[Vitamin B12 and transcobalamin in chronic myeloproliferative disorders]

Although vitamin B12 is an essential coenzyme for DNA synthesis, humans, like other mammals, are incapable of synthesizing it. The role of intrinsic factor (IF) in B12 absorption is widely known, but, in fact there exists a much more intricate and complex mechanism for the effective assimilation of this important trace element in humans. B12 binding proteins play important roles in all stages of vitamin B12 metabolism. They are involved not only in its absorption, but also in its transport in serum, uptake to cells, storage in organs, enterohepatic circulation, and elimination of its analogues. Besides IF, well-known as a vitamin B12 binding protein found in gastric juice, there are other kinds of binding proteins found in human serum which are composed to transcobalamin (TC) I, II and III. Elevation of the vitamin B12 level in chronic myelogenous leukemia was first reported in the 1950s. Since then, B12 elevation has been found to occur in other kinds of chronic myeloproliferative disorders (CMPDs) as well and to be caused by an increase of serum TC. In CMPDs, either TCI or TCIII increases, but, the degree of elevation and the type of TC involved differs for each disorder. This article describes the changes in TC of CMPD patients. With the induction of the developed radioimmunoassay for R-type B12 binding protein, many cases have been examined. In addition, detailed qualitative analysis using DEAE cellulose column chromatography has been included for conditions not previously reported.(ABSTRACT TRUNCATED AT 250 WORDS)