The mechanism of hepatic encephalopathy (HE) is still unknown. A characteristic amino acid pattern in HE has been described: an increased level of plasma free tryptophan, a fall in plasma branched chain amino acids (BCAA) valine, leucine and isoleucine and a rise in plasma aromatic amino acids (AAA) phenylalanine and tyrosine.1 The brain uptake of AAA would increase; the ensuing depletion of brain dopamine and norepinephrine and increase of brain octopamine, which is considered as a false neurotransmitter, would result in perturbation of cerebral neurotransmission.2
Acute hepatic encephalopathy in 70 cirrhotic patients was monitored during parenteral administration of amino acids between January 1979 and January 1984. The diagnosis of cirrhosis was confirmed by needle biopsy, and HE by conventional clinical and EEG parameters. The infusion of AA solutions was initiated 48 h after admission and during a 5-day period: 34 patients received a control aminoacid solution, a commercially available AA mixture (Azonutril), and 36 patients a modified solution enriched in BAA prepared from crystallized AA dissolved in distilled water. The calorie intake for both groups was 1600 calories per day from glucose and lipid emulsion. No significant difference was noted based on clinical evolution, even though the plasma AAA/BAA ratio was corrected using the modified AA solution. Of the 34 patients in Group 1: 10 improved, 14 were unchanged, 10 deteriorated and 7 died. Of the 36 patients in Group 2: 12 improved, 14 were unchanged, 10 deteriorated and 7 died. EEG tracing evolved in parallel fashion. The authors conclude that modified AA solutions are ineffective in the treatment of acute hepatic encephalopathy in cirrhotic patients.
