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Cobalamin (Vitamin B₁₂) and Holotranscobalamin Changes in Plasma and Liver Tissue in Alcoholics with Liver Disease

Departments of Preventive Medicine and Community Health, Medicine, and Liver Center, University of Medicine and Dentistry, New Jersey Medical School, Newark, New Jersey

Address reprint requests to: Herman Baker, Ph.D., UMDNJ, New Jersey Medical School, 65 Bergen Street, Martland GB-159, Newark, NJ 07107-3001

Objective: We wanted to know if alterations in plasma cobalamin (B₁₂) concentration and B₁₂ carriers, e.g., holotranscobalamins (holo TC), occur in blood and liver tissue from patients with severe alcoholic liver disease. Our purpose was to test the hypothesis that liver disease may disrupt B₁₂ distribution.

Method: Total B₁₂, as well as B₁₂ bound to transcobalamin I, II, III (holo TC), were measured to determine their concentration in plasma and in liver tissue; Poteriochromonas malhamensis—a protozoan reagent served to measure only metabolically active (true) B₁₂. Total B₁₂ as distributed in holo TC in plasma and liver tissue of healthy subjects (controls) were compared to patients with severe alcoholic liver disease.

Results: Severe liver disease initiates highly elevated B₁₂ levels in plasma and a lowered liver tissue total B₁₂ concentration. The percent of B₁₂ distributed to holo TC II is significantly depleted during liver disease. In contrast, holo TC I and III are elevated in plasma during liver disease and contain more B₁₂ than controls. Total B₁₂ and B₁₂ distributed to TC are lower in diseased liver tissue.

Conclusion: Severe alcoholic liver disease involves leakage of total B₁₂ from liver tissue into the plasma. Holo TC I and III concentration increases in plasma; this preserves the high plasma B₁₂ from being excreted. However, plasma holo TC II B₁₂ distribution is decreased, indicating that there is a depression of exogenous B₁₂ entering the plasma and tissues. In severe liver disease, liver tissue B₁₂ binding and storage by TC is disrupted and causes B₁₂ to leak out of the liver into the circulation. Eventually liver disease could produce enough severe tissue B₁₂ deficits to cause metabolic dysfunction despite elevated plasma total B₁₂. Elevation of plasma B₁₂, accompanied by a lowering of holo TC II distribution, seemed to be a useful index of liver disease severity suggesting preventative treatment.

Key words: vitamin B₁₂, holotranscobalamins, liver disease

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