Pathogenesis and Treatment of Hepatic Failure

Abstract

IN a review of hepatic coma published in this journal eleven years ago¹ the statement was made that, "in spite of a long-continued search for a metabolic toxin in liver coma, none has been demonstrated." Within a few years a continuing flood of papers on the biochemical and clinical effects of ammonia in hepatic coma was started by the observations that impending coma could be produced by ammonia-releasing substances such as cation-exchange resins, urea and dietary protein.^{2 3 4 5} It was fitting that this rediscovery of ammonia toxicity in liver disease was made at the same time in France,⁶ for it was . . .