scholarly journals Hematologic Responses and Concenrtation of Vitamin B12 in Serum and Urine following Oral Administration of Vitamin B12 without Intrinsic Factor

Blood ◽  
1954 ◽  
Vol 9 (5) ◽  
pp. 473-488 ◽  
Author(s):  
G. I. M. ROSS ◽  
D. L. MOLLIN ◽  
E. V. COX ◽  
C. C. UNGLEY
Keyword(s):  
Urinary Excretion ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Intrinsic Factor ◽  
Normal Subjects ◽  
Average Amount ◽  
Hematologic Response ◽  
B12 Deficiency ◽  
Oral Doses ◽  
Lower Urinary

Abstract Vitamin B12 in doses of 500 to 3000 µg. was given by mouth or by rectum to patients with megaloblastic anemia due to B12 deficiency and to normal subjects. Its absorption was studied by following the hematologic response and/or the changes in serum and urinary B12 concentrations by microbiologic assay with Euglena gracilis var. bacillaris. After oral doses of 1000 to 3000 µg. of B12 there was a definite but variable hematologic response in the thirty-five patients. The serum B12 concentrations, measured in eighteen of these patients, increased in the first twenty-four hours after the dose. The urinary excretion of B12 increased in fifteen out of sixteen patients, but the average amount excreted was only one quarter of that excreted after intramuscular injections producing comparable hematologic responses. The lower urinary excretion after the oral doses was associated with a lower total and uncombined B12 concentration in the serum. In the majority of patients serum B12 concentrations and urinary B12 excretion reached a maximum in the first six hours after the dose. After oral doses of 3000 µg. there was a rise in serum and urinary B12 in three out of four normal subjects. After doses of 500 µg., there was an increase in the serum B12 concentrations of two normal subjects and of one out of two patients with megaloblastic anemia, but there was no change in urinary B12 excretion. After rectal doses of 1000 or 3000 µg. there was evidence of absorption of the vitamin in seven out of eight patients with pernicious anemia.

scholarly journals Differentiation between Vitamin B12—deficient and Folic Acid—deficient Megaloblastic Anemias with C14—Histidine

Blood ◽  
1963 ◽  
Vol 21 (4) ◽  
pp. 447-461 ◽  
Author(s):  
MATHEWS B. FISH ◽  
MYRON POLLYCOVE ◽  
THOMAS V. FEICHTMEIR
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Specific Activity ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Normal Subjects ◽  
Intermediary Metabolism ◽  
Folic Acid Deficiency ◽  
Acid Deficiency ◽  
B12 Deficiency

Abstract Intermediary metabolism of the monocarbon pool and histidine in normal subjects and patients with megaloblastic anemia was studied by continuous measurement of pulmonary excretion of C14O2 and urinary excretion of C14 after injection of L-histidine-2(ring)-C14. Cumulative pulmonary and renal excretion of C14 for 1 month by two normal subjects approximates 45 per cent of the amount injected. Within 4 months after injection of the dose used in this study, the resultant average tissue radiation decreases below the average natural terrestrial and cosmic radiation level. Simultaneous determination of two parameters, (1) cumulative 1-hour pulmonary C14 excretion and (2) the time of occurrence of maximum C14O2specific activity (Tmax), may permit rapid and unequivocal differentiation between folic acid deficiency and vitamin B12 deficiency in the pathogenesis of megaloblastic anemia. Folio acid deficiency results in marked diminution of pulmonary C14 excretion (approximately 0.1 per cent of injection C14 in 1 hour) and marked prolongation of C14O2-specific activity Tmax (approximately 3 hours), while both parameters are normal (approximately 1 per cent and less than 1 hour, respectively) in patients with vitamin B12 deficiency and megaloblastic anemia. Measurement during periods of reticulocyte response to either folio acid or vitamin B12 demonstrate normal C14O2-specific activity Tmax but decreased pulmonary C14 excretion. These observations suggest that prolongation of C14O2-specific activity Tmax is a sensitive index of folic acid deficiency or block and that if Tmax is normal, pulmonary C14 excretion is a sensitive index of the relative partition of the active monocarbon pool between pathways for oxidation and pathways for nucleic acid synthesis. This type of breath analysis seems to provide a quantitative dynamic representation of metabolic function which may be particularly useful in differentiating between the alterations of intermediary metabolism that occur in patients with folic acid-deficient megaloblastic anemia and in patients with vitamin B12-deficient megaloblastic anemia.

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 Screening of vitamin B12 in children diagnosed as Autism Spectrum Disorder

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
M M Metyas ◽  
A S Abdelhakim ◽  
H H Ghandour
Keyword(s):  
Autism Spectrum Disorder ◽  
Vitamin B12 ◽  
Rating Scale ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Normal Subjects ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Control Group ◽  
B12 Deficiency

Abstract Background Vitamin B12 deficiency causes megaloblastic anemia and disorders of the nervous system. In Autism spectrum disorder intestinal problems in absorption of some minerals like Vitamin B12 which lead to Vitamin B12 deficiency. Aim of the Work to investigate level of vitamin B12 in autistic children in an attempt to reach such etiological factor and to be incorporated in management if proved. Patients and Methods a Case control study. The subjects of this study comprised a convenient sample of 15 children diagnosed as ASD and other 15 children not diagnosed as ASD as control group with age range between 3 years 8 months. Modified Arabic preschool language scale (PLS-4) Test, Stanford Binet intelligence scales, fifth edition were done for all children and Child autism rating scale (CARS) was done for children of 2 groups. Results Vitamin B12 level in ASD is significantly deficiency compared to the Vitamin B12 level of normal subjects. Conclusion Vitamin B12 in ASD was found to be decreased in cases group than the controls group also below the total language level of cases group than the controls group.

Homologous G776G Variant of Transcobalamin-II Gene is Linked to Vitamin B12 Deficiency

2020 ◽  
Vol 90 (1-2) ◽  
pp. 151-155
Author(s):  
Khalid M. Al-Batayneh ◽  
Mazhar Salim Al Zoubi ◽  
Bahaa Al-Trad ◽  
Emad Hussein ◽  
Wesam Al Khateeb ◽  
...  
Keyword(s):  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Intermediate Phenotype ◽  
Cobalamin Deficiency ◽  
Control Group ◽  
Jordanian Population ◽  
B12 Deficiency ◽  
Transcobalamin Ii

Abstract. Vitamin B12 (Cobalamin) deficiency, due to improper internalization of cobalamin, is a metabolic disorder prevalent in impoverished and elderly populations and is associated with megaloblastic anemia and dementia. It has been suggested that mutations in transcobalamin II ( TCN2) or gastric intrinsic factor (GIF) proteins can alter their binding efficiency to cobalamin or reduce the ability of their receptors to internalize them. In this case-control study, the correlation between vitamin B12 deficiency and alternative alleles of TCN2 and GIF was investigated in a Jordanian population. One hundred individuals with vitamin B12 deficiency (B12 < 200 mg/mL) were enrolled in our study to evaluate the TCN2 and GIF polymorphisms. The control group (B12 > 200 mg/mL) included 100 individuals. Our results indicated a significant association between the homologous variant of the TCN2 gene (G776G) and vitamin B12 deficiency, and an intermediate phenotype in heterozygous individuals ( p < 0.001, OR = 5.6, 95% CI = 2.95 to 10.63). The GIF gene, however, showed no correlation between the A68G variant and vitamin B12 deficiency ( p = 0.2). This study expounds the association of TCN2 polymorphism with cobalamin levels in a Jordanian population and highlights the necessity of further studies to elucidate the molecular basis and impact of TCN2 and GIF genes polymorphisms on vitamin B12 deficiency and associated disorders.

scholarly journals Studies of a Patient with Selective Deficiency in Absorption of Vitamin B12

Blood ◽  
1961 ◽  
Vol 18 (1) ◽  
pp. 48-60 ◽  
Author(s):  
E. COLLE ◽  
L. GREENBERG ◽  
WILLIAM KRIVIT
Keyword(s):  
Small Bowel ◽  
Urinary Excretion ◽  
Vitamin B12 ◽  
Functional Disability ◽  
Megaloblastic Anemia ◽  
Test Dose ◽  
Fecal Excretion ◽  
Normal Patient ◽  
Schilling Test ◽  
B12 Deficiency

Abstract A 2 year old girl with a megaloblastic anemia secondary to B12 deficiency was presented. The mechanism appeared to be a specific inability to absorb vitamin B12 from the small bowel in the absence of any other functional disability. Evidence of absorption of vitamin B12 was obtained when intestinal juice from a normal patient was administered with the test dose of vitamin B12. This evidence consisted of (1) an increased urinary excretion of the test dose (positive Schilling test), (2) a decreased fecal excretion of the labelled B12 and (3) the presence of significant counts over the liver (positive Glass test). A generalized malabsorption can only be totally and absolutely disproven by testing over many years. It is considered more probable, however, that this patient lacks an intestinal factor required for the absorption of vitamin B12.

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 EFEK FORTIFIKASI VITAMIN B12 TERHADAP KADAR VITAMIN B12 SERUM DAN HOMOSISTEIN SERUM PADA VEGETARIAN

2020 ◽  
Vol 11 (1) ◽  
pp. 114-120
Author(s):  
Susianto Susianto
Keyword(s):  
Vitamin B12 ◽  
Homocysteine Level ◽  
Megaloblastic Anemia ◽  
Serum Vitamin ◽  
Vitamin B12 Deficiency ◽  
Natural Sources ◽  
Serum Homocysteine ◽  
Microparticle Enzyme Immunoassay ◽  
B12 Deficiency ◽  
Community Trial

Introduction: Vegetarians consume plant-based foods with or without eggs and milk. Vegetarians are at risk of vitamin B12 deficiency, as natural sources of vitamin B12 are limited to animal-based foods. Vitamin B12 deficiency can lead to megaloblastic anemia, nerve damage and increase homocysteine level. Higher homocysteine level can increase the risk of coronary heart disease and stroke. The objective of this study was to investigate the effect of vitamin B12 fortification on the level of serum vitamin B12 and homocysteine in vegetarian. Method: The research design was an experimental study, community trial. The samples were 42 vegetarians with vitamin B12 deficiency (< 156 pmol/L) selected from 118 vegetarians as members of Indonesia Vegetarian Society (IVS) Pekanbaru, treated by vitamin B12 fortified oatmeal for three months from March to June 2010.  Serum vitamin B12 and homocysteine were measured by electrochemiluminescent immunoassay and microparticle enzyme immunoassay method respectively. Result: Prevalence of vitamin B12 deficiency in vegetarian was 35.6%. Statistical analysis showed a significant increase of serum vitamin B12 from 124.6 to 284.6 pmol/L (p=0.001) and significant decrease of serum homocysteine from 20.1 to 15.1 µmol/L (p=0.001). Conclusion: Consumption of vitamin B12 fortified oatmeal increases the level of serum vitamin B12 and decreases the level of serum homocysteine significantly in vegetarian with vitamin B12 deficiency.

scholarly journals Hematologic Manifestations of Vitamin B12 Deficiency in Swine

Blood ◽  
1951 ◽  
Vol 6 (10) ◽  
pp. 867-891 ◽  
Author(s):  
G. E. CARTWRIGHT ◽  
BETTY TATTING ◽  
JEAN ROBINSON ◽  
N. M. FELLOWS ◽  
F. D. GUNN ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Vitamin B12 ◽  
Liver Damage ◽  
Megaloblastic Anemia ◽  
Macrocytic Anemia ◽  
Vitamin B12 Deficiency ◽  
Deficiency Anemia ◽  
Severe Neutropenia ◽  
Pteroylglutamic Acid ◽  
B12 Deficiency

Abstract In an effort to produce a deficiency of vitamin B12 a total of 70 pigs were fed a purified diet containing soybean alpha protein in place of casein. One group of animals was started on the diet at 2 to 7 days of age. A second group began at 21 to 28 days of age. Methionine, iodinate casein, desiccated thyroid and pteroylglutamic acid were added to the diet of certain animals and! omitted from the diet of other pigs. In addition, 9 pigs were gastrectomized. Forty-three of the animals survived for a sufficiently long period of time for adequate evaluation of the results of the experiment. Severe liver damage was observed in 24 of the 25 animals autopsied. The only animal not showing liver damage received vitamin B12 from the beginning of the experiment. Necrosis of the liver cells, fatty infiltration, or both, occurred in the presence of a high fat diet containing apparently adequate amounts of protein, choline, vitamin E and methionine. These pathologic changes were apparently prevented but not reversed by the administration of vitamin B12. Growth of the animals on the above diets without added vitamin B12 was retarded as compared with the growth of animals on the same diet supplemented with this vitamin. The administration of vitamin B12 to the deficient animals resulted in rapid growth. Of the 39 animals not receiving vitamin B12 13 failed to develop anemia, 16 developed a mild anemia and in 10 a moderately severe anemia was present. When present the anemia was normocytic and in 24 pigs was accompanied by a moderately severe neutropenia. Differential cell counts on the sternal marrow were normal except for a slight increase in the proportion of normoblasts. These hematologic alterations were neither consistently or completely corrected by the administration of vitamin B12 in spite of the fact that definite and sometimes marked reticulocyte increases followed. When methionine deficiency was associated with vitamin B12 deficiency, anemia appeared to be more severe. The administration of aureomycin, an "animal protein factor," did not stimulate growth and failed to induce a hemopoietic response. There was no macrocytic anemia, the bone marrow was not megaloblastic, and neurologic disturbances or morphologic alterations in the neutrophils were not observed. These results are in contrast to those obtained in pigs with an experimentally produced deficiency of pteroylglutamic acid. Such animals develop macrocytic anemia, leukopenia and a macronormoblastic type of bone marrow. It is not possible to give with any assurance the reason why megaloblastic anemia was not produced in the "B12-deficient" animals. This may have been due to the fact that (1) the deficiency was not sufficiently severe to result in such a change in the hemopoietic system; or (2) because pteroylglutamic acid prevents the development of megaloblastic anemia even in the absence of vitamin B12.

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