scholarly journals Metabolic responses to low doses of cyanocobalamin in patients with megaloblastic anaemia

1968 ◽  
Vol 22 (4) ◽  
pp. 575-582 ◽  
Author(s):  
J. F. Adams ◽  
R. Hume ◽  
Elizabeth H. Kennedy ◽  
T. G. Pirrie ◽  
J. W. Whitelaw ◽  
...  
Keyword(s):  
Propionic Acid ◽  
Serum Iron ◽  
Serum Vitamin ◽  
Megaloblastic Anaemia ◽  
Cobalamin Deficiency ◽  
Metabolic Responses ◽  
Vitamin B ◽  
Acid Excretion ◽  
Transient Rise ◽  
Abrupt Rise

1. The metabolic responses to daily treatment with 1 μg cyanocobalamin were studied in sixteen patients with megaloblastic anaemia due to cobalamin deficiency.2. The fall in serum iron was sluggish in most patients. The pattern of reticulocyte responses varied widely, the most common being a plateau with suboptimal maximal value.3. Urinary propionic acid excretion before treatment was normal in two out of six patients. A transient rise during treatment was observed in two patients, possibly owing to demands on coenzyme stores. The fall in urinary propionic acid excretion during treatment was slow.4. Serum vitamin B12levels rose during treatment. In two patients an abrupt rise was found, possibly owing to release of stored cobalamin into the circulation.

Increased plasma homocysteine levels without signs of vitamin B12 deficiency in patients with multiple sclerosis assessed by blood and cerebrospinal fluid homocysteine and methylmalonic acid

2003 ◽  
Vol 9 (3) ◽  
pp. 239-245 ◽  
Author(s):  
M Vrethem ◽  
E Mattsson ◽  
H Hebelka ◽  
K Leerbeck ◽  
A Österberg ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Methylmalonic Acid ◽  
Haemoglobin Concentration ◽  
Serum Vitamin ◽  
High Serum ◽  
Plasma Homocysteine ◽  
Cobalamin Deficiency ◽  
Vitamin B ◽  
Plasma Thcy

Objective: The aim of this study was to evaluate if multiple sclerosis (MS) is associated with vitamin B12 (cobalamin) deficiency. Methods: We measured serum vitamin B12, plasma folate, serum methylmalonic acid (MMA), plasma homocysteine (tHcy) and also cerebrospinal fluid (C SF) MMA and tHcy in 72 patients with MS and 23 controls. Results: The mean plasma tHcy level was significantly increased in MS patients (11.6 mmol/L) compared with controls (7.4 mmol/L) (P =4-0.002). Seven patients showed low serum vitamin B12levels but only one of them had concomitant high plasma tHcy. None of them showed high serum MMA. Plasma or blood folate levels did not differ between MS patients and controls. We found no significant differences in mean values or frequency of pathological tests of serum B12, serum MMA, mean corpuscular volume (MC V), haemoglobin concentration, C SF tHcy or C SF MMA between patients and healthy subjects. There were no correlations between C SF and serum/plasma levels of MMA or tHcy. Serum vitamin B12, serum MMA, plasma tHcy, C SF Hcy or C SF MMA were not correlated to disability status, activity of disease, duration of disease or age. Conclusions:The relevance of the increased mean value of plasma tHcy thus seems uncertain and does not indicate functional vitamin B12 deficiency. We can not, however, exclude the possibility of a genetically induced dysfunction of the homocysteine metabolism relevant for the development of neuroinflammation/degeneration. O ur findings indicate that, regardless of a significant increase in plasma tHcy in MS patients, the MS disease is not generally associated with vitamin B12 deficiency since we did not find any other factors indicating vitamin B12 deficiency. A nalysis of C SF MMA and C SF tHcy, which probably reflects the brain vitamin B12 status better than serum, are not warranted in MS. We conclude that B12 deficiency, in general, is not associated with MS.

INFORMING DISINVESTMENT WITH LIMITED EVIDENCE: COBALAMIN DEFICIENCY IN THE FATIGUED

2015 ◽  
Vol 31 (3) ◽  
pp. 188-196
Author(s):  
George Mnatzaganian ◽  
Jonathan Karnon ◽  
John R. Moss ◽  
Adam G. Elshaug ◽  
Michael Metz ◽  
...  
Keyword(s):  
Input Parameter ◽  
Serum Vitamin ◽  
Evaluation Process ◽  
Cost Effective ◽  
Screening Tests ◽  
Cobalamin Deficiency ◽  
Vitamin B ◽  
Treatment Pathways ◽  
Published Evidence ◽  
The Face

Objectives:Health technology reassessment and disinvestment can be difficult due to uncertainties regarding available evidence. Pathology testing to investigate cobalamin (vitamin B12) deficiency is a strong case in point. We conducted a 3-month economic evaluation of five strategies for diagnosing and treating cobalamin deficiency in adult patients hypothetically presenting with new unexplained fatigue in the primary care setting. The first consultation per patient was considered. Screening tests other than serum cobalamin were not included.Methods: A cost-effectiveness analysis was undertaken using a decision tree to represent the diagnostic / treatment pathways, with relevant cost and utility scores assigned to different stages in the evaluation process. Input parameter values were estimated from published evidence, supplemented by expert opinion, with sensitivity analysis undertaken to represent parameter uncertainty.Results:Ordering serum vitamin B12to assess cobalamin deficiency among patients with unexplained fatigue was not cost-effective in any patient population, irrespective of pretest prevalence of this deficiency. For patients with a pretest prevalence above 1 percent, treating all with oral vitamin B12supplements without testing was most cost-effective, whereas watchful waiting with symptoms monitoring was most cost-effective for patients with lower pretest prevalence probabilities.Conclusions:Substantial evidence gaps exist for parameter estimation: questionable cobalamin deficiency levels in the fatigued; debatable treatment methods; unknown natural history of the condition. Despite this, we reveal a robust path for disinvestment decision making in the face of a paradox between the evidence required to inform disinvestment compared with its paucity in informing initial funding decisions.

Schizophrenia-like Psychoses of Epilepsy and Disturbances of Folate and Vitamin B12Metabolism Induced by Anticonvulsant Drugs

1967 ◽  
Vol 113 (501) ◽  
pp. 911-919 ◽  
Author(s):  
E. H. Reynolds
Keyword(s):  
Psychiatric Illness ◽  
Serum Vitamin ◽  
Anticonvulsant Drug ◽  
Megaloblastic Anaemia ◽  
Vitamin B ◽  
Normal Range ◽  
Drug Induced ◽  
Subacute Combined Degeneration ◽  
Epileptic Patients ◽  
Mental Symptoms

Since it was first described by Mannheimer, Pakesch, Reimer and Vetter in 1952 megaloblastic anaemia has come to be recognized as an occasional complication of anticonvulsant drug therapy. More recently a disturbance in folic acid and vitamin B12metabolism has been observed in many non-anaemic drug-treated epileptic patients (Hawkins and Meynell, 1958; Klipstein, 1964; Malpas, Spray and Witts, 1966; Reynolds, Milner, Matthews and Chanarin, 1966a). Reynoldset al.(1966a) found megaloblastic haemopoiesis in 38 per cent. and subnormal serum folates in over 75 per cent. of a series of 54 out-patient epileptics. In addition, serum vitamin B12levels, though still within the normal range, were significantly lower in the megaloblastic group of patients than in controls. They suggested (1) that the anti-folate effects of phenobarbitone, phenytoin and primidone may be related to their therapeutic actions, and (2) that prolonged drug-induced disturbances of folate and vitamin B12metabolism may be responsible for certain side-effects, particularly mental symptoms. The latter possibility is supported by the increasing recognition of psychiatric illness due to vitamin B12deficiency in the absence of anaemia or subacute combined degeneration of the cord. (Langdon, 1905; McAlpine, 1929; Holmes, 1956; Smith, 1960; Edwin, Holten, Norum, Schrumpf and Skaug, 1965; Strachan and Henderson, 1965).

scholarly journals Folate and vitamin B12: friendly or enemy nutrients for the elderly

2007 ◽  
Vol 66 (4) ◽  
pp. 548-558 ◽  
Author(s):  
Geraldine J. Cuskelly ◽  
Kathleen M. Mooney ◽  
Ian S. Young
Keyword(s):  
Folic Acid ◽  
Serum Vitamin ◽  
The Elderly ◽  
Megaloblastic Anaemia ◽  
Vitamin B ◽  
Folic Acid Fortification ◽  
The Usa ◽  
Criteria For Diagnosis ◽  
Folate And Vitamin B12 ◽  
The Uk

In the UK vitamin B12deficiency occurs in approximately 20% of adults aged >65 years. This incidence is significantly higher than that among the general population. The reported incidence invariably depends on the criteria of deficiency used, and in fact estimates rise to 24% and 46% among free-living and institutionalised elderly respectively when methylmalonic acid is used as a marker of vitamin B12status. The incidence of, and the criteria for diagnosis of, deficiency have drawn much attention recently in the wake of the implementation of folic acid fortification of flour in the USA. This fortification strategy has proved to be extremely successful in increasing folic acid intakes pre-conceptually and thereby reducing the incidence of neural-tube defects among babies born in the USA since 1998. However, in successfully delivering additional folic acid to pregnant women fortification also increases the consumption of folic acid of everyone who consumes products containing flour, including the elderly. It is argued that consuming additional folic acid (as ‘synthetic’ pteroylglutamic acid) from fortified foods increases the risk of ‘masking’ megaloblastic anaemia caused by vitamin B12deficiency. Thus, a number of issues arise for discussion. Are clinicians forced to rely on megaloblastic anaemia as the only sign of possible vitamin B12deficiency? Is serum vitamin B12alone adequate to confirm vitamin B12deficiency or should other diagnostic markers be used routinely in clinical practice? Is the level of intake of folic acid among the elderly (post-fortification) likely to be so high as to cure or ‘mask’ the anaemia associated with vitamin B12deficiency?

Nutritional B12 Deficiency in Infants of Vitamin B12-Deficient Mothers

2011 ◽  
Vol 81 (5) ◽  
pp. 328-334 ◽  
Author(s):  
Oya Halicioglu ◽  
Sezin Asik Akman ◽  
Sumer Sutcuoglu ◽  
Berna Atabay ◽  
Meral Turker ◽  
...  
Keyword(s):  
Megaloblastic Anemia ◽  
Maternal Diet ◽  
Clinical Manifestations ◽  
Serum Vitamin ◽  
Failure To Thrive ◽  
Clinical Findings ◽  
Vitamin B ◽  
Animal Products ◽  
Hematological Evaluation ◽  
Nutritional Vitamin

Aim: Nutritional vitamin B12 deficiency in infants may occur because the maternal diet contains inadequate animal products. Clinical presentations of the infants who had nutritional vitamin B12 deficiency were analyzed in this study. Subjects and Methods: Patients with nutritional vitamin B12 deficiency were enrolled in the study between 2003 and 2010. The diagnosis was based on a nutritional history of mothers and infants, clinical findings, hematological evaluation, and low level of serum vitamin B12. Results: Thirty children aged 1 - 21 months constituted the study group. Poverty was the main cause of inadequate consumption of animal products of the mothers. All infants had predominantly breastfed. The most common symptoms were developmental delay, paleness, apathy, lethargy, anorexia, and failure to thrive. Hematological findings were megaloblastic anemia (83.3 %), thrombocytopenia (30 %), and severe anemia (13.3 %). All of the mothers had low serum B12 levels; eight of them had megaloblastic anemia. Conclusion: The unusual clinical manifestations of vitamin B12 deficiency may also be seen apart from neurological and hematological findings. Nutritional vitamin B12 deficiency due to maternal deficiency might be a serious health problem in infants. Therefore, screening and supplementation of pregnant and lactating women to prevent infantile vitamin B12 deficiency should be considered.

Serum Vitamin B12 Concentrations among Mothers and Newborns and Follow-up Study to Assess Implication on the Growth Velocity and the Urinary Methylmalonic Acid Excretion

2009 ◽  
Vol 79 (56) ◽  
pp. 297-307 ◽  
Author(s):  
Laila Hussein ◽  
Sahar Abdel Aziz ◽  
Salwa Tapouzada ◽  
Boehles
Keyword(s):  
Early Diagnosis ◽  
Growth Velocity ◽  
Methylmalonic Acid ◽  
Post Partum ◽  
Serum Vitamin ◽  
Vitamin B ◽  
Postnatal Life ◽  
Negative Consequences ◽  
Metabolic Marker ◽  
Biochemical Measurement

Objective:Cobalamin (B12) deficiency has been reported in infants born to mothers with low cobalamin intake. Early diagnosis of vitamin B12 deficiency in infants is critical for the prevention of neurobehavioral disorders. We investigated the relationship between serum vitamin B12 level in newborns and in their healthy mothers who consumed an omnivorous diet. Anthropometry was studied longitudinally to assess the growth velocity of the infants. Urinary methylmalonic acid (MMA) excretion of 6-month old infants was compared retrospectively as the biomarker correlated with the initial serum vitamin B12 concentrations. Methods: Serum cobalamin and blood hemoglobin were determined in 84 pairs of newborns and their mothers. Urinary MMA excretion was measured in the same subjects during the first 6 months of the post partum period. Results: At birth, median serum cobalamin levels were 152.0 pmol/L in the mothers and 296.6 pmol/L in the newborns. Maternal and neonatal serum cobalamin levels had no effect on growth velocity during the first six months of postnatal life. Serum maternal and neonatal cobalamin levels were inversely associated with urinary MMA excretion. Conclusion: Early diagnosis of vitamin B12 status in neonates and infants is crucial, particularly in nutritionally deprived areas. Biochemical measurement of plasma cobalamin or its metabolic marker MMA is highly recommended. Urinary MMA measurement in cobalamin diagnostics provides an advantage in that blood sampling is not required. A vitamin B12 taskforce should be created to alleviate vitamin deficiency and its negative consequences.

scholarly journals Masked vitamin B12 and folate deficiency in the elderly

1985 ◽  
Vol 54 (3) ◽  
pp. 613-619 ◽  
Author(s):  
G. M. Craig ◽  
C. Elliot ◽  
K. R. Hughes
Keyword(s):  
Clinical Investigation ◽  
Binding Capacity ◽  
Serum Vitamin ◽  
The Elderly ◽  
Folate Deficiency ◽  
Significant Negative Correlation ◽  
Serum Folate ◽  
Fe Deficiency ◽  
Vitamin B ◽  
Geriatric Unit

1. A high incidence of vitamin B12 or folate deficiency, or both, may be found in the elderly, particularly those in hospital. This report concerns fifty cases detected in an inner-city-area geriatric unit during the course of routine clinical investigation. The majority had none of the classical haematological signs of vitamin B12 or folate deficiency, and all the patients reported had a mean corpuscular volume (MCV) of less than 100 fl.2. There was a significant negative correlation between the MCV and the erythrocyte folate (P< 0.01), supporting earlier published work using a low serum folate as an index of folate deficiency.3. There was no correlation between the MCV and the serum vitamin B12. Published work differs on this point.4. Serum iron, total Fe-binding capacity and percentage Fe saturation results were available in forty patients in this series. There was a significant positive correlation between the serum Fe and the MCV (P<0.01) and 34% of patients had haematological evidence of Fe deficiency. In the majority, however, there was no evidence that associated Fe deficiency had masked the haematological signs of vitamin B12 or folate deficiency.5. More attention should be paid to the problem of ‘masked’ vitamin B12 and folate deficiency in the elderly. There is a case for routine screening of the elderly for vitamin B12 and folate deficiency irrespective of the MCV.

The Serum Vitamin B12 in the Elderly

1966 ◽  
Vol 8 (4) ◽  
pp. 220-225 ◽  
Author(s):  
A.A. Dawson ◽  
D. Donald
Keyword(s):  
Serum Vitamin ◽  
The Elderly ◽  
Vitamin B
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