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June 1973

Lean Reye Syndrome

Author Affiliations

Pediatric Neurology Unit Massachusetts General Hospital Boston, MA 02114

Am J Dis Child. 1973;125(6):900-901. doi:10.1001/archpedi.1973.04160060096025

To the Editor.  —The report by Glasgow et al1 on the occurrence of Reye syndrome in the absence of severe fatty infiltration of the liver represents both some useful clinical observation and a disservice to the effort to define Reye syndrome more precisely. The latter objection arises, in part, from a most dubious clinical example (case 1). The history, physical examination, course, and presence of hypoglycemia, while not unlike some cases of Reye syndrome, are certainly nonspecific. The mildly elevated serum glutamic oxaloacetic transaminase (SGOT) and minimally elevated serum glutamic pyruvic transaminase (SGPT) are hardly diagnostic, although not inconsistent with values in certain other cases reported from the same laboratory. The prothrombin activity and the venous ammonia level are not out of the range of values seen in the control group of patients illustrated in Fig 1 of the companion article by Glasgow et al.2 Furthermore, the slight fat

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