Blizzard et al1 were among the first to suggest that maternal autoimmune thyroid disease (AITD) may be of pathogenic significance in the development of neonatal hypothyroidism. Matsuura et al2 first described the occurrence of transient neonatal hypothyroidism due to the transplacental passage of maternal immunoglobulins that inhibited the binding of thyrotropin to its receptor on the thyrotrope membrane. Since then, the role of AITD in the pathogenesis of both transient and permanent forms of this disorder has been subjected to renewed investigation. Many antibodies of diverse biological activity have been found in the serum samples of women with known or subclinical AITD who have delivered infants with neonatal hypothyroidism. These include IgGs that: (1) inhibit binding of thyrotropin to its receptor (TBIIg, measured in a radioreceptor assay), (2) inhibit thyrotropin-mediated growth of thyroid cells (TGIIg, assessed by the effect of serum immunoglobulins on thyrotropin-induced increase in nuclear DNA
ROOT AW. The Role of Maternal Autoimmune Thyroid Disease in Neonatal Hypothyroidism. Am J Dis Child. 1992;146(9):1029–1030. doi:10.1001/archpedi.1992.02160210031015
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