and infant and combined clinical and assay data are compatible with the following interpretations.Abstract:
These studies in a mother and child describe the effects of multiple antibodies directed against the TSH receptor that influenced thyroid function in the fetus and infant. Blood was taken periodically for 6 months from a child (C3) whose mother (M) was known to have in her serum immunoglobulin G (IgG) that contained thyroid-stimulating antibody (TSAb), an inhibitor of TSAb and TSH binding and action, and an enhancer of TSH binding to its receptor, the last activity presumed to enhance both TSH and TSAb action. We correctly predicted that C3 and an older sibling, C2, would have delayed onset of hyperthyroidism (∼45 days of age) due to interaction of these antibodies. In addition, in both C2 and C3, fetal hyperthyroidism in the second trimester was postulated, and therefore, M was given propylthiouracil from then until term (C2) or 8 months (C3), with associated return of the fetal heart rate to normal in the one fetus (C3) in whom this was monitored. IgG was purified from C3's serum samples and tested for ...read more
Citations
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Journal ArticleDOI
Autoantibodies to the thyrotropin receptor.
TL;DR: This review considers recent developments in the understanding of the properties of TRAb, particularly measurement of the antibodies and their sites of action and synthesis and indicates that TSH receptor antibodies nearly always act as TSH agonists in patients with a history of Graves' hyperthyroidism.
Journal ArticleDOI
Brief report: congenital hyperthyroidism caused by a mutation in the thyrotropin-receptor gene.
Peter Kopp,J. Van Sande,Jasmine Parma,L Duprez,H Gerber,E Joss,J L Jameson,Jacques Emile Dumont,Gilbert Vassart +8 more
TL;DR: A molecular basis for autonomous thyroid function has been found in some patients with hyperfunctioning thyroid adenomas, and somatic mutations in stimulatory G (guanine nucleotide–binding) have been found.
Journal ArticleDOI
Fetal and neonatal hyperthyroidism.
TL;DR: Hyperthyroid neonates may be treated with antithyroid drugs, beta-adrenergic receptor blocking agents, iodine, or iodinated contrast agents, and at times, with glucocorticoids and digoxin, and the time course of thyrotoxicosis depends on etiology.
Journal ArticleDOI
Fetal and neonatal hyperthyroidism and hypothyroidism due to maternal TSH receptor antibodies.
J.M. McKENZIE,M. Zakarija +1 more
TL;DR: There is evidence that in some patients the lack of goiter is associated with the presence in the blood of an antibody that inhibits the binding of TSH to its receptor, which prevents TSH from stimulating the thyroid and constitutes an acceptable explanation for an agoitrous state.
Journal ArticleDOI
Neonatal thyroid disorders
TL;DR: Hypothyroxinaemia, which is common in the preterm infant, and thyrotoxicosis, which are rare, are important neonatal thyroid disorders.
References
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Journal ArticleDOI
Pregnancy-associated Changes in the Thyroid-Stimulating Antibody of Graves' Disease and the Relationship to Neonatal Hyperthyroidism
M. Zakarija,J. M. Mckenzie +1 more
TL;DR: A pattern, related to pregnancy, of a decline in TSAb concentration or a subsequent postpartum increase was observed in the majority of subjects, and apparently, neonatal hyperthyroidism due to transplacental passage of TSAb occurred only when this decline did not reduce the concentration to a low value.
Journal ArticleDOI
Clinical Significance of Assay of Thyroid-Stimulating Antibody in Graves' Disease
TL;DR: Measurement of thyroid-stimulating antibody appears effectively to reflect activity of the underlying disturbance in Graves' disease.
Journal ArticleDOI
Clinical Experience with a Human Thyroid Cell Bioassary for Thyroid-Stimulating Immunoglobin *
TL;DR: A sensitive, specific, and practical bioassay for thyroid-stimulating immunoglobulin (TSI) is now available for clinical use and correlated well with relapse or remission after antithyroid drug therapy.
Journal ArticleDOI
Immunoglobulin G Inhibitor of Thyroid-stimulating Antibody Is a Cause of Delay in the Onset of Neonatal Graves' Disease
TL;DR: The data are compatible with a concept that this mother's IgG contained thyroid-stimulating antibody (TSAb) and another moiety that inhibited TSAb through an action on the thyroid cell membrane, thus delaying the onset of hyperthyroidism in the neonate until the inhibiting IgG was metabolically cleared to an ineffective concentration.
Journal ArticleDOI
Studies on the cyclic AMP response to thyroid stimulating immunoglobulin (TSI) and thyrotropin (TSH) in human thyroid cell monolayers.
Basil Rapoport,Basil Rapoport,Sebastiano Filetti,Sebastiano Filetti,Neal A. Takai,Neal A. Takai,P. Seto,P. Seto,G. Halverson,G. Halverson +9 more
TL;DR: Investigation of the cultured human thyroid cell bioassay for thyroid stimulating immunoglobulin (TSI) and thyrotropin and the present state of the TSI assay found human thyroid cells obtained from patients with Graves' disease are relatively insensitive to TSI stimulation in NaCl(-) medium.
Related Papers (5)
Pregnancy-associated Changes in the Thyroid-Stimulating Antibody of Graves' Disease and the Relationship to Neonatal Hyperthyroidism
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Fetal and neonatal hyperthyroidism and hypothyroidism due to maternal TSH receptor antibodies.
J.M. McKENZIE,M. Zakarija +1 more