[Transcobalamin II dynamics in a plasma turnover study of patients with lupus erythematosus. Preliminary report]

Increased serum levels of the essential vitamin B12 binding protein, transcobalamin II (TC2) were previously observed in autoimmune disease. The periods of raised serum level correlated with clinical disease activity in patients with SLE and dermatomyositis. The correlation of serum levels with disease activity in a large group of 44 Swiss SLE patients was shown to be most reliable for TC2, when compared to certain established serological markers such as complement factors C3 and C4, antinuclear antibody titer or antinative DNA antibodies. Several questions were raised: Why is the TC2 level elevated in active SLE? Is the accumulation in serum due to lack of TC2 uptake by the cell or is it due to stimulation of synthesis? Answers were sought by applying a plasma turnover test for TC2 to the SLE patients. After 400 ng/kg cyanocobalamin (i.m.) the TC2 level decreased, due to preferential uptake of holo TC2 by the cells. Total TC2 levels were determined by radioimmunoassay. Normalisation of the plasma level and corresponding reappearance of apo TC2 was interpreted as newly synthesized TC2. Twelve SLE patients and six healthy controls were investigated. One SLE patient was treated with a higher cobalamin dose (200 micrograms) to ensure complete saturation of TC2. The TC2 level decrease after cobalamin injection was comparable in controls and patients, independently of the state of the disease. Normalisation of plasma levels was significantly faster, elevation above starting levels was observed, in 3 of 5 SLE patients exhibiting active disease. In the remaining 9 patients normalisation of the plasma level was comparable to the control group. Our conclusions are that TC2 uptake, in other words TC2 consumption by the cell, is unchanged in SLE, and that an increased rate of TC2 synthesis may be the cause of elevated plasma levels in active SLE.