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Serum Vitamin B12 Content and Unsaturated Vitamin B12-Binding Capacity in Myeloproliferative Disease: Value in Differential Diagnosis and as Indicators of Disease Activity

HARRIET S. GILBERT, M.D., F.A.C.P.; STEPHEN KRAUSS, M.D.; BERNARD PASTERNACK, PH.D.; VICTOR HERBERT, M.D.; and LOUIS R. WASSERMAN, M.D., F.A.C.P.
Ann Intern Med. 1969;71(4):719-729. doi:10.7326/0003-4819-71-4-719
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SUMMARY:

The serum unsaturated vitamin B12-binding capacity (UBBC) was found to be of value in distinguishing polycythemia vera from other conditions that are accompanied by an elevated hematocrit or an absolute erythrocytosis and as an indicator of disease activity in polycythemia vera. The serum vitamin B12 level was of lesser value. Increased levels of serum vitamin B12 were observed in 36% and increased levels of UBBC in 70% of patients with untreated polycythemia vera and related myeloproliferative disorders, as contrasted with normal serum vitamin B12 levels in 98% and normal UBBC in 87% of cases of spurious (relative) polycythemia and isolated erythrocytosis (secondary and unclassified polycythemia). Serum vitamin B12 and UBBC levels in polycythemia vera treated only with phlebotomy did not differ from values in untreated cases, whereas patients whose erythroid activity had been controlled by myelosuppressive therapy had levels comparable to those in normal subjects. UBBC values were positively correlated with erythroid activity and leukocyte count. Serial observations indicated that changes in UBBC accompanied and in some cases preceded the occurrence of response and relapse in patients receiving myelosuppressive therapy. Changes in serum B12 levels did not parallel the erythroid response to therapy, nor were B12 levels correlated with the blood count, spleen size, or uric acid values. Chromatographic separation of unsaturated B12 binders showed an increase in both alpha and beta components. The frequent observation of elevated B12 binders without a concomitant rise in serum B12 content in patients with polycythemia vera suggests that some of the B12-binding protein of alpha mobility that is elaborated is abnormal in that it does not bind endogenous vitmain B12.

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