Summary. Chronic myeloid leukaemia (CML) and pernicious anaemia (PA) coexisted in a 51‐yr‐old man (who also had myasthenia gravis). His serum vitamin B12 level was normal instead of the high value expected in CML, or the low value expected in PA. Short‐term culture of his peripheral blood cells showed deranged DNA synthesis of the type observed in vitamin B12 deficiency, indicating that his ‘normal’ serum vitamin B12 level was not associated with normal amounts of vitamin B12 available to his CML cells. A tracer dose of 0.45 μg of[57 Co]vitamin B12 disappeared abnormally slowly from his serum over 24 hr (as previously observed by others in patients with either CML or PA). A therapeutic injection of vitamin B12 appeared to disappear abnormally slowly from his serum over a period of 2 yr. His serum showed a markedly elevated unsaturated vitamin B12 binding capacity, with a less sharp increase in percentage of vitamin B12 binding α as compared to β globulin than usually expected in CML. Withholding therapeutic vitamin B12 for 2 yr has been associated with stabilization of his WBC at the 40 000‐50 ooo/μl range. Although this association could be chance rather than cause and effect, the patient does represent an ‘experiment of nature’ involving vitamin B12 metabolism and does raise the question as to whether his leukaemia is retarded by his deficiency of vitamin B12, which results from inadequate absorption of vitamin B12 and possibly from elevated serum vitamin B12 binding a globulin rendering his circulating vitamin B12 metabolically inert.

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A B S T R A C T Human granulocytes (G) contain a vitamin Ba-binding protein (B12BP).There is evidence that chronic myelogenous leukemia leukocytes (CMLL) may synthesize B12BP. Our prior studies suggested that intact, living intravascular G synthesize and release such protein into extracellular compartments in vivo.In the present study, CMLL were incubated in Trisbuffered Hank's basal salt solution (pH 7.2) containing 0.1% human serum albumin to study release of B12BP into the medium. B,2BP was released continuously and in increasing amounts over a 5 hr period at 370C; this release was inhibited almost completely when the cells were incubated at 4VC and by about half as much in the presence of N-ethylmaleimide (1 mmole/liter). Cycloheximide (50 ,gg/ml) had no effect on the release of B12BP but significantly inhibited incorporation of leucine-'H into leukocyte protein. G incubated with 20 mg/ml of compound 48/80, an experimental histamine-releasing agent, had a 6-fold increase in release of B12BP over a 2 hr period. Subcellular fractionation studies of human granulocytes demonstrate that most of the B12BP is associated with the granular (20,000 g) layer with an excellent correlation observed between its subcellular distribution and that of acid phosphatase.These findings suggest that the release of B12BP from G is mediated by an active process and provide further evidence that granulocytes are secretory as well as phagocytic cells.

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