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Tryptophan and hepatic coma.

J Ono, D G Hutson, R S Dombro

    Gastroenterology
    |February 1, 1978
    PubMed
    Summary
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    Elevated cerebrospinal fluid (CSF) tryptophan levels are linked to hepatic coma pathogenesis. Increased plasma free tryptophan, free fatty acids, and decreased albumin characterize hepatic coma, distinguishing it from stable cirrhosis.

    Area of Science:

    • Biochemistry
    • Neuroscience
    • Hepatology

    Background:

    • Hepatic coma is a severe complication of liver cirrhosis.
    • Tryptophan metabolism is altered in liver disease.
    • The role of specific amino acids in hepatic encephalopathy requires further clarification.

    Purpose of the Study:

    • To investigate the role of tryptophan in the pathogenesis of hepatic coma.
    • To compare plasma and cerebrospinal fluid (CSF) tryptophan levels in patients with hepatic coma, stable cirrhosis, and healthy controls.

    Main Methods:

    • Measured plasma and CSF tryptophan levels.
    • Assessed plasma free fatty acids, competing amino acids, and albumin levels.
    • Compared biochemical parameters across three patient groups: hepatic coma, stable cirrhosis, and controls.

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    Main Results:

    • CSF tryptophan levels were elevated in hepatic coma patients compared to stable cirrhotic patients.
    • Elevated CSF tryptophan in hepatic coma correlated with increased plasma free tryptophan concentrations.
    • Hepatic coma patients exhibited increased plasma free fatty acids and decreased serum albumin.

    Conclusions:

    • Increased plasma free tryptophan, influenced by free fatty acids and albumin levels, is a key factor in hepatic coma.
    • Tryptophan accumulation in the central nervous system contributes to the development of hepatic coma.
    • Tryptophan is the only amino acid significantly elevated in the CSF of hepatic coma patients compared to those with stable cirrhosis.