Serum vitamin B12, serum and red cell folates, vitamin B12 and folic acid binding proteins in women taking oral contraceptives.

Serum and red cell folate, FABP, serum vitamin B12 and vitamin B12 binding proteins were determined in 20 women taking oral contraceptives continuously for at least one year. Studies were also performed on 50 apparently healthy women with history of never taken or not taking oral contraceptives for at least one year as a control group. Serum vitamin B12 level, UBBC and TBBC in women taking oral contraceptives were slightly but not significantly lower than those of the control group. TCI and TCIII increased with a decreased TCII, so that UBBC was within the normal limit. Serum folate was non-significantly lower while red cell folate was significantly lower in the oral contraceptive group than those of the control group. However, all cases of the former showed red cell folate over 200 ng/ml. A highly significant increased serum FABP was demonstrated in the women taking oral contraceptives. This was probably due to the increased synthesis of the FABP in order to bind more folate from the low serum folate and the hormonally induced stimulation.

Vitamin B12 and vitamin B12 binding proteins in liver diseases.

Serum vitamin B12 and vitamin B12 binding proteins (transcobalamins, TCS) were determined in patients with malaria, amoebic liver abscess, carcinoma of the liver, infectious hepatitis, cirrhosis and chronic myelocytic leukemia (CML) as well as in 60 blood donor subjects. Serum vitamin B12 in patients with infectious hepatitis, cirrhosis and CML were higher than that of the normal subjects. The values of unsaturated vitamin B12 binding capacity (UBBC) in patients with carcinoma of the liver, infectious hepatitis, cirrhosis were lower while that of patients with CML were higher than that of the normal subjects. A markedly increased TCI and decreased TCII was observed in patients with CML while these changes was much less in patients with other liver diseases. The difference was possibly due to a flooding of vitamin B12 from damaged liver cells into the circulation and the decreased synthesis of transcobalamins in patients with liver diseases while the increased granulocytes, the source of TCI, was much increased in patients with CML.