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Vitamin B12 deficiency: case report and review of literature.
Hasbaoui, BE, Mebrouk, N, Saghir, S, Yajouri, AE, Abilkassem, R, Agadr, A
The Pan African medical journal. 2021;:237
Abstract
Vitamin B12 deficiency in early childhood is an important cause of neurodevelopmental delay and regression. Most of these cases occur in exclusively breast-fed infants of deficient mothers. Symptoms and signs of vitamin B12 deficiency appear between the ages of 2 to 12 months and include vomiting, lethargy, failure to thrive, hypotonia, and arrest or regression of developmental skills. Approximately one half of this cases exhibit abnormal movements, variously described as tremors, twitches, chorea, or myoclonus. Urinary concentrations of methylmalonic acid and homocysteine are characteristically elevated in vitamin B12 deficiency. Hyperglycinuria is sometimes present. The early diagnosis and treatment of vitamin B12 deficiency is crucial for significant neurological impairment and long-term prognosis. Treatment with vitamin B12 corrects these metabolic abnormalities very rapidly (within a few days). Vitamin B12 supplementation of pregnant women may prevent neurological and neuroradiological findings of the infants. Because of the importance of vitamin B12 in the development of the foetal and neonatal brain, vegetarian and vegan mothers should be aware of the severe and not fully-reversible damages caused by insufficient nutritional intake of vitamin B12 during pregnancy and lactation. Therefore, efforts should be directed to prevent its deficiency in pregnant and breastfeeding women on vegan diets and their infants. It is also important to take the nutritional history of both infants and their mothers for the early prevention and treatment. Here an interesting case of vitamin B12 deficiency in a 10-month-old boy presented with psychomotor regression, hypotonia and lethargy.
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Persistently increased vitamin B12 concentration due to cobalamin macrocomplexes: a case report and review of the literature.
Rodríguez, JAD, García, MIP, Bauça, JM, Mullor, RV, Barceló, A
Clinical chemistry and laboratory medicine. 2020;(10):e237-e239
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3.
How I treat anemia in pregnancy: iron, cobalamin, and folate.
Achebe, MM, Gafter-Gvili, A
Blood. 2017;(8):940-949
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Abstract
Anemia of pregnancy, an important risk factor for fetal and maternal morbidity, is considered a global health problem, affecting almost 50% of pregnant women. In this article, diagnosis and management of iron, cobalamin, and folate deficiencies, the most frequent causes of anemia in pregnancy, are discussed. Three clinical cases are considered. Iron deficiency is the most common cause. Laboratory tests defining iron deficiency, the recognition of developmental delays and cognitive abnormalities in iron-deficient neonates, and literature addressing the efficacy and safety of IV iron in pregnancy are reviewed. An algorithm is proposed to help clinicians diagnose and treat iron deficiency, recommending oral iron in the first trimester and IV iron later. Association of folate deficiency with neural tube defects and impact of fortification programs are discussed. With increased obesity and bariatric surgery rates, prevalence of cobalamin deficiency in pregnancy is rising. Low maternal cobalamin may be associated with fetal growth retardation, fetal insulin resistance, and excess adiposity. The importance of treating cobalamin deficiency in pregnancy is considered. A case of malarial anemia emphasizes the complex relationship between iron deficiency, iron treatment, and malaria infection in endemic areas; the heightened impact of combined etiologies on anemia severity is highlighted.
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Effect of folic acid, vitamin B6 and vitamin B12 supplementation on mortality and cardiovascular complication among patients with chronic kidney disease: an evidence-based case report.
Nursalim, A, Siregar, P, Widyahening, IS
Acta medica Indonesiana. 2013;(2):150-6
Abstract
AIM: to determine whether the administration of folic acid, vitamin B6 and vitamin B12 would lead to reduction of cardiovascular complication and mortality among CKD patients. METHODS a search was conducted on PubMed and Google. The selection of title and abstract was conducted using inclusion and exclusion criterias, which led to six relevant articles. The selected studies were critically appraised for its validity, importance and applicability. RESULTS the administration of folic acid and vitamin B reduce homocysteine level among CKD patients. Despite homocysteine level reduction, all six studies reported similar findings that folic acid and vitamin B supplementation did not significantly reduce cardiovascular complication and mortality. CONCLUSION treatment with folic acid, vitamin B6 and vitamin B12 did not reduce cardiovascular complication and mortality among CKD patients.
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Imerslund-Gräsbeck syndrome in a 25-month-old Italian girl caused by a homozygous mutation in AMN.
De Filippo, G, Rendina, D, Rocco, V, Esposito, T, Gianfrancesco, F, Strazzullo, P
Italian journal of pediatrics. 2013;:58
Abstract
Imerslund-Gräsbeck syndrome is a rare autosomal recessive disorder, characterized by vitamin B12 deficiency due to selective malabsorption of the vitamin and usually results in megaloblastic anemia appearing in childhood. It is responsive to parenteral vitamin B12 therapy.The estimated prevalence (calculated based on Scandinavian data) is less than 6:1,000,000. However, many cases may be misdiagnosed.When there is reasonable evidence to suspect that a patient suffers from IGS, a new and straightforward approach to diagnosis is mutational analysis of the appropriate genes. We report for the first time the case of a girl of Italian ancestry with IGS genetically confirmed by the detection of a homozygous missense mutation in the AMN gene (c.208-2 A > G).
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Nitrous oxide "whippit" abuse presenting with cobalamin responsive psychosis.
Sethi, NK, Mullin, P, Torgovnick, J, Capasso, G
Journal of medical toxicology : official journal of the American College of Medical Toxicology. 2006;(2):71-4
Abstract
INTRODUCTION Nitrous oxide is a commonly abused inhalant drug. It is known to precipitate vitamin B12 deficiency when used chronically and acutely, especially in people having marginal vitamin B12 reserve. CASE REPORT We are presenting a case of nitrous oxide "whippit" abuse in a thirty-three-year-old male with bizarre behavior and delusions. The patient had low normal levels of vitamin B12 (202 pg/ml), but he had markedly high methylmalonyl CoA (1078 nmol/L) and homocysteine (48.4 mcmol/L). Treatment with intramuscular cobalamin led to a resolution of his psychosis. DISCUSSION This case report highlights the need to consider vitamin B12 deficiency in patients who arrive at a hospital with psychiatric manifestations and who report having a history of nitrous oxide exposure or abuse in the recent or remote past. A review of the literature on the neuropsychological manifestations of vitamin B12 deficiency is provided.
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Potential outcome factors in subacute combined degeneration: review of observational studies.
Vasconcelos, OM, Poehm, EH, McCarter, RJ, Campbell, WW, Quezado, ZM
Journal of general internal medicine. 2006;(10):1063-8
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Abstract
BACKGROUND Subacute combined degeneration is an acquired myelopathy caused by vitamin B12 deficiency. Therapy with B12 leads to improvement in most but to complete recovery in only a few patients. Prognostic indicators in subacute combined degeneration are unknown; therefore, predicting complete recovery of neurologic deficits is challenging. PURPOSE To identify potential correlates of outcome and to generate hypotheses concerning predictors of complete resolution of neurologic deficits in subacute combined degeneration. DATA SOURCE We searched EMBASE (1974 to October 2005), MEDLINE (1968 to October 2005), and references from identified reports. REPORTS SELECTION Reports of patients with subacute combined degeneration containing results of magnetic resonance imaging (MRI) and description of outcome and 1 patient treated by the authors. DATA EXTRACTION, SYNTHESIS We extracted data from 45 reports and 57 patients (36 males, 21 females; age range: 10 to 81) with a diagnosis of subacute combined degeneration, and estimated the strength of association between clinical, laboratory, and radiological factors and complete resolution of signs and symptoms. RESULTS Eight patients (14%) achieved clinical resolution and 49 (86%) improved with B12 therapy. The absence of sensory dermatomal deficit, Romberg, and Babinski signs were associated with a higher complete resolution rate. Patients with MRI lesions in < or = 7 segments and age less than 50 also appear to have higher rates of complete resolution. CONCLUSIONS B12 therapy is reported to stop progression and improve neurologic deficits in most patients with subacute combined degeneration. However, complete resolution only occurs in a small percentage of patients and appears to be associated with factors suggestive of less severe disease at the time of diagnosis.
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Diagnosing vitamin B-12 deficiency on the basis of serum B-12 assay.
Devalia, V
BMJ (Clinical research ed.). 2006;(7564):385-6