Abstract
THE CURRENT THERAPY of hepatoencephalopathy has consisted principally of a regimen of dietary protein restriction and antibiotics. 1,2 In these studies we have attempted to invoke an immune mechanism to inhibit bacterial urease present in the gastrointestinal tract and thus decrease the quantity of ammonia transported to the liver for detoxification. Administration of ammonium salts or of substances which can be enzymatically broken down to ammonia will produce hepatic coma in patients with liver disease. 3-5 Proteins and their derivatives exposed to bacterial enzymes in the gastrointestinal tract are a constant source of ammonia. 6-8 Under normal circumstances ammonia so produced is carried via the portal circulation to the liver where it is converted to urea and is thereby diverted from the systemic circulation. 9,10 Many patients with hepatic coma have an elevated concentration of ammonia in the blood. 11,12 This blood ammonium concentration represents a balance between production in
Published Version
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