vitamin-b-12 and Myeloproliferative-Disorders

Anemia is a common problem in primary care. Classification based on mean cell volume narrows the differential diagnosis and directs testing. A marked macrocytosis is characteristic of vitamin B12 and folate deficiencies, certain medications, and primary bone marrow disorders. The three most common causes of microcytic anemia are iron deficiency, thalassemia trait, and anemia of inflammation. Additional laboratory testing is required for diagnosis. Determination of the rate of development of anemia and examination of a blood smear may provide diagnostic clues to guide more specialized testing. Diagnosis of iron, vitamin B12, or folate deficiency mandates determination of the underlying cause.

Topics: Alcohol Drinking; Anemia, Iron-Deficiency; Anemia, Macrocytic; Blood Cell Count; Diagnosis, Differential; Drug-Related Side Effects and Adverse Reactions; Female; FIGLU Test; Folic Acid; Folic Acid Deficiency; Humans; Liver Diseases; Myeloproliferative Disorders; Predictive Value of Tests; Primary Health Care; United States; Vitamin B 12; Vitamin B 12 Deficiency; Women's Health

Topics: Anemia; Gastritis, Atrophic; Humans; Liver Diseases; Luminescent Measurements; Myeloproliferative Disorders; Radioligand Assay; Reference Values; Specimen Handling; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Adrenal Cortex Hormones; Aged; Alkaline Phosphatase; Androgens; Antineoplastic Agents; Blood Cell Count; Blood Transfusion; Chromosome Aberrations; Chromosome Disorders; Folic Acid; Humans; Leukocytes; Middle Aged; Muramidase; Myeloproliferative Disorders; Peroxidase; Preleukemia; Prognosis; Pyridoxine; Vitamin B 12

Topics: Anemia, Pernicious; Blood Volume; Blood Volume Determination; Chromium Isotopes; Cobalt Isotopes; Erythrocyte Aging; Erythrocytes; Erythropoiesis; Hematologic Diseases; Humans; Intestinal Absorption; Iodine Radioisotopes; Iron; Iron Isotopes; Myeloproliferative Disorders; Phosphorus Isotopes; Radioisotopes; Radionuclide Imaging; Schilling Test; Serum Albumin, Radio-Iodinated; Surface Properties; Vitamin B 12

FIP1L1-PDGFRA-positive myeloid neoplasm with eosinophilia (F/P+ MN-eo) is a rare disease: robust epidemiological data are lacking and reported issues are scarce, of low sample-size and limited follow-up. Imatinib mesylate (IM) is highly efficient but no predictive factor of relapse after discontinuation has yet been identified. One hundred and fifty-one patients with F/P+ MN-eo (143 males; mean age at diagnosis 49 years; mean annual incidence: 0.18 case per million population) were included in this retrospective nationwide study involving all French laboratories who perform the search of F/P fusion gene (study period: 2003-2019). The main organs involved included the spleen (44%), skin (32%), lungs (30%), heart (19%) and central nervous system (9%). Serum vitamin B12 and tryptase levels were elevated in 74/79 (94%) and 45/57 (79%) patients, respectively, and none of the 31 patients initially treated with corticosteroids achieved complete hematologic remission. All 148 (98%) IM-treated patients achieved complete hematologic and molecular (when tested, n = 84) responses. Forty-six patients eventually discontinued IM, among whom 20 (57%) relapsed. In multivariate analysis, time to IM initiation (continuous HR: 1,01 [0.99-1,03]; P = .05) and duration of IM treatment (continuous HR: 0,97 [0,95-0,99]; P = .004) were independent factors of relapse after discontinuation of IM. After a mean follow-up of 80 (56) months, the 1, 5- and 10-year overall survival rates in IM-treated patients were 99%, 95% and 84% respectively. In F/P+ MN-eo, prompt initiation of IM and longer treatment durations may prevent relapses after discontinuation of IM.

Topics: Adrenal Cortex Hormones; Adult; Disease-Free Survival; Eosinophilia; Female; France; Hematologic Neoplasms; Humans; Incidence; Male; Middle Aged; mRNA Cleavage and Polyadenylation Factors; Myeloproliferative Disorders; Oncogene Proteins, Fusion; Receptor, Platelet-Derived Growth Factor alpha; Retrospective Studies; Survival Rate; Tryptases; Vitamin B 12

Topics: Female; Humans; Male; Middle Aged; Myeloproliferative Disorders; Pathology, Molecular; Up-Regulation; Vitamin B 12

Myeloproliferative disorders are characterized by proliferation of 1 or more lineage of hematologic cells. Rapid proliferation of cells may lead to depletion of vitamin B12, which may be falsely elevated by conventional assays in these disorders. We evaluated vitamin B12 status with conventional vitamin B12 assay and levels of serum methylmalonic acid (MMA), serum holotranscobalamin (holoTC), and plasma homocysteine in myeloproliferative disorders.. In 58 patients who had myeloproliferative disorders and normal serum creatinine levels, we measured levels of vitamin B12, MMA, holoTC, and homocysteine. Correlations were evaluated between these tests, with MMA as the reference standard for vitamin B12 deficiency.. Prevalence of vitamin B12 deficiency was 69%, despite high serum vitamin B12 levels. Levels of holoTC of 40.6 pmol/L or less and homocysteine of greater than 14 mol/L were the best cutoff levels with sensitivity values of 75% and 70%, specificity values of 80% and 68%, and positive predictive values of 88% and 80%. Logistic regression showed that cutoff values of holoTC of 40.6 pmol/L or less and homocysteine of greater than 14 mol/L resulted in odds ratio 15.5 for low versus high holoTC, and odds ratio 5.4 for high versus low homocysteine, to confirm vitamin B12 deficiency.. Patients who had myeloproliferative disorders had a high prevalence of vitamin B12 deficiency, despite high serum vitamin B12 levels. Therefore, vitamin B12 status should be evaluated in patients with myeloproliferative disorders. Holotranscobalamin level may be the best initial test and may replace vitamin B12 assay to accompany MMA and homocysteine levels.

Topics: Aged; Female; Follow-Up Studies; Humans; Male; Methylmalonic Acid; Middle Aged; Myeloproliferative Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Elevation of the methylmalonic acid level is a sensitive marker of vitamin B(12) deficiency. Our cross-sectional observational study of 33 patients with myeloproliferative disorders found that 9 patients, 27.27% had occult deficiency despite having normal to elevated serum vitamin B(12) levels. Early detection of vitamin B(12) deficiency by using the methylmalonic acid measurement may prevent significant neurologic and hematologic complications in patients with myeloproliferative disorders. In patients with myeloproliferative disorders, normal to high serum vitamin B(12) concentrations have often been reported. The primary objective of this study was to determine whether normal or elevated serum vitamin B(12) levels in myeloproliferative disorders might actually mask the true underlying vitamin B(12) deficiency in some patients. Thirty-three patients (12 men, 21 women; mean age, 70.55 years [range, 37-90 years]) with polycythemia vera (n = 13), essential thrombocythemia (n = 12), chronic myelogenous leukemia (n = 5), and idiopathic myelofibrosis (IMF) (n = 3) were accrued over a period of 1 year, from March 2009 to February 2010. From all of the subjects, serum vitamin B(12) level, methylmalonic acid level, a basic complete blood cell count panel, and liver and renal function tests were obtained. Normal to elevated serum vitamin B(12) levels were recorded in all the patients. However, elevated serum methylmalonic acid levels were found in 9 (27.27%) patients, with a prevalence of 2 patients with polycythemia vera, 23% in polycythemia vera, 4 patients with essential thrombocythemia, 33.3% in essential thrombocythemia, 1 patient with chronic myelogenous leukemia, 20% in chronic myelogenous leukemia, and 2 patients with idiopathic myelofibrosis, 66.7% in IMF. Our data suggest that 27.27% of the total enrolled patients had occult vitamin B(12) deficiency despite normal to elevated vitamin B(12) levels on regular serum vitamin B(12) testing.

Topics: Adult; Aged; Aged, 80 and over; Cross-Sectional Studies; Humans; Methylmalonic Acid; Middle Aged; Myeloproliferative Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Diagnosis, Differential; Female; Humans; Middle Aged; Myeloproliferative Disorders; Radioimmunoassay; Vitamin B 12

Since serum tryptase levels are elevated in some patients with myeloproliferative disorders, we examined their utility in identifying a subset of patients with hypereosinophilic syndrome (HES) and an underlying myeloproliferative disorder. Elevated serum tryptase levels (> 11.5 ng/mL) were present in 9 of 15 patients with HES and were associated with other markers of myeloproliferation, including elevated B12 levels and splenomegaly. Although bone marrow biopsies in these patients showed increased numbers of CD25+ mast cells and atypical spindle-shaped mast cells, patients with HES and elevated serum tryptase could be distinguished from patients with systemic mastocytosis and eosinophilia by their clinical manifestations, the absence of mast cell aggregates, the lack of a somatic KIT mutation, and the presence of the recently described fusion of the Fip1-like 1 (FIP1L1) gene to the platelet-derived growth factor receptor alpha gene (PDGFRA). Patients with HES and elevated serum tryptase were more likely to develop fibroproliferative end organ damage, and 3 of 9 died within 5 years of diagnosis in contrast to 0 of 6 patients with normal serum tryptase levels. All 6 patients with HES and elevated tryptase treated with imatinib demonstrated a clinical and hematologic response. In summary, elevated serum tryptase appears to be a sensitive marker of a myeloproliferative variant of HES that is characterized by tissue fibrosis, poor prognosis, and imatinib responsiveness.

Topics: Adolescent; Adult; Aged; Amino Acid Sequence; Base Sequence; Benzamides; Biopsy; Bone Marrow; Chromosomes, Human, Pair 4; Endomyocardial Fibrosis; Eosinophils; Female; Fibrosis; Gene Deletion; Humans; Hypereosinophilic Syndrome; Imatinib Mesylate; Leukocytes, Mononuclear; Lung Diseases; Male; Mast Cells; Mastocytosis; Middle Aged; Molecular Sequence Data; mRNA Cleavage and Polyadenylation Factors; Myeloproliferative Disorders; Oncogene Proteins, Fusion; Piperazines; Prognosis; Pyrimidines; Receptor, Platelet-Derived Growth Factor alpha; Reverse Transcriptase Polymerase Chain Reaction; RNA; Serine Endopeptidases; Splenomegaly; Tryptases; Vitamin B 12

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)

Topics: Blast Crisis; Chronic Disease; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Myeloproliferative Disorders; Transcobalamins; Vitamin B 12

Serum vitamin B12 levels were measured in 300 Indian subjects, comprising 165 haematologically normal volunteers, 78 cases of nutritional megaloblastic anaemia and 57 patients with myeloproliferative disorders. Each sample was assayed by three different techniques: i) a microbiological assay using Euglena gracilis as the test organism; ii) radioisotope dilution assay, using pure intrinsic factor as the B12 binder and haemoglobin-coated charcoal for separation of bound from free vitamin B12; iii) radioisotope dilution assay using intrinsic factor as the vitamin B12 binder and DEAE cellulose for separation of bound from free vitamin B12. Results by the three methods correlated closely at normal and high levels of serum B12: at low levels microbiological assay and radio-assay using haemoglobin-coated charcoal correlated well but DEAE cellulose failed to detect 16 of 68 patients with vitamin B12 deficiency. The radioisotope dilution assay tended to yield higher values of serum vitamin B12 than did the microbiological assay. In none of the healthy volunteers was a clearly low value found by any of the techniques, but 20 of them had low serum B12 levels. Radioisotope dilution assay using haemoglobin-coated charcoal is recommended as an accurate assay procedure for developing countries like India, where ready-made kits are not easily available and vitamin B12 deficiency states are common.

Topics: Anemia, Megaloblastic; DEAE-Cellulose; Evaluation Studies as Topic; Humans; India; Microbiological Techniques; Myeloproliferative Disorders; Radioisotope Dilution Technique; Vitamin B 12

Topics: Anemia; Biological Assay; Humans; Liver Neoplasms; Myeloproliferative Disorders; Pancreatitis; Radioisotope Dilution Technique; Reference Values; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Chronic Disease; Humans; Myeloproliferative Disorders; Transcobalamins; Vitamin B 12

Our information about cobalamin transport in the blood is largely based on studies of unsaturated cobalamin-binding proteins. Therefore, the distribution of endogenous cobalamin among these proteins was examined. Normally, R binder (transcobalamin I) carries most of the cobalamin circulating at any given moment, but the proportion varies greatly. Transcobalamin II carries a larger fraction of the cobalamin present in portal vein blood than in hepatic and axillary vein blood. In disease, transcobalamin II occasionally holds the bulk of the vitamin present in peripheral blood. Such was observed in three patients showing quantitative changes of unsaturated binder (either diminished R binder or increased transcobalamin II), but in two cases of chronic liver disease this was independent of unsaturated transcobalamin levels. Four patients with low serum cobalamin levels maintained normal distribution, indicating proportional cobalamin depletion from both binder pools. Small amounts of vitamin were attached in many sera to minor binders, and occasionally seemed to circulate free. These results demonstrate that assumptions that cobalamin is always attached largely to transcobalamin I are not warranted. Cobalamin distribution appears to be governed by many factors, of which the amounts of the binding proteins is only one.

Topics: Axillary Vein; Health Status; Hematologic Diseases; Hepatic Veins; Humans; Liver Diseases; Multiple Myeloma; Myeloproliferative Disorders; Portal Vein; Transcobalamins; Vitamin B 12

Topics: Antibodies, Antinuclear; Bone Marrow; Chronic Disease; Cytodiagnosis; Female; Humans; Leukemia; Middle Aged; Myeloproliferative Disorders; Neutrophils; Vitamin B 12

Methods for the rapid quantitation on unsaturated transcobalamin II (TC II) and R-binders in serum following separation of these binders using a) adsorption by uncoated charcoal, b) adsorption by Quso G32, c) precipitation with ammonium sulphate, and d) acidification of serum, have been compared with the standard gel filtration technique. In serum from healthy subjects and patients with elevated R-binders, the serum acidification and Quso methods yielded results in closest agreement with those obtained by gel filtration. When TC II was markedly elevated, the recommended concentration of Quso failed to remove all TC II from serum. Both the serum acidification and Quso methods are suitable for routine use, providing that with the latter method the concentration of Quso is increased when elevated levels of TC II are anticipated, as, eg, in severe jaundice. All the rapid methods tested yielded clinically significant results in patients with myeloproliferative disorders.

Topics: Acids; Adsorption; Blood Chemical Analysis; Blood Proteins; Charcoal; Chemical Precipitation; Chromatography, Gel; Female; Humans; Myeloproliferative Disorders; Pregnancy; Protein Binding; Transcobalamins; Vitamin B 12

Seven patients with MP and four controls were injected with 0.04 to 0.05 microgram of [57Co] cyanocobalamin i.m. or i.v. in order to study the shift of binding with time and the conversion of one Cbl to another. The initial pattern of binding reflected the proportion of the apo forms of TC II and R binders. In MP there was more initial binding of the injected Cbl to R-type binders and less to TC II. During the first 48 hr after intake, the injected Cbl remained mostly as cyanocobalamin. Some adenosylcobalamin appeared transiently in both control and MP subjects. Radioactive methylcobalamin did not appear in the circulation until after 48 hr, and the conversion of cyanocobalamin to methylcobalamin within the circulation was greater in MP subjects. Serum from some subjects converted small amounts of cyanocobalamin to all other forms in vitro by a heat-stable, extracellular property which was abolished by dialysis of the serum. This property of serum could have accounted for the early conversion to adenosylcobalamin but not, at least as an in vitro phenomenon, to the late appearance of methylcobalamin. Although the expected increases and abnormal patterns of R binders were observed in MP, these abnormalities could not be correlated with the increased conversion to plasma methylcobalamin. During the first 6 hr after injection the R binder-Cbl designated as alpha 2-R-Cbl disappeared from the circulation at a rate faster than that of alpha 1-R-Cbl. Subsequently the alpha 2 and alpha 1 components of R binder-Clb cleared at the same rate, and this rate was the same for both control and MP subjects.

Topics: Carrier Proteins; Humans; Injections, Intramuscular; Injections, Intravenous; Myeloproliferative Disorders; Time Factors; Transcobalamins; Vitamin B 12

Three siblings with a lifelong history of a bleeding disorder and thrombocytopenia died from a myeloproliferative disease. In 2, the terminal event resembled juvenile chronic myelogenous leukemia, and in the third, the diagnosis was acute monocytic leukemia. A family study revealed that the mother and 5 other siblings had a variety of hematologic abnormalities. These included chronic thrombocytopenia, abnormal platelet function, elevated concentrations of HgbF or serum vitamin B12, and low leukocyte alkaline phosphatase (LAP) scores either singly or in combination. At the time of study, none had evidence of malignancy. Members of this family have a myeloproliferative disorder that has the potential for terminating in nonlymphocytic leukemia, a combination of events which appears not to have been reported previously.

Topics: Adolescent; Adult; Alkaline Phosphatase; Blood Platelet Disorders; Child; Child, Preschool; Family Characteristics; Female; Fetal Hemoglobin; Humans; Infant; Leukemia, Monocytic, Acute; Leukemia, Myeloid; Leukocytes; Male; Myeloproliferative Disorders; Pedigree; Thrombocytopenia; Vitamin B 12

Topics: Acrylates; Animals; Carcinogens; Drug Synergism; Indoles; Male; Mice; Mice, Inbred C57BL; Myeloproliferative Disorders; Time Factors; Vitamin B 12

Topics: Aged; Anemia, Megaloblastic; Chronic Disease; Female; Humans; Male; Middle Aged; Myeloproliferative Disorders; Polycythemia; Vitamin B 12

The unsaturated vitamin B12 binding capacity of whole serum (UBBC) and of the three transcobalamins (TC) has been studied in patients with various haematological diseases including myeloproliferative disorders (MPD) and acute leukaemia. The binding capacity of TC I and TC III was increased in MPD; TC I being particularly high in chronic granulocytic leukaemia (CGL) and TC III especially raised in polycythaemia rubra vera (PRV) and in infectious leucocytosis. The binding capacity of both TC I and TC III correlated with blood neutrophil count and the ratio TC III/TC I was low in CGL and increased in PRV. TC II was increased in acute myelogenous leukaemia, during remission and blast cell crisis of CGL and in refractory anaemia with excess of myeloblasts but not in acute lymphoblastic leukaemia (ALL). TC II correlated inversely with blood neutrophil count. There is an inverse ratio between TC II and TC I at least in myelogenous leukaemia. These abnormalities are discussed in relation to granulocyte kinetics. TC III and TC I reflect probably the total body granulocyte pool and share some biochemical and immunological properties supporting the view that they have a common origin in the more mature stages of the granulocyte cell line while TC II probably originates partly in more primitive granulocytes.

Topics: Anemia, Aplastic; Blood Cell Count; Blood Proteins; Humans; Leukemia; Leukemia, Lymphoid; Leukemia, Myeloid; Leukocyte Count; Leukocytosis; Myeloproliferative Disorders; Neutrophils; Polycythemia Vera; Primary Myelofibrosis; Transcobalamins; Vitamin B 12

Topics: Humans; Myeloproliferative Disorders; Vitamin B 12

Topics: Adult; Anemia, Pernicious; Chronic Disease; Female; Humans; Infant, Newborn; Leukemia, Myeloid; Male; Maternal-Fetal Exchange; Multiple Myeloma; Myeloproliferative Disorders; Placenta; Polycythemia Vera; Pregnancy; Primary Myelofibrosis; Vitamin B 12

Topics: Anemia; Carrier Proteins; Chromatography, DEAE-Cellulose; Electrophoresis; Humans; Leukemia; Liver Diseases; Metabolic Clearance Rate; Molecular Weight; Mucoproteins; Myeloproliferative Disorders; Vitamin B 12

Topics: Blood Proteins; Carrier Proteins; Humans; Leukemoid Reaction; Leukocytes; Myeloproliferative Disorders; Protein Binding; Vitamin B 12

Topics: Agranulocytosis; Anemia, Aplastic; Anemia, Macrocytic; Bone Marrow; Chronic Disease; Folic Acid; Humans; Leukemia, Myeloid; Leukocyte Count; Leukocytes; Muramidase; Myeloproliferative Disorders; Neutrophils; Polycythemia Vera; Protein Binding; Vitamin B 12

Topics: Agammaglobulinemia; Agranulocytosis; Anemia; Anemia, Hemolytic; Anemia, Hypochromic; Anemia, Macrocytic; Anemia, Sideroblastic; Antineoplastic Agents; Bone Marrow Diseases; Elliptocytosis, Hereditary; Female; Folic Acid; Folic Acid Deficiency; Humans; Iron; Myeloproliferative Disorders; Polycythemia Vera; Pregnancy; Primary Myelofibrosis; Spherocytosis, Hereditary; Thalassemia; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Adsorption; Anemia, Pernicious; Autoradiography; Cellulose; Cobalt Isotopes; Cyanides; Electrophoresis; Filtration; Humans; Kinetics; Myeloproliferative Disorders; Plasma; Protein Binding; Vitamin B 12

Topics: Anemia, Pernicious; Colorimetry; Gastrectomy; Humans; Malonates; Myeloproliferative Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Adult; Aged; Blood Proteins; Bloodletting; Chlorambucil; Chromatography; Cyclophosphamide; Diagnosis, Differential; Hematocrit; Humans; Middle Aged; Myeloproliferative Disorders; Polycythemia; Polycythemia Vera; Protein Binding; Vitamin B 12

Topics: Aged; Antigen-Antibody Reactions; Binding Sites; Biological Assay; Blood Protein Electrophoresis; Bone Marrow Diseases; Chromatography; Chromatography, Gel; Cobalt Isotopes; Euglena; Glycoproteins; HeLa Cells; Humans; Male; Molecular Weight; Myeloproliferative Disorders; Phosphorus Isotopes; Polycythemia Vera; Vitamin B 12

Topics: Alpha-Globulins; Beta-Globulins; Cellulose; Charcoal; Cobalt Isotopes; Diagnosis, Differential; Humans; Leukemia, Myeloid; Leukocytosis; Methods; Myeloproliferative Disorders; Polycythemia Vera; Vitamin B 12

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Bone Marrow Diseases; Chromosome Aberrations; Chromosome Disorders; Chromosomes, Human, 1-3; Chromosomes, Human, 13-15; Chromosomes, Human, 4-5; Chronic Disease; Diagnosis, Differential; Female; Hemorrhage; Hemostasis; Hepatomegaly; Humans; Leukemia, Myeloid; Leukocytes; Male; Megakaryocytes; Middle Aged; Myeloproliferative Disorders; Polycythemia Vera; Primary Myelofibrosis; Splenomegaly; Thrombocytosis; Vitamin B 12

Topics: Acute Disease; Adult; Blood Transfusion; Bone Diseases; Bone Marrow Diseases; Bone Marrow Examination; Chloramphenicol; Female; Folic Acid; Hepatitis A; Hip Joint; Humans; Myeloproliferative Disorders; Prednisone; Testosterone; Vitamin B 12

Topics: Blood; Bone Marrow Diseases; Corrinoids; Humans; Leukemia; Myeloproliferative Disorders; Vitamin B 12

Topics: Bone Marrow; Bone Marrow Diseases; Hematologic Diseases; Hodgkin Disease; Humans; Leukemia; Myeloproliferative Disorders; Polycythemia Vera; Vitamin B 12

Topics: Bone Marrow; Bone Marrow Diseases; Humans; Leukemia; Leukemia, Myeloid; Myeloproliferative Disorders; Neoplasms; Vitamin B 12