February 1976, Vol 130, No. 2 >

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Article | February 1976

Pathogenesis and Therapy of Neonatal Graves Disease

DELBERT A. FISHER, MD

Am J Dis Child. 1976;130(2):133-134. doi:10.1001/archpedi.1976.02120030023003.

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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

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Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature

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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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