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Several investigators have documented the fact that chronic myelocytic leukemia (CML) is as- sociated with increases in serum vitamin B12 concentrations which may be of the order of 20 to 40 times the normal value (1-4).Less striking and less consistent elevations have been found in other myeloproliferative disorders.These include acute myelocytic leukemia (1, 3, 4), myeloid metaplasia (2-4), polycythemia vera associated with mye- locytic leukemia (4) and Di Guglielmo's disease (5).Elevations have also been reported in pa- tients with solid tumors when there are metastases to the liver (3, 6).The present study was de- signed to investigate in vivo the role that gastro- intestinal absorption, plasma transport and renal excretion of vitamin B12 play in producing this abnormality.Previous in vivo studies have dealt with the fate of a large intravenously administered dose of ra- (lioactive B1, (7, 8).In the present studies a dose of approximately 0.5 ug of Co58B12 was chosen, since this is within the limits of the estimated daily requirement of B12 (9).Oral administration was used so that gastrointestinal absorption could be evaluated and a physiologic pattern of plasma concentrations and excretion could be obtained.Twenty-four subjects have been studied, six of whom had CML. MATERIALS AND METHODSMaterials.Co58B12 1 had an original specific activity of 3.0 Atc per jig.
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Weinstein et al. (1960) studied this question.
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