Massive Vitamin B12 Therapy in Pernicious Anemia

1950 ◽  
Vol 17 (3) ◽  
pp. 166-168 ◽  
Author(s):  
D. W. BORTZ ◽  
J. D. BATTLE
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia

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.

Metabolic Interrelationship between Vitamin B12 and Ascorbic Acid in Pernicious Anemia

Blood ◽  
1968 ◽  
Vol 31 (1) ◽  
pp. 55-65 ◽  
Author(s):  
SIGMUND BENHAM KAHN ◽  
ISADORE BRODSKY ◽  
Sandra A. Fein
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Vitamin B12 Deficiency ◽  
Biochemical Index ◽  
Plasma Ascorbate ◽  
B12 Deficiency ◽  
Future Work

Abstract An interrelationship between vitamin C and vitamin B12 was studied in three patients with vitamin B12 deficiency associated with pernicious anemia. Subnormal plasma ascorbate concentrations were found prior to therapy confirming previous observations. Following vitamin B12 administration and utilizing methylmalonate (MMA) excretion as a biochemical index of vitamin B12 deficiency, low plasma ascorbate concentrations persisted until MMA excretion was abolished. In two patients, RBC vitamin B12 activity was also serially measured in order to evaluate its sensitivity as an index of vitamin B12 stores when compared to MMA excretion. The data demonstrate that in these two vitamin B12-deficient patients undergoing slow repletion therapy, RBC vitamin B12 activity returns to normal before MMA excretion is abolished. Whether continued MMA excretion in these patients indicates a greater sensitivity of MMA excretion as an index of deficiency of vitamin B12 stores than does RBC vitamin B12 activity remains to be answered by future work.

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.

scholarly journals Chromosomal Aberrations in Pernicious Anemia

Blood ◽  
1965 ◽  
Vol 25 (5) ◽  
pp. 662-682 ◽  
Author(s):  
KOSMAS A. KIOSSOGLOU ◽  
W. J. MITUS ◽  
WILLIAM DAMESHEK
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Chromosomal Aberrations ◽  
Peripheral Blood ◽  
Vitamin B12 Deficiency ◽  
Common Finding ◽  
Morphological Abnormalities ◽  
G 21 ◽  
B12 Deficiency ◽  
Chromatin Material

Abstract Numerical and morphologic chromosomal aberrations were demonstrated in three cases of pernicious anemia in relapse. The morphological abnormalities including chromatid breaks, gaps and "giant" chromosomes were reduced in remission following vitamin B12 therapy. The numerical changes consisted of aneuploidy (45 and 44 chromosomes) with the most common finding encountered (6 to 100 per cent of the cells) being monosomy involving the G 21 chromosome. This was present, not only in the marrow cells, but also in other tissues, e.g., peripheral blood and possibly skin fibroblasts, thus suggesting a more generalized disorder. The numerical anomalies persisted in remission. It is postulated that the structural anomalies, namely chromatid breaks, gaps, acentric fragments and "giant" chromosomes are related to vitamin B12 deficiency and are correctable. The cause of the aneuploidy, since it was not correctable by treatment, is not clear. Since the patients were not studied before the disease had ensued, a congenital or acquired predisposition to megaloblastosis on the basis of G 21 monosomy cannot be excluded. The origin and significance of the extra chromatin material translocated onto the short arms of G 21 chromosomes in cases 1 and 3 remains unexplained.

scholarly journals Vitamin B12 Malabsorption Due to Intrinsic Factor Deficiency in Indian Subjects

Blood ◽  
1972 ◽  
Vol 40 (5) ◽  
pp. 747-753 ◽  
Author(s):  
H. G. Desai ◽  
F. P. Antia
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Indian Population ◽  
Intrinsic Factor ◽  
Subacute Combined Degeneration ◽  
Factor Deficiency ◽  
Vitamin B12 Absorption ◽  
Intrinsic Factor Deficiency ◽  
Intrinsic Factor Antibody ◽  
Vitamin B12 Malabsorption

Abstract Sixteen patients (from Bombay) with severe vitamin B12 malabsorption due to intrinsic factor deficiency, presenting as subacute combined degeneration of the cord (7), tropical sprue (3), anemia (2), thyrotoxicosis (2), diabetes mellitus (1), and pain in the abdomen (1), are reported. The difficulties of establishing a definite diagnosis of pernicious anemia in Indian population are described. The lower incidence of circulating intrinsic factor antibody (IFA) in Indian patients with histamine-fast achlorhydria and poor vitamin B12 absorption is emphasized. The necessity of separating atrophic gastritis, with severely impaired vitamm B12 absorption, from pernicious anemia on the basis of absence or presence of IFA in serum and/or gastric juice cannot be overemphasized.

Effect of D-Sorbitol on Absorption of Vitamin B12 by Pernicious Anemia Patients.

1958 ◽  
Vol 99 (1) ◽  
pp. 257-259 ◽  
Author(s):  
L. Ellenbogen ◽  
V. Herbert ◽  
W. L. Williams
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia

scholarly journals Megaloblastic Anemia Associated with Anatomic Lesions in the Small Intestine

Blood ◽  
1955 ◽  
Vol 10 (8) ◽  
pp. 771-787 ◽  
Author(s):  
R. B. THOMPSON ◽  
C. C. UNGLEY
Keyword(s):  
Small Intestine ◽  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Megaloblastic Anemia ◽  
The Other ◽  
Intestinal Lesion ◽  
Laboratory Findings ◽  
Relationship Of ◽  
The Relationship

Abstract This paper describes the development of anemia in six patients with strictures and anastomoses in the small intestine. The marrow proved to be megaloblastic in three instances, and megaloblastic change is presumed in the other three because of the clinical and laboratory findings, and the characteristic hemopoietic response to liver therapy. Responses to crude and refined liver extracts and vitamin B12 compared unfavorably with those to be expected in Addisonian pernicious anemia; they were similar to the poorer responses often observed in megaloblastic anemia associated with idiopathic steatorrhea. The relationship of the intestinal lesion to the development of megaloblastic anemia is briefly discussed.

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.

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