Vitamin B6 repletion in cirrhosis with oral pyridoxine: Failure to improve amino acid metabolism

Authors

  • J. Michael Henderson FRCS,

    Corresponding author
    1. Departments of Surgery, Biochemistry and Biostatistics, Emory University School of Medicine, Atlanta, Georgia 30322
    • Department of Surgery, Emory University Hospital (F510), 1364 Clifton Rd. NE, Atlanta, Georgia 30322
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  • Steven S. Scott,

    1. Departments of Surgery, Biochemistry and Biostatistics, Emory University School of Medicine, Atlanta, Georgia 30322
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  • Alfred H. Merrill,

    1. Departments of Surgery, Biochemistry and Biostatistics, Emory University School of Medicine, Atlanta, Georgia 30322
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  • Bettye Hollins,

    1. Departments of Surgery, Biochemistry and Biostatistics, Emory University School of Medicine, Atlanta, Georgia 30322
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  • Michael H. Kutner

    1. Departments of Surgery, Biochemistry and Biostatistics, Emory University School of Medicine, Atlanta, Georgia 30322
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Abstract

This study evaluated the effect of daily oral pyridoxine supplementation in patients with cirrhosis. Eight subjects were treated with 25 mg of pyridoxine for 28 days. Before and after the supplementation period, B6 status was assessed by measuring fasting plasma vitamer levels and response to a 25 mg oral pyridoxine load. In addition, a 24-hr urine collection was analyzed during each load study for B6 metabolites. The data indicated that supplementation achieved repletion of peripheral B6 stores, as evidenced by: (i) a significant (p < 0.005) rise in fasting plasma pyridoxal phosphate after supplementation (mean ± S.D. = 56.8 ± 30.5 nmoles per liter) as compared to initial levels (17.0 ± 17.8 nmoles per liter); (ii) a higher (p < 0.05) percentage excretion of the pyridoxine load as urinary 4-pyridoxic acid (31.0 ± 9.3%) compared to the initial load (19.6 ± 5.8%), and (iii) a postsupplementation area under the plasma concentration vs. time curve for pyridoxal phosphate (377 ± 529 nmoles·hr per liter), which was decreased (p < 0.005) from the presupplementation value (934 ± 756 nmoles·hr per liter). The postsupplementation fasting plasma pyridoxal phosphate concentrations were within the normal range. The consequences of B6 repletion on amino acid metabolism were measured by oral protein loads (n = 4) or oral methionine loads (n = 4). No significant changes were observed for methionine or any other amino acid in regard to plasma fasting concentration, peak concentration or AUC. Although the vitamin B6 deficiency of cirrhosis was corrected by daily oral pyridoxine supplementation, there was apparently no improvement in the deranged amino acid metabolism.

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