VARIABLE RESPONSE TO VITAMIN B12 OF MEGALOBLASTIC ANEMIA OF INFANCY

PEDIATRICS ◽  
1949 ◽  
Vol 4 (6) ◽  
pp. 723-729
Author(s):  
CALVIN W. WOODRUFF ◽  
HOWARD W. RIPY ◽  
J. CYRIL PETERSON ◽  
WILLIAM J. DARBY
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Variable Response ◽  
Pteroylglutamic Acid

Two cases of megaloblastic anemia in infancy have improved following treatment with vitamin B12. A third case failed to respond to this factor but subsequently responded to pteroylglutamic acid (folic acid). It is suggested that megaloblastic anemia may be a syndrome which embraces more than one entity.

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.

Brief Report: Observations on Conjugated and Unconjugated Blood Folate Levels in Megaloblastic Anemia and the Effects of Vitamin B12

Blood ◽  
1965 ◽  
Vol 26 (3) ◽  
pp. 354-359 ◽  
Author(s):  
K. N. JEEJEEBHOY ◽  
S. M. PATHARE ◽  
J. M. NORONHA
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Cellular Level ◽  
B12 Deficiency

Abstract Vitamin B12 deficiency was associated with a rise in unconjugated folates and marked depletion of intracellular conjugated folates. The changes could be reversed by giving vitamin B12. These results probably indicate a way by which vitamin B12 and folic acid are interrelated at the cellular level.

scholarly journals Congenital Familial Megaloblastic Anemia

Blood ◽  
1971 ◽  
Vol 37 (6) ◽  
pp. 615-623 ◽  
Author(s):  
BEATRICE C. LAMPKIN ◽  
ALLAN PYESMANY ◽  
CAROL B. HYMAN ◽  
DENMAN HAMMOND
Keyword(s):  
Bone Marrow ◽  
Folic Acid ◽  
Dna Synthesis ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Vitamin Deficiency ◽  
Preliminary Step ◽  
Orotic Aciduria

Abstract Two sisters with a previously unreported megaloblastic anemia unassociated with a deficiency of either folic acid or vitamin B12 are described. Deficiencies of these vitamins were ruled out by standard studies. All other previously reported forms of megaloblastic anemia not secondary to a vitamin deficiency, such as orotic aciduria, were also excluded by appropriate studies. Optimal hemoglobin responses were obtained after the administration of large amounts of both vitamin B12 and folic acid. Because of this hemoglobin response, the conversion of deoxyuridine-5-monophosphate to deoxythymidine-5-monophosphate in vitro was examined in bone marrow samples from both patients using a modification of a method described by Killmann.18 This preliminary step in DNA synthesis was found to be normal. The results of this test and the optimal hemoglobin response after administration of both vitamins suggest that both folic acid and vitamin B12 may be necessary at some other preliminary step in DNA synthesis.

scholarly journals Experimental Production of Nutritional Macrocytic Anemia in Swine

Blood ◽  
1952 ◽  
Vol 7 (10) ◽  
pp. 992-1004 ◽  
Author(s):  
G. E. CARTWRIGHT ◽  
BETTY TATTING ◽  
DORIS KURTH ◽  
M. M. WINTROBE
Keyword(s):  
Bone Marrow ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Soybean Protein ◽  
Macrocytic Anemia ◽  
Experimental Production ◽  
Vitamin Supplement ◽  
Normal Limits ◽  
Erythroid Hyperplasia ◽  
Pteroylglutamic Acid

Abstract A total of 20 swine were fed a diet adequate in all known respects except that soybean protein was substituted for casein, succinylsulfathiazole and a folic acid antagonist were added, and vitamin B12 and pteroylglutamic acid were withheld from the vitamin supplement. The animals developed macrocytic anemia, leukopenia and neutropenia, accompanied by erythroid hyperplasia of the bone marrow. Tue erythroblasts consisted mainly of immature macronormoblasts but a few atypical megaloblasts were also observed. The anemia responded rapidly and completely to the administration of both vitamin B12 and pteroylglutamic acid. The administration of pteroylglutamic acid alone resulted in an immediate return of the blood and bone marrow to within normal limits but after several months there was a partial hematologic relapse in spite of continued therapy with this vitamin. The administration of vitamin B12 alone resulted in only partial remission of the anemia and the bone marrow remained macronormoblastic although the megaloblasts tended to disappear. Growth of the animals was stimulated by the administration of either vitamin but the administration of both vitamins simultanseously resulted in the greatest rate of growth. No manifestations of neurologic disturbances or of inscreased pigment excretion were observed in the deficient swine.

scholarly journals Microspectrophotometric Determination of Desoxyribosenucleic Acid in Megaloblasts of Pernicious Anemia

Blood ◽  
1951 ◽  
Vol 6 (4) ◽  
pp. 344-349 ◽  
Author(s):  
EDWARD H. REISNER ◽  
ROY KORSON
Keyword(s):  
Bone Marrow ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Blood Cells ◽  
Nuclear Dna ◽  
Liver Extract ◽  
Megaloblastic Anemia ◽  
Gradual Loss

Abstract 1. In 9 patients with various types of megaloblastic anemia responding to treatment with vitamin B12, folic acid or liver extract, no significant deviations from the normal amounts of total or polymerized DNA were observed in the nuclei of red blood cells in marrow smears. 2. During the maturation of megaloblasts in the bone marrow there is a gradual loss of nuclear DNA. 3. This pattern is quantitatively and qualitatively similar for normal marrow and for that of pernicious anemia in relapse and after treatment.

scholarly journals Absorption of Physiologic Doses of Folic Acid in Subjects with Tropical Sprue Responding to Tetracycline Therapy

Blood ◽  
1969 ◽  
Vol 34 (2) ◽  
pp. 191-203 ◽  
Author(s):  
FREDERICK A. KLIPSTEIN
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Day Treatment ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Tropical Sprue ◽  
Response To Therapy ◽  
Serum Folate ◽  
Fecal Excretion ◽  
Hematologic Response

Abstract The response to therapy with oral tetracycline has been assessed in three subjects with tropical sprue, all of whom presented with a megaloblastic anemia due to combined folate and vitamin B12 deficiency, and all of whom were shown to have normal absorption prior to treatment of a physiologic dose of 25 µg. of folic acid, as tested by assay of the fecal excretion of a tritium-labeled test dose. Treatment was associated with clinical and intestinal improvement and a hematologic response in all three subjects. The serum folate concentration rose to normal in one subject and the absorption of a pharmacologic dose of folic acid was normal when tested by microbiologic assay at the termination of the 20 day treatment period in all three. In contrast, both the absorption and serum concentrations of vitamin B12 remained subnormal. These observations confirm the fact that folate deficiency can be present in some subjects with tropical sprue in whom the absorption of a physiologic dose of folic acid is normal. They suggest that in this circumstance folate repletion and the hematologic response secondary to tetracycline therapy in tropical sprue is mediated by a factor other than the absorption of crystalline folic acid; it is likely that this factor is increased absorption of dietary polyglutamate forms of folate.

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.

Vitamin B12 and folic acid associated megaloblastic anemia: Could it mislead the diagnosis of breast cancer?

2019 ◽  
Vol 89 (5-6) ◽  
pp. 255-260
Author(s):  
Inanc Karakoyun ◽  
Can Duman ◽  
Fatma Demet Arslan ◽  
Anil Baysoy ◽  
Banu Isbilen Basok
Keyword(s):  
Breast Cancer ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Normal Group ◽  
Ca 125 ◽  
Folic Acid Deficiency ◽  
Acid Deficiency ◽  
B12 Deficiency

Abstract. CA 15-3 is a tumor-associated antigen and is overexpressed in breast tumors, and may also be high in some other non-cancerous conditions. The aim of this study was to investigate the effect of megaloblastic anemia due to vitamin B12 or folic acid deficiency on the levels of tumor markers. Five-year patient data were retrospectively analyzed. The associations between megaloblastic anemia due to vitamin B12 deficiency and CA 15-3, CA 125, CA 19-9, CEA, and AFP levels were analyzed. Furthermore, association between CA 15-3 level and megaloblastic anemia due to folic acid deficiency was evaluated. Median CA 15-3 level was 38.1 U/mL in the group with megaloblastic anemia due to vitamin B12 deficiency(n = 15), 46.7 U/mL in the group with megaloblastic anemia related to folic acid deficiency (n = 3), and 17.8 U/mL in the normal group(n = 1724). CA 15-3 levels were significantly higher among patients with vitamin B12- and folic acid-associated megaloblastic anemia compared to the normal group (p = 0.001 and p = 0.005, respectively). Megaloblastic anemia due to vitamin B12 deficiency was not associated with any significant differences in CA 125, CA 19-9, CEA, or AFP levels compared to the normal group (p = 0.777, p = 0.327, p = 0.577, and p = 0.197, respectively). The numbers of anemic and normal subjects compared in these tests were 12 vs. 1501, 17 vs. 1827, 4 vs. 897, and 8 vs. 1041, respectively. In conclusion, megaloblastic anemia results in ineffective erythropoiesis, and increased levels of CA 15-3 may be associated with this issue. Clinicians should take this into account when evaluating for a pre-diagnosis of breast cancer.

scholarly journals Comparative Assessment of Vitamin-B12, Folic Acid and Homocysteine Levels in Relation to p53 Expression in Megaloblastic Anemia

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0164559 ◽  
Author(s):  
Manish K. Yadav ◽  
Nandini M. Manoli ◽  
SubbaRao V. Madhunapantula
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Comparative Assessment ◽  
P53 Expression

CLINICAL AND EPIDEMIOLOGICAL PROFILE OF CHILDREN WITH MEGALOBLASTIC ANEMIA AT A TERTIARY CARE HOSPITAL IN WESTERN INDIA: A CROSS SECTIONAL STUDY

2021 ◽  
pp. 35-38
Author(s):  
Anjali Sharma ◽  
Anand Deshpande ◽  
Chhavi Sauparna ◽  
Zeeshan Ahmed
Keyword(s):  
Bone Marrow ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Tertiary Care ◽  
Neurological Manifestation ◽  
Vitamin B ◽  
Western India ◽  
Care Hospital ◽  
Vitamin B 12

Background: In India most cases of Megaloblastic anemia are caused by nutritional deciency of vitamin B12 and Folic acid. Initial workup include Complete Blood Count(CBC), Peripheral blood smear(PBS) ,Vitamin B12 asssay, folic acid assay and Bone marrow if required. Therefore, this study is planned to study the clinical and laboratory prole of children with Megaloblastic anemia and to study the clinical outcome of children with Megaloblastic anemia Methods: The study was a prospective observational study conducted among 60 children with megaloblastic anemia, aged 1- 12 years. Demographic data, clinical symptoms and signs, laboratory ndings, serum B12 and Folic acid ,Bone marrow report and stool routine microscopy report were collected. Chi square test was applied. Results: Among the 60 children 40% were female sand 60% were males. The age of the study population ranged from a minimum of 1 month to a maximum of 12 years with a mean(SD) of 8.08 (± 5.45).Majority of children (41.6%) were in age group of 6 months- 1 year. Most common symptoms fever and most common sign is pallor. More than fty percent cases presented with severe anemia. Many cases reported late, leading to delay in diagnosis leads to poor outcome. Developmental delay (neurological manifestation) is strongly associated with vitamin B 12 deciency as compared to folic acid deciency. (p value <0.05) Conclusions: There is a slight female preponderance seen in megaloblastic anemia, probably due to reduced attention to girl children in the study group. neurological manifestation is strongly associated with vitamin B 12 deciency as compared to folic acid deciency.

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