Since the early stage of vitamin B
12 investigations in clinical field arround 1950, it has been well known that hypercobalaminemia was one of the characteristics in human leukemias, especially in chronic granulocytic leukemia without any reasonable explanations as to its mechanism. This study was undertaken to elucidate the mechanism of hypercobalaminemia in leukemia, from the view-point of B
12 values in sera, leukocytes and urine as well as the identification of four B
12 forms of derivatives, that is, Cyanocobalamin (CN-B
12), Hydroxocobalamin (OH-B
12), DBCC and Methylcobalamin (CH
3-B
12). Hypercobalaminemia in plasma was found to be mostly significant in cases of chronic granulocytic leukemia, but high B
12 contents in leukocytes were found to be significant in cases of acute granulocytic leukemia. High serum B
12 contents were corrected following the decrease of leukocytes counts after the administration of the antileukemic agents, but were not influenced by the spontaneous increase or decrease of leukocytes counts without any drugs administration. Following the drug administration, high urinary excretion of B
12 which occurred intermittently was found in course of leukemia, especially of chronic granulocytic leukemia. As to the percent distribution of CN-B
12, OH-B
12, DBCC and CH
3-B
12, it was found that approximately a half of B
12 derivatives was CH-B
12 in sera, leukocytes and urine of chronic granulocytic leukemia as well as of normals and it was concluded that the increased B
12 contents in blood and urine of leukemia were not due to the increase of one specialized form of B
12 derivatives. The percent distribution of four B
12 derivatives which bound to the increased Transcobalamin I in chronic granulocytic leukemia were also found to be similar to the patterns of whole plasma, demonstrating predominantly in CH
3-B
12 contents, while the B
12 derivatives pattern in Transcobalamin II were found to be the same percent distribution in three derivatives of CH
3-B
12, DBCC and OH-B
12 except CN-B
12 fraction. From the obtained results which are described above, the discussion is extended to the possible mechanism of hypercobalaminemia and hypercobalaminuria in leukemic patients in terms of the granulocytes turnover and destruction.
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