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Hepatic Encephalopathy

  • Arthur J.l. Cooper
  • , Fred Plum
  • , Alan H. Lockwood
  • , David W. Mccandless
  • , Peter G. Traber
  • , Milton M. Lieberthal
  • , Parker Vanamee
  • , Saul W. Brusilow
  • , Richard Traystman
  • , Cosmo L. Fraser
  • , Allen I. Arieff
  • Cornell University
  • University of Texas Health Science Center at Houston
  • Northwestern University
  • University of Cincinnati
  • Memorial Sloan-Kettering Cancer Center
  • Johns Hopkins University
  • University of California at San Francisco

Research output: Contribution to journalLetterpeer-review

6 Scopus citations

Abstract

To the Editor: The Medical Progress article on hepatic encephalopathy by Fraser and Arieff (Oct. 3 issue)1 contains several errors that could lead to mistakes of understanding or treatment. It states, “After ammonia is generated [in the gut], it is transported through the portal circulation to the liver, where it is normally converted to urea.” However, 30 to 40 percent of ammonia is also converted to glutamine in the liver.2 The authors imply that an increased cerebral catabolism of amino acids results in elevated ammonia concentrations in the hyperammonemic brain. The five cited references are inappropriate. The best evidence suggests…

Original languageEnglish
Pages (from-to)784-787
Number of pages4
JournalNew England Journal of Medicine
Volume314
Issue number12
DOIs
StatePublished - Mar 20 1986

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