The article by Hollingsworth and Mabry that appears in this issue of the Journal (p 148) provides interesting and important supplemental information to the authors' earlier article.1 These articles present convincing evidence that at least some cases of congenital Graves disease (perhaps 20% to 30%) are not transient and emphasize that the disease is not benign. The mortality is in the range of 15% to 20%, and sequels, including premature synostosis and minimal brain dysfunction, are common, particularly in the cases with a persistent or recurrent course. The authors suggest that the neonatal disease is not due to transplacentally acquired long-acting thyroid stimulator (LATS), but rather that the LATS serves only as an immunologic marker or incitant in a genetically preselected population.
This is a provocative hypothesis and seems credible for the infants with prolonged disease (more than six months). However, for those with transient disease of less than
FISHER DA. Pathogenesis and Therapy of Neonatal Graves Disease. Am J Dis Child. 1976;130(2):133–134. doi:10.1001/archpedi.1976.02120030023003
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