The report on aspirin hepatitis by Zucker and colleagues in this issue of the Journal (page 1433) is the latest in a series of recent publications concerned with this phenomenon.1-5 These reports follow at least two earlier communications on the same subject about 20 years ago.6,7 Elevated activity of serum glutamic oxaloacetic and pyruvic transaminases (SGOT and SGPT) and other evidence of hepatotoxicity have been observed in patients receiving relatively high doses of aspirin or other salicylates such as choline salicylate or sodium salicylate. Most, but not all, of the reported cases involved children with rheumatic fever or rheumatoid arthritis rather than adults. One of the two patients reported by Zucker et al, as well as the three patients described by Seaman et al,5 had systemic lupus erythematosus. Evidence of liver injury usually appeared at plasma salicylate concentrations above 25 mg/100 ml and disappeared promptly when salicylate
LEVY G, YAFFE SJ, SMITH CA. Clinical Implications of Salicylate-Induced Liver Damage. Am J Dis Child. 1975;129(12):1385–1386. doi:10.1001/archpedi.1975.02120490003001
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