Encephalopathy, oxygen consumption, visceral amino acid clearance, and mortality in cirrhotic surgical patients.

TitleEncephalopathy, oxygen consumption, visceral amino acid clearance, and mortality in cirrhotic surgical patients.
Publication TypeJournal Article
Year of Publication1984
AuthorsLoda M, Clowes GH, Nespoli A, Bigatello L, Birkett DH, Menzoian JO
JournalAm J Surg
Date Published1984 Apr
KeywordsAdult, Aged, Amino Acids, Amino Acids, Branched-Chain, Ammonia, Female, Hemodynamics, Hepatic Encephalopathy, Humans, Liver Cirrhosis, Male, Metabolic Clearance Rate, Middle Aged, Octopamine, Oxygen Consumption, Phenylalanine, Tyrosine

To assess the relationship of the high mortality of coma in cirrhotic surgical patients to defects in energy metabolism, reduced utilization of amino acids by the liver and other visceral tissues, oxygen consumption, central plasma clearance rate of amino acids (CPCR of amino acids), and the plasma concentrations of plasma inducing factors were measured in a series of 59 cirrhotic patients. They were classed as alert, encephalopathic, and comatose (Groups A, E, and C, respectively). The comatose group was set apart from the other two by a significantly higher mortality of 83 percent (p less than 0.005) combined with a lower whole body oxygen consumption of 103 +/- 6.8 ml/min per m2 compared with 135 +/- 10 ml/min per m2 in alert patients and 159 +/- 12 ml/min per m2 in the encephalopathic patients (p less than 0.01) and CPCR of amino acids of only 120 +/- 20 ml of plasma/min per m2 compared with 240 +/- 30 ml of plasma/min per m2 in the alert patients and 300 +/- 50 in the encephalopathic patients (p less than 0.01). An inverse correlation of tyrosine and phenylalanine concentrations existed with both whole body oxygen consumption (r = -0.56, p less than 0.01) and also with total amino acid clearance (r = -0.61, p less than 0.01). Tyrosine and phenylalanine concentrations also correlated directly with the octopamine concentration (r = 0.64, p less than 0.01). Thus, we conclude that coma is a symptom of hyperaminoacidemia, but that death is the result of impaired oxidative energy production and a deficiency of amino acid clearance for synthesis of proteins required for survival.

Alternate JournalAm J Surg
PubMed ID6424488
Related Faculty: 
Massimo Loda, M.D.

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