The relationship between pyridoxal phosphate deficiency and activities of serum and liver aminotransferases was studied in 12 patients with alcoholic hepatitis. Plasma pyridoxal phosphate and the activities of liver aminotransferases were initially decreased in the patients, as compared with mean values in controls with normal hepatic histology. Addition of pyridoxal phosphate to liver homogenates increased liver alanine aminotransferase, but not aspartate aminotransferase, in all patients with initially low plasma pyridoxal phosphate. After 1 mo of abstinence from alcohol, with intake of an adequate diet and pyridoxine supplementation, plasma pyridoxal phosphate increased in all patients with initially low values (p less than 0.02). Serum aspartate aminotransferase decreased, whereas serum alanine aminotransferase increased, resulting in a decrease in their ratio in serum (p less than 0.001). Liver alanine aminotransferase increased (p less than 0.005), whereas liver aspartate aminotransferase remained unchanged. These data suggest that pyridoxal 5'-phosphate depletion is partially responsible for the low serum alanine to aspartate aminotransferase ratio that is typical of patients with alcoholic hepatitis.
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Exp Biol Med (Maywood)
January 2025
[This retracts the article DOI: 10.1258/ebm.2011.
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Engelhardt Institute of Molecular Biology of the Russian Academy of Sciences, Vavilov street, 32, Moscow, 119991, Russia.
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