Andres, E. et al. Vitamin B12 (cobalamin) deficiency in elderly patients. CMAJ 171, 251-259

Department of Internal Medicine, Medical Clinic B, Strasbourg University Hospitals, Strasbourg, France.
Canadian Medical Association Journal (Impact Factor: 5.96). 09/2004; 171(3):251-9.
Source: PubMed


Vitamin B12 or cobalamin deficiency occurs frequently (> 20%) among elderly people, but it is often unrecognized because the clinical manifestations are subtle; they are also potentially serious, particularly from a neuropsychiatric and hematological perspective. Causes of the deficiency include, most frequently, food-cobalamin malabsorption syndrome (> 60% of all cases), pernicious anemia (15%-20% of all cases), insufficient dietary intake and malabsorption. Food-cobalamin malabsorption, which has only recently been identified as a significant cause of cobalamin deficiency among elderly people, is characterized by the inability to release cobalamin from food or a deficiency of intestinal cobalamin transport proteins or both. We review the epidemiology and causes of cobalamin deficiency in elderly people, with an emphasis on food-cobalamin malabsorption syndrome. We also review diagnostic and management strategies for cobalamin deficiency.

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    • "An even higher prevalence of 30% to 40% is reported for malnourished and sick elderly people.1 Cobalamin serves as a cofactor for methionine synthase and L-methylmalonyl-coA mutase. People with cobalamin deficiency may experience megaloblastic anemia, subacute combined degeneration of the spinal cord, peripheral polyneuropathy, cognitive impairment, and mental changes.2 Cobalamin deficiency is due to malabsorption of food-bound cobalamin and/or insufficient dietary intake. "
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    ABSTRACT: Background The gold standard for cobalamin deficiency treatment is administration of cobalamin by intramuscular injection. The injection is painful and inconvenient, particularly for elderly persons. Cobalamin might also be administered intranasally. Previous studies do not provide insight into the pharmacokinetics of intranasal cobalamin administration in comparison with cobalamin injection. Aim To quantify the pharmacokinetics of intranasally and intramuscularly administered cobalamin to determine if intranasal administration might be an alternative for intramuscular administration. Methods Ten inpatients and outpatients of a geriatrics unit were recruited and randomly assigned to receive a single dose of 1000 μg cobalamin administered either by intranasal spray or intramuscular injection (5 per group). Inclusion criteria were written informed consent, age >65 years, and a cobalamin serum concentration <200 pmol/L. Total cobalamin serum concentrations were determined 10 times within 48 hours after administration. The differences in Cmax, Tmax, and AUC0–48 h per administration route were statistically compared using ANOVA. Results The average Cmax was 1 nmol/L after intranasal and 38.5 nmol/L after intramuscular administration. The average Tmax for intranasal and intramuscular administration was 42 minutes versus 342 minutes, respectively, and the AUC0–48 h was 1.3 µmol/L/min versus 45.4 µmol/L/min, respectively. These values also differed significantly (P<0.05). The estimated bioavailability of the intranasal administration was 2%. Conclusions The pharmacokinetics of intranasal and intramuscular cobalamin administration in elderly, cobalamin-deficient patients differ significantly. However, the estimated 2% bioavailability of cobalamin after intranasal administration makes intranasal cobalamin administration a potentially interesting administration route for elderly patients. Netherlands Trial Registry identifier: NTR 3005.
    Current Therapeutic Research 12/2014; 76:21–25. DOI:10.1016/j.curtheres.2014.01.001 · 0.45 Impact Factor
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    • "Vitamin B12 deficiency is common, with an estimated prevalence of 15% in patients >60 years of age. Although most cases are clinically subtle, vitamin B12 deficiency may sometimes present with florid disease [1,2]. When present, symptoms and signs can be broadly classified into hematological and neurological categories. "
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    ABSTRACT: Introduction Although vitamin B12 deficiency is a well-known cause of hematological and neuropsychiatric illness, the presentation of combined severe pancytopenia, demyelination and prominent psychiatric impairment is rare. Case presentation We present a case of a previously healthy 55-year-old East African man with severe vitamin B12 deficiency (serum vitamin B12 22pmol/L) secondary to pernicious anemia. He had a severe hypoproliferative megaloblastic anemia with hemolysis (hemoglobin 61g/L, mean corpuscular volume 99fL, reticulocytes 0.8%, haptoglobin undetectable), leukopenia (2.7×109/L), thrombocytopenia (96×109/L), ataxia with central demyelination, and megaloblastic madness. The patient’s anemia, myelopathy and psychiatric condition responded well to parenteral vitamin B12 replacement therapy, with significant improvement seen within weeks. Conclusion Hematological manifestations of vitamin B12 deficiency are typically inversely correlated with the presence and severity of neuropsychiatric impairment. Although uncommon, a presentation with severe hematological and neuropsychiatric disease can occur, as illustrated by this case. Its presence may help guide diagnosis as well as provide clinically important prognostic information.
    Journal of Medical Case Reports 08/2014; 8(1):277. DOI:10.1186/1752-1947-8-277
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    • "In the Chilean population, we found in older adults a prevalence of B12 deficiency of 12% (B125148 pmol/l) and 25.4% of marginal deficiency (B12 between 148 and 221 pmol/l) (Sánchez et al. 2010). This prevalence would be the result of age-related gastric atrophy, low acid, and intrinsic factor production (Carmel et al. 1988; Suter et al. 1991; Andres et al. 2004; Clarke et al. 2004). Many studies have supported the usefulness of neurophysiological evaluation of the corticospinal tract in patients with myelopathies of different cause (Abbruzzese et al. 1988; Maertens de Noordhout et al. 1991; Chistyakov et al. 1995). "
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    ABSTRACT: Abstract Introduction: Vitamin B12 deficiency causes neurologic and psychiatric disease, especially in older adults. Subacute combined degeneration is characterized by damage to the posterior and lateral spinal cord affecting the corticospinal tract. Objective: To test corticospinal tract projections using motor evoked potentials (MEPs) by transcranial magnetic stimulation (TMS) in asymptomatic older adults with low vitamin B12 (B12) levels. Methods: Cross-sectional study of 53 healthy older adults (>70 years). MEPs were recorded in the abductor pollicis brevis and tibialis anterior muscles, at rest and during slight tonic contraction. Central motor conduction time (CMCT) was derived from the latency of MEPs and peripheral motor conduction time (PMCT). Neurophysiological variables were analyzed statistically according to B12 status. Results: Median age was 74.3 ± 3.6 years (58.5% women). Twenty-six out of the 53 subjects had low vitamin B12 levels (B12 < 221 pmol/l). MEPs were recorded for all subjects in upper and lower extremities. There were no significant differences in either latency or amplitude of MEPs and CMCT between low and normal B12 groups. There was a significant PMCT delay in the lower extremities in the low B12 group (p = 0.014). Conclusions: No subclinical abnormality of the corticospinal tract is detected in asymptomatic B12-deficient older adults. The peripheral nervous system appears to be more vulnerable to damage attributable to this vitamin deficit. The neurophysiological evaluation of asymptomatic older adults with lower B12 levels should be focused mainly in peripheral nervous system evaluation.
    Somatosensory & Motor Research 04/2014; 31(3). DOI:10.3109/08990220.2014.897603 · 0.64 Impact Factor
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