Transient Hypothyroidism in Infants due to Maternal TSH-Receptor Blocking Antibodies-Character of Their IgG and Long-Term Prognosis of Their Infants

Abstract

Transient neonatal hypothyroidism in infants born to mothers with chronic thyroidism, first reported in 1960 by Sutherland et al.^l), has been established as an important diseases entity in the newborn period. Transplacental transfer of TSH-receptor blocking antibodies has been defined as the cause of the disease.) Although similar cases have been reported since then,^{3) 4)} the clinical features, as well as the prognosis of each case, varied greatly. That is, most of infants developed normally; however, some infants were physically, mentally or emotionally retarded in spite of intensive treatment during the newborn period,¹⁾ and their condition was quite different from that found in congenital hypothyroidism. It is not clear whether the difference was due to the nature of TSH-receptor blocking antibodies in the mother or to the severity of thyroid suppression during the fetal and newborn periods. It was suggested that the IgG in the mother’s serum not only inhibited TSH binding to its receptor, but also blocked TSH-stimulated cAMP response, TSH-stimulated iodine uptake, organification and ³H-thymidine incorporation into DNA in cultured thyroid cells: that is, it blocked post-receptor processes.⁴⁾ The purposes of this paper are twofold: 1) To study more precise mechanism and to evaluate the possible involvement of GTP-binding protein of the inhibition of adenylate cyclase activities using porcine thyroid cells. 2) To establish a basis for the long-term prognosis of these patients, particularly of two of the sibling sets, whose mothers were once hypothyroid and were euthyroid during pregnancy.