Letter to the Editor

PEDIATRICS ◽  
1994 ◽  
Vol 93 (4) ◽  
pp. 695-695
Author(s):  
Margretta R. Seashore
Keyword(s):  
Folic Acid ◽  
American Academy ◽  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Vitamin B12 Deficiency ◽  
The Other ◽  
American Academy Of Pediatrics ◽  
B12 Deficiency ◽  
Few Data ◽  
Number Of Individuals

The American Academy of Pediatrics Committee on Genetics thanks Dr Herbert for his comments, and would like to address his concerns as follows. Pernicious anemia. There are few data in the literature that address the issue of folic acid and vitamin B12 deficiency. Estimates suggest that the masking of pernicious anemia by folate rarely takes place with an intake of folate < 5 mg per day. On the other hand, there is evidence that a number of individuals with vitamin B12 deficiency have neurological symptoms without any anemia.

scholarly journals Prevalence of Iron, Folic Acid and Vitamin B12 Deficiency in Patients with Thalassemia Minor

2013 ◽  
Vol 7 (4) ◽  
pp. 83 ◽  
Author(s):  
Suheyl Asma ◽  
Cigdem Gereklioglu ◽  
Ahmet Erdogan ◽  
Mahmut Yeral ◽  
Mutlu Kasar ◽  
...  
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Vitamin B12 Deficiency ◽  
Thalassemia Minor ◽  
B12 Deficiency ◽  
Iron Folic Acid

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.

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 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.

The Effect of Vitamin B12 Deficiency on Methylfolate Metabolism and Pteroylpolyglutamate Synthesis in Human Cells

1974 ◽  
Vol 47 (6) ◽  
pp. 617-630
Author(s):  
A. Lavoie ◽  
E. Tripp ◽  
A. V. Hoffbrand
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Direct Effect ◽  
Vitamin B12 Deficiency ◽  
Pernicious Anaemia ◽  
Normal Subjects ◽  
Normal Cells ◽  
Methyl Group ◽  
Consistent Effect ◽  
B12 Deficiency

1. The uptake of 14C from [methyl-14C]methyItetrahydrofolate was significantly reduced in the phytohaemagglutinin (PHA)-stimulated lymphocytes from nine patients with untreated pernicious anaemia compared with the uptake in seven normal subjects. 2. The uptake of 14C from [14C]methyltetrahydrofolate by the lymphocytes from seven of the patients with pernicious anaemia was consistently increased by addition of vitamin B12in vitro. 3. The proportion of 14C taken up from [14C]methyltetrahydrofolate transferred to non-folate compounds was found to be significantly reduced in the PHA-stimulated lymphocytes from nine patients with untreated pernicious anaemia compared with the proportion transferred in the PHA-stimulated lymphocytes from seven normal subjects. Addition of vitamin B12in vitro consistently increased the transfer in vitamin B12-deficient cells but had no consistent effect in normal cells. 4. Normal and vitamin B12-deficient PHA-stimulated lymphocytes took up [3H]folic acid and after 72 h incubation converted this largely into pteroylpolyglutamate forms. 5. The proportion of labelled lymphocyte folate as pteroylpolyglutamate after incubation with [3H]folic acid was the same in vitamin B12-deficient as in normal lymphocytes and the proportion of pteroylpolyglutamates formed in vitamin B12-deficient lymphocytes was unaffected by addition of vitamin B12in vitro. 6. No radioactivity could be decteted in pteroylpolyglutamates after incubating normal PHA-stimulated lymphocytes with [14C]methyltetrahydrofolate for 72 h, suggesting that pteroylpolyglutamate forms of folate cannot be made directly from methyltetrahydrofolate. 7. These results are consistent with the ‘methyltetrahydrofolate trap’ hypothesis in vitamin B12 deficiency. It is suggested that reduced synthesis of pteroylpolyglutamates reported by others in vitamin B12-deficient cells may be secondary to the failure of removal of the methyl group from methyltetrahydrofolate rather than to a direct effect of vitamin B12 deficiency on the enzyme responsible for pteroylpolyglutamate synthesis. 8. Reduced entry of methyltetrahydrofolate into vitamin B12-deficient cells may be secondary to failure of conversion of this compound into tetrahydrofolate.

scholarly journals Severe Vitamin B12 Deficiency in Pregnancy Mimicking HELLP Syndrome

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Shravya Govindappagari ◽  
Michelle Nguyen ◽  
Megha Gupta ◽  
Ramy M. Hanna ◽  
Richard M. Burwick
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Thrombotic Microangiopathy ◽  
Hellp Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Vitamin B12 Deficiency ◽  
Severe Vitamin ◽  
Elevated Liver Enzymes ◽  
B12 Deficiency ◽  
In Pregnancy

Severe vitamin B12 deficiency may present with hematologic abnormalities that mimic thrombotic microangiopathy disorders such as hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. We report a patient diagnosed with severe vitamin B12 deficiency, following termination of pregnancy for suspected preeclampsia and HELLP syndrome at 21 weeks’ gestation. When hemolysis and thrombocytopenia persisted after delivery, testing was performed to rule out other etiologies of thrombotic microangiopathy, including atypical hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and vitamin B12 deficiency. This work-up revealed undetectable vitamin B12 levels and presence of intrinsic factor antibodies, consistent with pernicious anemia. Parenteral B12 supplementation was initiated, with subsequent improvement in hematologic parameters. Our case emphasizes the importance of screening for B12 deficiency in pregnancy, especially in at-risk women with unexplained anemia or thrombocytopenia. Moreover, providers should consider B12 deficiency and pernicious anemia in the differential diagnosis of pregnancy-associated thrombotic microangiopathy.

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