scholarly journals The Kinetics of Intravenously Injected Radioactive Vitamin B12: Studies on Normal Subjects and Patients with Chronic Myelocytic Leukemia and Pernicious Anemia

Blood ◽  
1960 ◽  
Vol 15 (5) ◽  
pp. 646-661 ◽  
Author(s):  
EUGENE A. BRODY ◽  
SOLOMON ESTREN ◽  
LOUIS R. WASSERMAN
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Total Gastrectomy ◽  
Binding Capacity ◽  
Intrinsic Factor ◽  
Normal Subjects ◽  
High Serum ◽  
Malabsorption Syndrome ◽  
Chronic Myelocytic Leukemia ◽  
Myelocytic Leukemia

Abstract 1. Studies of the fate of intravenously injected radioactive vitamin B12 have been performed in patients with normal, low and high serum concentrations of vitamin B12. 2. Abnormal plasma disappearance curves were noted in chronic myelocytic leukemia, pernicious anemia in relapse and in remission, total gastrectomy and malabsorption syndrome. 3. In chronic myelocytic leukemia, the slow clearance of plasma radioactivity may be explained by the increased binding capacity of the plasma proteins for vitamin B12. 4. Plasma clearance of radioactivity is slower than normal in pernicious anemia, even in remission. The failure of the disappearance curve to return to normal in pernicious anemia in complete remission suggests the existence of a plasma "B12-transferase," whose function is to transfer circulating B12 to the tissues. The disappearance curves suggest that the amount of such "B12-transferase" is diminished in pernicious anemia, total gastrectomy and certain Cases of malabsorption syndrome. 5. A relationship between a hypothetical "B12-transferase" and intrinsic factor is discussed.

scholarly journals Co60 Vitamin B12 Binding Capacity of Human Leukocytes

Blood ◽  
1962 ◽  
Vol 19 (2) ◽  
pp. 229-235 ◽  
Author(s):  
LEO M. MEYER ◽  
EUGENE P. CRONKITE ◽  
INEZ F. MILLER ◽  
CLAIRE W MULZAC ◽  
IRVING JONES
Keyword(s):  
Vitamin B12 ◽  
Human Serum ◽  
Polycythemia Vera ◽  
Binding Capacity ◽  
Chronic Myelocytic Leukemia ◽  
Nonspecific Binding ◽  
Two Phase ◽  
Intact Cells ◽  
Myelocytic Leukemia ◽  
Neutrophilic Leukocytes

Abstract 1. Mature neutrophilic leukocytes show the highest Co60B12 binding capacity. 2. Less mature granulocytes, "blast" forms and eosinophils have little or no Co60B12 binding capacity. 3. Disintegrated mature leukocytes from chronic myelocytic leukemia and polycythemia vera show higher B12 binding capacity than intact cells. 4. Mature leukocytes from patients with chronic myelocytic leukemia and polycythemia vera show a two-phase B12 curve suggesting specific and nonspecific binding, similar to that observed in human serum. 5. Disintegration products from mature neutrophilic leukocytes probably contribute largely to increased B12 binding capacity of serum in chronic myelocytic leukemia and polycythemia vera.

scholarly journals The Plasma Clearance and Urinary Excretion of Parenterally Administered 58Co B12

Blood ◽  
1956 ◽  
Vol 11 (1) ◽  
pp. 31-43 ◽  
Author(s):  
D. L. MOLLIN ◽  
W. R. PITNEY ◽  
S. J. BAKER ◽  
J. E. BRADLEY
Keyword(s):  
Urinary Excretion ◽  
Vitamin B12 ◽  
Plasma Clearance ◽  
Vitamin B12 Deficiency ◽  
Normal Subjects ◽  
Normal Serum ◽  
Chronic Myelocytic Leukemia ◽  
Intravenous Injections ◽  
Myelocytic Leukemia ◽  
B12 Deficiency

Abstract Intravenous injections of 1.5 µg. of 58Co B12 were given to subjects with normal serum B12 concentrations, to patients with vitamin B12 deficiency and to patients with chronic myelocytic leukemia. The rate of plasma clearance of radioactivity after this dose was slowest in patients with chronic myelocytic leukemia and patients with pernicious anemia in severe relapse. In patients with vitamin B12 deficiency, serum B12 concentrations were estimated microbiologically at frequent intervals after the injection. There was a good correlation between the results obtained by microbiological assay and as calculated from plasma radioactivity. Significant differences were not observed between the urinary excretion of radioactivity by normal subjects and patients with B12 deficiency.

scholarly journals Identification of the Vitamin B12-Binding Protein in the Serum of Normals and of Patients with Chronic Myelocytic Leukemia

Blood ◽  
1958 ◽  
Vol 13 (8) ◽  
pp. 740-747 ◽  
Author(s):  
ROBERT S. MENDELSOHN ◽  
DONALD M. WATKIN ◽  
ANN P. HORBETT ◽  
JOHN L. FAHEY
Keyword(s):  
Vitamin B12 ◽  
Binding Protein ◽  
Qualitative Difference ◽  
Normal Subjects ◽  
Paper Electrophoresis ◽  
Normal Serum ◽  
Chronic Myelocytic Leukemia ◽  
Myelocytic Leukemia ◽  
Abnormal Metabolism

Abstract Vitamin B12-binding proteins in the serum of normal subjects and of patients with chronic myelocytic leukemia have been compared. The in-vivo-bound B12 was utilized to identify the binding protein. Column protein chromatography and block and paper electrophoresis were employed individually and in combination to characterize the B12-binding protein. B12 was found to be bound primarily to an alpha-l globulin in both normal individuals and in patients with chronic myelocytic leukemia. No qualitative difference was found in these proteins. The increased amounts of B12-binding protein in the serum of patients with chronic myelocytic leukemia would seem to be attributable to abnormal metabolism of the same protein that binds B12 in normal serum.

scholarly journals Metabolic Interrelations between Gastric Intrinsic Hematopoietic Factor and Vitamin B12

Blood ◽  
1954 ◽  
Vol 9 (12) ◽  
pp. 1127-1140 ◽  
Author(s):  
GEORGE B. JERZY GLASS ◽  
LOIS C. LILLICK ◽  
LINN J. BOYD ◽  
CARRIE GUNNIS ◽  
LUCY GORMAN CORTI
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Total Gastrectomy ◽  
Macrocytic Anemia ◽  
Intrinsic Factor ◽  
The Body ◽  
Urinary Output ◽  
Blood Levels ◽  
Factor Concentrate ◽  
Hematopoietic Response

Abstract The concentration of vitamin B12 in blood serum and its excretion in the urine were assayed by the E. coli mutant technic in two patients after total gastrectomy and by use of the more sensitive Euglena gracilis method in four cases of pernicious anemia in relapse and 1 case of well controlled nutritional macrocytic anemia. Following parenteral administration of 100 µg. vitamin B12 intramuscularly to two patients with total gastrectomy, much higher blood levels were observed within the first few hours than those reported by others under similar circumstances in normals. Following oral administration of vitamin B12 together with a potent intrinsic factor concentrate from hog stomach, a rise in blood levels of vitamin B12 was observed in patients with pernicious anemia. The normal serum levels of vitamin B12 could not be maintained, however, for the entire duration of the oral treatment, in spite of the apparent hematologic and clinical remission. The urinary output of vitamin B12 was in all instances less than 0.5 per cent of the total dose of vitamin B12 ingested during the experimental period, in spite of an optimal or suboptimal hematopoietic response obtained. A similar situation existed in patients with total gastrectomy, as well as in the patient with controlled macrocytic nutritional anemia, when vitamin B12 was ingested alone or with intrinsic factor concentrate. The intensity of the obtained hematopoietic response in patients with pernicious anemia indicates the absorption of much larger amounts of vitamin B12 from the intestine than is indicated by the total urinary output of vitamin B12; therefore the anchorage and retention of a large part of vitamin B12 in the storage depots of the body after its absorption from the intestine must occur. A sharp increase in the urinary output of vitamin B12 was observed during or immediately following the hematopoietic response in all patients with pernicious anemia treated orally with vitamin B12 and intrinsic factor concentrate, i.e., coincident with or immediately following the reticulocyte peak in blood. Similar observation was reported by the authors in the previous series of investigations. Of many possible interpretations of this finding, the most plausible appears to be the metabolic release of free vitamin B12 from its complex binding in the body during hyperactivity of the hematopoietic organs and its escape through the kidneys.

scholarly journals Polycythemia Rubra Vera With Pernicious Anemia Some Observations on Vitamin B12 Metabolism

Blood ◽  
1969 ◽  
Vol 34 (1) ◽  
pp. 14-24 ◽  
Author(s):  
ROBERT E. SAGE
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Parietal Cell ◽  
Intrinsic Factor ◽  
Serum Levels ◽  
High Serum ◽  
Normal Serum ◽  
Polycythemia Rubra Vera ◽  
The One ◽  
Symptoms And Signs

Abstract A patient with polycythemia rubra vera developed symptoms and signs of pernicious anemia three years after institution of therapy for the polycythemia. This is the first satisfactorily documented report of this sequence. Strict criteria utilized make both diagnoses unequivocal. Autoantibody studies, the first performed in such a patient, show the presence of parietal cell and intrinsic factor autoantibodies but no antibodies to other tissues. Vitamin B12 requirements have been excessive despite high or high normal serum levels and extreme marrow sensitivity to withdrawal of the Vitamin is evident in the presence of these high serum levels. Studies on Vitamin B12 binding proteins showed an elevation in α binding globulin with reversal of the α to β ratio. It is suggested that this protein is physiologically abnormal. The literature is briefly reviewed regarding the pathogenesis of the two disorders with the conclusion that their appearance in the one patient represents purely a chance phenomenon.

A case report on Subacute Combined Degeneration of spinal cord in children – A rare neurological manifestation in Vitamin B12 deficiencies

2017 ◽  
Vol 6 (12) ◽  
pp. 5562
Author(s):  
Tiana Mary Alexander ◽  
Vineeta Pande ◽  
Sharad Agarkhedkar ◽  
Dnyaneshwar Upase
Keyword(s):  
Spinal Cord ◽  
Case Report ◽  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Chronic Diarrhea ◽  
Megaloblastic Anemia ◽  
Vegetarian Diet ◽  
Malabsorption Syndrome ◽  
Subacute Combined Degeneration ◽  
B12 Deficiency

Megaloblastic anemia is a common feature between 6 months – 2 years and rarely occurs after 5 years of age, especially in a child consuming non-vegetarian diet. B12 deficiency may occur after 5 years of age because of chronic diarrhea, malabsorption syndrome, or intestinal surgical causes. Pernicious anemia causes B12 deficiency, but nutritional B12 deficiency with subacute combined degeneration causing ataxia is rare.

scholarly journals Circulating antibody to transcobalamin II causing retention of vitamin B12 in the blood

Blood ◽  
1977 ◽  
Vol 49 (6) ◽  
pp. 987-1000 ◽  
Author(s):  
R Carmel ◽  
B Tatsis ◽  
L Baril
Keyword(s):  
Vitamin B12 ◽  
Binding Capacity ◽  
Megaloblastic Anemia ◽  
Serum Vitamin ◽  
Vitamin B12 Deficiency ◽  
High Serum ◽  
The Status ◽  
B12 Deficiency ◽  
Long Acting

A patient with recurrent pulmonary abscess, weight loss, and alcoholism was found to have extremely high serum vitamin B12 and unsaturated vitamin B12-binding capacity (UBBC) levels. While transcobalamin (TC) II was also increased, most of his UBBC was due to an abnormal binding protein which carried greater than 80% of the endogenous vitamin B12 and was not found in his saliva, granulocytes, or urine. This protein was shown to be a complex of TC II and a circulating immunoglobulin (IgGkappa and IgGlambda). Each IgG molecule appeared to bind two TC II molecules. The reacting site did not interfere with the ability of TC II to bind vitamin B12, but did interfere with its ability to transfer the vitamin to cells in vitro. The site was not identical to that reacting with anti-human TC II antibody produced in rabbits. Because of this abnormal complex, 57Co-vitamin B12 injected intravenously was cleared slowly by the patient. However, no metabolic evidence for vitamin B12 deficiency was demonstrable, although the patient initially had megaloblastic anemia apparently due to folate deficiency. The course of the vitamin B12-binding abnormalities was followed over 4 yr and appeared to fluctuate with the status of the patient's illness. The IgG-TC II complex resembled one induced in some patients with pernicious anemia by intensive treatment with long-acting vitamin B12 preparations. The mechanism of induction of the antibody formation in our patient is unknown.

scholarly journals Chronic Atrophic Gastritis with Negative Intrinsic Factor and Parietal Cell Antibody Presenting as a Severe Hemolytic Anemia

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
G. F. Cittolin-Santos ◽  
S. Khalil ◽  
J. K. Bakos ◽  
K. Baker
Keyword(s):  
Vitamin B12 ◽  
Atrophic Gastritis ◽  
Pernicious Anemia ◽  
Hemolytic Anemia ◽  
Parietal Cell ◽  
Intrinsic Factor ◽  
Peripheral Blood Smear ◽  
Chronic Atrophic Gastritis ◽  
Cell Antibody ◽  
Parietal Cell Antibody

A 28-year-old Caucasian male with Hashimoto’s disease and vitiligo presented with two weeks of dizziness on exertion following pharyngitis which was treated with prednisone 40 mg by mouth once a day for five days. Initial workup revealed anemia, elevated lactate dehydrogenase (LDH), and low haptoglobin. He underwent workup for causes of hemolytic anemia which was remarkable for a peripheral blood smear with hypersegmented neutrophils and low vitamin B12 levels concerning for pernicious anemia. Parietal cell and intrinsic factor antibodies were negative, and he then underwent an esophagogastroduodenoscopy with biopsy. The biopsy was negative for Helicobacter pylori, and the immunohistochemical stains were suggestive of chronic atrophic gastritis. He was started on vitamin B12 1,000 mcg intramuscular injections daily. His hemoglobin, LDH, and haptoglobin normalized. Given the absence of the parietal cell antibody and intrinsic factor antibody, this is a rare case of seronegative pernicious anemia.

scholarly journals Absorption of Liver-bound Vitamin B12 in Relation to Intrinsic Factor

Blood ◽  
1968 ◽  
Vol 32 (2) ◽  
pp. 313-323 ◽  
Author(s):  
KUNIO OKUDA ◽  
ISAO TAKARA ◽  
TERUMI FUJII
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Rat Liver ◽  
Intrinsic Factor ◽  
In Vitro Digestion ◽  
Enhanced Absorption ◽  
Biochemical Studies ◽  
Peptide Complexes ◽  
Liver Powder

Abstract Rat liver containing radioactive native B12 was prepared by repeated injections of 57Co-OH-B12, and absorption of liver B12 was measured in patients with pernicious anemia and in subjects without stomach, using physiologic doses. It was found that absorption of liver B12 was very poor, not superior to that of free OH-B12, and coadministration of IFC markedly enhanced absorption. In vitro digestion of rat liver with several enzymes, as determined from liberation of dialyzable radioactivity, suggested its easy digestibility. Biochemical studies of the dialyzable products of liver containing 57Co-B12 failed to demonstrate any detectable quantities of radioactivity other than free 57Co-OH-B12. A study in which cow liver powder mixed with a small quantity of 57Co-CN-B12 was fed to humans and digestion of liver was estimated from the reduction in absorption of radioactivity, indicated that most of the extractable liver B12 was liberated free in the intestine. Thus, no evidence has been obtained for the production of B12-peptide complexes from liver by digestion that require no IF for absorption.

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