Since 1912, more than 30 case reports of congenital Graves' disease have appeared in the American and European literature.1,2 In each reported case, during pregnancy the mother either manifested thyrotoxicosis or still exhibited exophthalmos from previous Graves' disease. Except for five reported deaths, all infants recovered within a few months. These findings suggest that neonatal thyrotoxicosis is due to transplacental transfer from the mother of some stimulating factor which is gradually excreted or metabolized by the infant.
Rosenberg et al,2 reported the first case of neonatal thyrotoxicosis in which both thyrotropin (TSH) and "long-acting thyroid stimulator" (LATS) were measured by the in vivo mouse thyroid I131 release assay.3,4 LATS activity was found in both the mother's and infant's sera, and the authors suggested that transplacental transfer of this substance was responsible for the infant's thyrotoxicosis and exophthalmos.
This paper will report a thyrotoxic infant whose sera