Transferrin metabolism in alcoholic liver disease

Authors

  • Barry J. Potter Ph.D.,

    Corresponding author
    1. Academic Department of Medicine, The Royal Free Hospital, London NW3 2QG, England
    Current affiliation:
    1. The Polly Annenberg Levee Hematology Center, Department of Medicine, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, New York 10029
    • Polly Annenberg Levee Hematology Center and Hepatic Research Group (Department of Medicine), Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, New York 10029
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  • Roger W. G. Chapman,

    1. Academic Department of Medicine, The Royal Free Hospital, London NW3 2QG, England
    Current affiliation:
    1. Gastroenterology Unit, The John Radcliffe Hospital, Headington, Oxford OX2 6HE, England
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  • Rosa M. Nunes,

    1. Academic Department of Medicine, The Royal Free Hospital, London NW3 2QG, England
    Current affiliation:
    1. The Polly Annenberg Levee Hematology Center, Department of Medicine, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, New York 10029
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  • Dario Sorrentino,

    1. Academic Department of Medicine, The Royal Free Hospital, London NW3 2QG, England
    Current affiliation:
    1. Gastrointestinal Research Unit, Department of Medicine, University of California, San Francisco, California 94143
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  • Sheila Sherlock

    1. Academic Department of Medicine, The Royal Free Hospital, London NW3 2QG, England
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Abstract

The metabolism of transferrin was studied using purified 125I-labeled transferrin in 11 alcoholic patients; six with fatty liver and five with cirrhosis. Six healthy subjects whose alcohol intake was les than 40 gm daily were studied as a control group.

There were no significant differences in the mean fractional catabolic rate and plasma volume in the alcoholic groups when compared with control subjects. A significantly decreased mean serum transferrin concentration was found in the alcoholic cirrhotic patients (1.8 ± 0.3 gm per liter vs. 2.9 ± 0.2; p < 0.01), resulting from diminished total body synthesis (0.9 ± 0.2 mg per kg per hr vs. 1.8 ± 0.2; p < 0.01). In contrast, in the patients with alcoholic fatty liver, the mean total body transferrin synthesis (2.4 ± 0.3 mg per kg per hr) was significantly increased when compared with controls (p < 0.05).

For all the alcoholic patients, the serum transferrin correlated with transferrin synthesis (r = +0.70; p < 0.01) but the serum iron did not.

These results suggest that, in alcoholic cirrhosis, transferrin synthesis is decreased, probably reflecting diminished synthetic capacity by the liver. In contrast, in patients with alcoholic fatty liver, transferrin turnover is accelerated.

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