Fetal and neonatal hyperthyroidism and hypothyroidism due to maternal TSH receptor antibodies.
Autoimmune thyroid disease is a generic term that includes Graves' disease and Hashimoto's thyroiditis. In the former, there is overactivity of the thyroid due to the action of a thyroid-stimulating antibody (TSAb). Pathogenesis of Hashimoto's thyroiditis is largely cell-mediated immune destruction of the thyroid. Nonetheless, there may be either a goiter or an atrophic gland. 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. This TSH-binding inhibiting antibody (TBIAb), therefore, prevents TSH from stimulating the thyroid and constitutes an acceptable explanation for an agoitrous state. Collectively, TSAb and TBIAb, both of which are IgG, are known as TSH receptor antibodies (TRAb).
Department of Medicine, University of Miami School of Medicine, Florida.
J M
JM
McKenzie
M
M
Zakarija
D001323:Autoantibodies / Q000032:analysis* / Q000276:immunology; D005260:Female; D005315:Fetal Diseases / Q000175:diagnosis / Q000209:etiology*; D005333:Fetus / Q000276:immunology; D006801:Humans; D006980:Hyperthyroidism / Q000151:congenital / Q000209:etiology*; D007074:Immunoglobulin G / Q000276:immunology; D018828:Immunoglobulins, Thyroid-Stimulating; D007231:Infant, Newborn; D008431:Maternal-Fetal Exchange; D011247:Pregnancy / Q000276:immunology; D011989:Receptors, Thyrotropin / Q000276:immunology*
D001323:Autoantibodies; D007074:Immunoglobulin G; D018828:Immunoglobulins, Thyroid-Stimulating; D011989:Receptors, Thyrotropin