Vitamin B12 Binding Proteins in Liver Disease

Vitamin B₁₂ binding proteins were studied in patients with acute and chronic liver disease, and compared with vitamin B₁₂ binders in chronic myeloid leukemia. In acute viral hepatitis marked elevation of serum vitamin B₁₂ was common. Although the serum vitamin B₁₂ rose as high as that found in chronic myeloid leukaemia the unsaturated vitamin B₁₂ binding capacity (UBBC) was markedly elevated in the latter condition, whereas it was decreased in acute liver disease. In cirrhosis a moderate increase of serum vitamin B₁₂ and UBBC was common. Urinary vitamin B₁₂ excretion increased significantly only when the serum vitamin B₁₂ became markedly elevated in hepatitis. As in chronic myeloid leukaemia the alpha-globulin vitamin B₁₂-binder carried the bulk of the elevated serum vitamin B₁₂ in acute liver disease; the beta-globulin vitamin B₁₂-binder was decreased in serum but seemed to be the predominant binder in urine. This suggests that renal loss of beta-globulin binder is greater than renal loss of alpha-globulin binder. Only minor albumin binding of vitamin B₁₂ in liver disease was found in spite of marked elevation of the serum vitamin B₁₂ level. In cirrhosis the serum alpha-globulin binder was often increased and beta-globulin binder decreased. The cause and significance of these findings are discussed. The ability of serum vitamin B₁₂-binders of liver disease to ‘transfer’⁵⁷Co-B₁₂ to tissue was investigated in an in vitro rat liver homogenate system. In a limited study, vitamin B₁₂ uptake appeared to be within normal limits, except for suboptimal uptake from the beta-globulin binder in cirrhotic serum. Poor vitamin B₁₂ uptake from chronic myeloid leukaemia serum (in particular alpha-globulin binder) was confirmed.