Manifestation Of Vitamin B12 Deficiency Research Articles

Vitamin B12 and homocysteine in patients with major depressive disorder

ABSTRACT Background: Alterations in the level of neurotransmitters are evident in patients with major depressive disorder (MDD). Vitamin B12 mediates the synthesis of neurotransmitters, and hence, vitamin B12 deficiency could be associated with depression. Aims and Objectives: To assess the levels of serum vitamin B12, homocysteine (Hcy), and haematological profiles in patients of MDD. Materials and Methods: Fifty-nine patients with MDD were recruited based on ICD-10 criteria. Severity of depression was assessed by HAM-D scale. Vitamin B12, Hcy levels, and haematological profiles were analysed. Results: Vitamin B12 was deficient or depleted in all patients with MDD. The median level of vitamin B12 in serum was 164.2 pg./ml and significantly lower in patients with severe MDD. The mean value of Hcy was 18.34 μmol/L, which was high compared to the normal reference range. The red cell distribution width (RDW-CV) varied significantly between the three groups of MDD patients. Patients consuming non-vegetarian food had a significantly higher median value of serum vitamin B12. Conclusion: Vitamin B12 deficiency is found in patients with MDD and varies inversely with severity of MDD. Hcy is found to be higher in patients with MDD. The manifestation of depressive symptoms precedes the more commonly known haematological manifestations of vitamin B12 deficiency in this study.

Establishing the Law of Parsimony in a Case of Restless Legs Syndrome

Restless legs syndrome (RLS) is a common movement disorder characterized by uncomfortable sensations in the lower limbs relieved by limb movements. Clinical studies have established a possible association between RLS and vitamin B12 deficiency but not a causal one. RLS has rarely been reported as an isolated neurological manifestation of vitamin B12 deficiency. In this case report, we described a 24-year-old young man with RLS who responded poorly to symptomatic therapy. The etiological evaluation suggested vitamin B12 deficiency secondary to pernicious anemia. The patient responded rapidly to vitamin B12 supplementation and clinical manifestations of RLS resolved, suggesting a possible causal relationship.

A review on vitamin B12 deficiency induced by metformin

Multiple studies have established a higher prevalence of vitamin B12 deficiency in patients who have type 2 diabetes mellitus (T2DM). Metformin is prescribed as the 1st line oral glucose-lowering medication for individuals with T2DM. However, metformin therapy has been linked to vitamin B12 malabsorption, which can result in both biochemical and clinical manifestations of vitamin B12 deficiency. The long-term use of metformin is associated with a significant decrease in vitamin B12 levels, particularly in doses greater than 2000 mg per day over a period of 4 years. Vitamin B12 is a water-soluble vitamin. It acts as a cofactor for enzymes involved in DNA synthesis and neuroprotection at the cellular level. Hence, vitamin B12 deficiency can lead to various clinical consequences, including hematologic abnormalities such as megaloblastic anemia and hypersegmented neutrophil formation, peripheral neuropathy, and progressive axonal demyelination, hyperhomocysteinemia (HHcy). The latest "standards of medical care in diabetes-2017" issued by the American diabetes association recommends periodic assessment of B12 status and, if necessary, the use of B12 replacement therapy in diabetic patients taking metformin. In order to address the vitamin B12 deficiency associated with metformin several therapies are available including prophylactic supplements of calcium and vitamin B12, discontinuation of metformin, and replenishment of vitamin B12 stores through intramuscular or oral therapy. It is important to regularly monitor vitamin B12 levels for at least annually to prevent complications of vitamin B12 deficiency and continue with supplementation if metformin is still being used.

Characterizing Vitamin B12 Deficiency in Neurology Outpatients: A Retrospective Observational Study.

Clinical manifestations of vitamin B12 deficiency are varied and may result in missed or delayed diagnosis. This investigation explores the diverse clinical manifestations and demographic characteristics of vitamin B12 deficiency in neurology outpatients, aiming to enhance timely diagnosis and outcomes. The severity of vitamin B12 deficiency was classified as absolute (≤150 pg/mL) or borderline deficiency (150-300 pg/mL). We conducted a retrospective analysis of 165 outpatients with vitamin B12 deficiency at the department of neurology between May 2020 and May 2021. Absolute vitamin B12 deficiency was found in 23.0% of the patients. The most common age range was 50-60 years, the most common cause was vegetarianism, and the most common symptom was headache. Epileptiform symptoms were more likely to occur in younger patients (<20 years old) with vitamin B12 deficiency, whereas psychiatric symptoms were more likely to occur in older patients (>70 years old). Vegetarians, salivation, and nonmegaloblastic anemia were more obvious in patients with absolute vitamin B12 deficiency, whereas headaches often showed borderline B12 deficiency. The clinical characteristics of vitamin B12 deficiency are complex and nonspecific. The diagnosis should be based on multiple factors.

Neurological manifestations of vitamin B12 deficiency: A cross sectional study

Neurological manifestations of vitamin B12 deficiency: A cross sectional study

Pseudo-Orthostatic Tremor as a Manifestation of Vitamin B12 Deficiency: A Case Report

Vitamin B12 deficiency has long been known to present with various neurological manifestations, but only rarely presents as movement disorders, especially in adults. We present the case of a 30-year-old vegan male presenting with tremors on both legs when standing which was relieved by vitamin B12 supplementation. To the best of our knowledge, this is the first documented case of slow orthostatic tremor or pseudo-orthostatic tremor caused by vitamin B12 deficiency. Key words: Vitamin B12 Deficiency, Cobalamin, Vegan, Movement Disorders, Tremor, Orthostatic Tremor, Shaky-leg Syndrome, Electromyography

When two becomes one: neurological manifestation of vitamin B12 deficiency

article: When two becomes one: neurological manifestation of vitamin B12 deficiency - Gazzetta Medica Italiana - Archivio per le Scienze Mediche 2022 November;181(11):888-91 - Minerva Medica - Journals

Neuropsychiatric manifestations in vitamin B12 deficiency.

Vitamin B12 deficiency can have distressing neuropsychiatric symptoms. It can have an etiological role in clinical presentations like depression, anxiety, psychosis, dementia, and delirium, requiring screening of at-risk populations. Few mechanisms that underlie the neuropsychiatric manifestations of B12 deficiency include alteration in one-carbon metabolism, genetic vulnerability, and alteration in folate metabolism. Maintaining a high serum B12 level in elderly can be protective against Alzheimer's disease (AD). In an established AD, its deficiency is associated with higher cognitive decline and risk for delirium. The other mental changes associated with B12 deficiency include apathy, agitation, impaired concentration, insomnia, persecutory delusions, auditory and visual hallucinations, and disorganized thought-process. Besides serum vitamin B12, plasma methylmalonic acid (MMA) and homocysteine helps in diagnosis. The chapter focuses on early recognition and effective treatment of these neuropsychiatric manifestations of vitamin B12 deficiency.

Subacute combined degeneration of spinal cord, optic atrophy and thrombocytopenia without anemia secondary to B12 deficiency

Long-standing vitamin B12 deficiency can lead to neurological manifestations such as optic atrophy and subacute combined degeneration of the cord without causing significant anemia. In addition, folic acid supplementation could mask the hematological manifestations of vitamin B12 deficiency and delay the presentation of neurological manifestations We present a case of a 32-year-old vegan woman on long-term sodium valproate and folic acid treatment presenting with progressive weakness of bilateral lower limbs for three months and reduced vision in both eyes for two weeks duration. Further evaluation revealed optic atrophy, combined degeneration of the spinal cord, macrocytosis, thrombocytopenia, and severely deficient serum B12 levels. With B12 replacement therapy, the patient’s overall wellbeing improved.

A Case of Subacute Combined Degeneration as a Manifestation of Pernicious Anaemia

Vitamin B12 deficiency affects multiple systems, including the central and peripheral nervous systems, producing a vast spectrum of neurological symptoms. It is particularly important due to its insidious presentation and because it can evolve to spastic paraplegia with permanent sequelae. The authors describe a case of a woman with asthenia, bilateral lower limb weakness, urinary retention, and faecal incontinence, with no structural cause on imaging studies. Blood tests showed anaemia (haemoglobin: 6.8 g/dL) and vitamin B12 deficiency (&lt;100 pg/mL). After upper digestive endoscopy compatible with chronic atrophic gastritis and positive for anti-intrinsic factor antibodies was obtained, the diagnosis of subacute combined degeneration due to vitamin B12 deficiency in the context of pernicious anaemia was admitted. Although this entity is a rare cause of myelopathy, it is a frequent manifestation of vitamin B12 deficiency. Clinical suspicion is fundamental since the reversibility of the neurological lesion is dependent on early treatment.

Chronic Atrophic Gastritis Presenting as Hemolytic Anemia due to Severe Vitamin B12 Deficiency

Vitamin B12 is an essential nutrient which plays an important role in neurological function, hematopoiesis, and DNA synthesis. Low levels usually stem from either poor intake or a malabsorptive process. Presently, the most common cause of vitamin B12 deficiency is food-bound cobalamin malabsorption, which occurs when there is impaired release of vitamin B12 from ingested food due to an outstanding factor preventing the release of the nutrient from its transport protein. Such causes include achlorhydria, gastritis, gastrectomy, or the use of PPIs or antacids. A rarer cause is autoimmune chronic atrophic gastritis, resulting in pernicious anemia. In this disease process, there is destruction of parietal cells and thus a reduction in intrinsic factor, which is essential to the absorption of vitamin B12. Deficiency will result in a variety of abnormalities including but not limited to pancytopenia, paresthesias, and neuropsychiatric symptoms. A rare manifestation of vitamin B12 deficiency is hemolytic anemia, which occurs due to intramedullary and extramedullary dysfunction. This case describes a 46-year-old male with no past medical history who presented with chest pain, fatigue, and progressive weakness, found to have hemolytic anemia, ultimately attributed to vitamin B12 deficiency. Antiparietal cell antibodies and intrinsic factor antibodies (IFA) were both negative. Still, the patient underwent an endoscopy with biopsies of the stomach; pathology was consistent with chronic metaplastic atrophic gastritis. The patient improved with intramuscular vitamin B12 supplementation. This case highlights both a rare cause and presentation of vitamin B12 deficiency. Patients with autoimmune chronic atrophic gastritis should have antiparietal cell or intrinsic factor antibodies. Still, seronegative patients have been reported, like this patient. Additionally, hemolytic anemia secondary to vitamin B12 deficiency is uncommon. The presentation will usually mirror that of a thrombotic microangiopathy (TMA), including hemolytic anemia with schistocytes on peripheral blood smear and thrombocytopenia, as it did in this patient. This clinical entity is described as pseudothrombotic microangiopathy and is crucial to identify in order to prevent the initiation of invasive treatment strategies such as plasmapheresis.

Vitamin B12 Deficiency-Related Pseudo-Thrombotic Microangiopathy Might be Misdiagnosed and Treated with Plasma Product Therapy: Review of the Literature and Analysis of the Reported Cases

Introduction: Pseudo-thrombotic microangiopathy (pseudo-TMA) is a recognized clinical manifestation of vitamin B12 deficiency, manifested as microangiopathic hemolytic anemia, schistocytosis, high serum lactate dehydrogenase (LDH), and low plasma haptoglobin. Such cases have been misdiagnosed as thrombotic thrombocytopenic purpura and patients were subjected to treatment with plasma product therapy. We conducted literature search and analysis of cobalamin deficiency-pseudo thrombotic microangiopathy (pseudo-TMA) cases from published literature.Material & Methods: We performed comprehensive literature search in PUBMED, EMBASE, SCOPUS and GOOGLE SCHOLAR databases using the terms “B12 AND microangiopathy”, “cobalamin AND microangiopathy”, “B12 AND thrombotic thrombocytopenic purpura”, “cobalamin AND thrombotic thrombocytopenic purpura”, “pernicious anemia AND microangiopathy”, “pernicious anemia AND thrombotic thrombocytopenic purpura”, “B12 AND schistocytes”, “cobalamin AND schistocytes”, “pernicious anemia AND schistocytes”. We extracted data from eligible cases and analyzed them. The primary endpoint was to determine the frequency of use of plasma product therapy (plasma transfusion and/or plasma exchange). The secondary endpoint was to identify the clinical and laboratory differences between the cases treated with plasma products and cobalamin therapy versus those treated with cobalamin therapy only. The distribution of each categorical variable was be summarized in terms of its frequencies and percentages. Continuous variables were compared between groups (plasma product therapy versus no-plasma therapy) by non-parametric methods. Chi-square test or Fisher exact test was used to assess differences between categorical variables.Results: Total of 8116 citations were identified from the literature search and 4880 duplicates were identified and removed. In addition, 3200 ineligible citations were excluded. A total of 36 patients were available for analysis. Patient characteristics were described in Table 1. After comparison of clinical and laboratory variables between plasma therapy group and non-plasma therapy group, we found that patients who were treated with plasma therapy had much lower platelet count of 41 x 109/L whereas 100 x 109/L in non-plasma therapy group with p-value of <0.000. No other differences were identified between both groups.Conclusions: 38.8% of reported cases of cobalamin deficiency-related pseudo-TMA were treated with plasma product therapy. Median duration of symptom was 2 weeks before the correct diagnosis was made. Seemingly, low platelet count appeared to be the basis on deciding the use of plasma product therapy. However, we could not confirm if thrombocytopenia was the main clinical factor to consider “true” TMA. Moreover, schistocytes were present in 30 out of 36 cases; thus the presence of schistocytes was not the main clinical aspect leading to the decision to use plasma product therapy. No other clinical or laboratory aspects were different between the two groups. Improved awareness of this condition in the hematology community and reaching the precise diagnosis is critical to avoid unnecessary and expensive plasma product therapy. [Display omitted] DisclosuresRojas Hernandez:Daichii Sankyo: Research Funding. Oo:Daichii Sankyo: Research Funding.

Vitamin B12 Deficiency and Psychiatric Manifestations-A Consise Review

Vitamin B12 deficiency may contribute to the pathogenesis of neuropsychiatric disorders such as mental confusion, memory changes, cognitive slowing, mood disorder, violent behaviour, fatigue, delirium and paranoid psychosis. Vitamin B12 plays a crucial role in cell reproduction, normal erythropoiesis, nucleoprotein and myelin synthesis, normal growth, DNA synthesis, and one carbon metabolism. Vitamin B12 helps in synthesis of methionine from homocysteine and conversion of methylmalonylcoA to succinylcoA. Methionine is converted to SAM which donates its methyl group to myelin, membrane phospholipids and various neurotransmitters and free THF is liberated from N5 methyl THF which is used in synthesis of purine, pyrimidine and nucleic acid. An elevated level of Hcy as a neurotoxin was also shown to affect the redox signalling pathways in neurons through the generation of reactive oxygen species (ROS) and a decrease in endogenous antioxidants. If patterns of DNA methylation in redox-related genes can modulate cognitive impairment caused by vitamin B12 deficiency and hyperhomocysteinaemia is therefore of interest, low levels of vitamin B12 can cause serious cognitive dysfunction. Psychiatric symptoms attributable to vitamin B12 deficiency have been described for decades. The earlier studies are for the most part in accord with more recent ones, despite being diagnostically less precise in psychological and hematologic terms. These symptoms tend to fall into many clinically distinct categories: slow cerebration; confusion; memory changes; delirium, with or without hallucinations and/or delusions; depression; acute psychotic states; and more rarely) reversible manic and schizophreniform states. In conclusion, psychiatric disorders can be rare manifestations of vitamin B12 deficiency, which are reversible with therapy. Serum Vitamin B12 level should be checked in patients with psychiatric manifestations as it results in neuro psychiatric manifestations such as peripheral neuropathy, myeloneuropathy, cerebellar ataxia, optic atrophy, delirium, dementia, psychosis and mood disorders

VITAMIN B12 AND FOLIC ACID STATUS AMONG DISPLACED PREGNANT WOMEN ATTENDING ANTENATAL CARE CLINIC IN DOMIZ CAMP OF A SYRIAN REFUGEES /KURDISTAN REGION, IRAQ

Background: Vitamin B12, folic acid and their relevant biomarkers are essential micronutrients for healthy fetal growth and development. Thus, deficiency in the levels of these vitamins and relevant biomarkers during pregnancy leads to many adverse outcomes for both mother and fetus.&#x0D; Objective: The current research project aims to detect the status of vitamin B12 and Folic acid and relevant biomarkers such as Homocysteine, Methylmalonic acid and Holotranscobalamin among displaced pregnant women attending antenatal care in Domiz Camps Clinic of Syrian refugees.&#x0D; Methods and Subjects: This cross-sectional research was performed at Syrian refugee’s camps in Domiz- Duhok city, Kurdistan Region, Iraq, from February 2019 until June 2019. This study included 540 pregnant women whose ages ranged between 15-44 years. Participants were subdivided into three groups based on their trimesters. Each group included 180 pregnant women. Vitamin B12 and folic acid were measured by Automatic Clinical Chemistry Analyzer COBAS 6000 while Methylmalonic acid (MMA), Homocysteine (Hcy), and Holotranscobalamin (HoloTc) were measured by ELISA.&#x0D; Results: The results of the current study revealed that the prevalence of vitamin B12 insufficiency (&lt;200 pg/mL) was high across all three trimesters, which constitutes 73% in the total cohort. The mean vitamin B12 (pg/mL) during 1st semester was within the normal range (226.5± 6.95), whereas during the 2nd and 3rd semesters it was significantly (P&lt;0.0001) low (179.25± 4.52 and 151.60±4.32, respectively). Prevalence of folic acid (ng/ml) insufficiency (&lt;3.8 ng/mL) was 11.5% in total subjects and means of folic acid during the 3 semesters were 11.2± 0.41, 11.0± 0.41 and 9.2±0.41), respectively. Methylmalonic acid levels (umol/L) also showed a highly significant (P &lt; 0.001) differences between the three semesters. The mean MMA levels during the three semesters were 0.130±0.003, 0.142±0.002, and 0.154± 0.003, respectively. Whereas homocysteine (umol/L) showed non-significant (P=0.2085) differences between all trimesters; and their levels were 7.6± 0.45, 8.0± 0.39, and 8.6± 0.42. respectively. Furthermore, Holotranscobalamin also showed non-significant (P=0.883) difference between studied trimesters; and its level during the three trimesters were 137.4± 2.86, 135.1± 3.25 and 137.16± 4.20 pmol/l, respectively. From the total sum, 22.2% of the total pregnant women showed an increased MMA level (more than 0.280 umol/l), and 18.5% of the total participant showed an elevated level of Hcy (more than 15 umol/l). Whereas as only 7.9% of 540 pregnant women showed low level of HoloTc less than 40 pmol/l. From the total cohort, only 7.03% showed combining lowered HoloTc level plus elevated MMA and Hcy level which indicates the manifestation of vitamin B12 deficiency during pregnancy.

Vitamin B12 Deficiency Observed in Children With First Afebrile Seizures.

Objective: Vitamin B12 deficiency can lead to many different types of neurological symptoms and seizure can be seen as the first symptom. In the present study, we aimed to evaluate patients with seizures who were found to have vitamin B12 deficiency and whose seizures resolved with vitamin B12 treatment.Methods: A total of 26 infants were included in this retrospective study. The patients were evaluated in terms of clinical findings, laboratory tests including homocysteine, electrophysiological studies, neuroimaging studies, and other neurological examination findings.Results: Of 26 patients, 14 (53.8%) were male. The mean age of the patients was 8±4.8 months. Sixteen patients had generalized tonic-clonic seizures, and two patients had epileptic spasm (West syndrome)-type seizures. Six patients had abnormal discharge on electroencephalography. Twelve patients had abnormal findings in brain magnetic resonance imaging studies. Homocysteine ​​level was high in all patients at admission.Conclusion: The presence of seizures, including infantile spasm, is a very important and treatable manifestation of vitamin B12 deficiency. Considering the irreversible sequelae of increased homocysteine, vitamin B12 supplementation administered for an appropriate period and at an appropriate dose both prevents the use of unnecessary antiepileptic drugs and eliminates the need for unnecessary tests and examinations.

Analisis Kadar Nrf2 plasma Pada Tikus dengan Defisisensi Vitamin B12

Background. Vitamin B12 deficiency is a significant problem, particularly in developing countries. The increasing complexity of the Vitamin B12 molecule, the deficiency condition, causes a complex cell level disorder. The clinical manifestation of vitamin B12 deficiency is anemia, but it is believed that due to the complexity of vitamin B12, there are still other molecular disorders. This study aims to establish the pathway of damage caused by vitamin B12 deficiency in the Nrf2 molecule.&#x0D; Methods. An animal experiment involving 12 male Sprague Dawley rats were randomly divided into control and 16-week treatment. There are two research groups, namely the control group and the treatment group. The control group was given a standard diet, while the treatment group was assigned a vitamin B12 deficiency diet. At the end of treatment, The levels of vitamin B12 in the liver tissue and plasma NRF2 were measured.&#x0D; Statistical Analysis. Nrf2 and vitamin B12 levels were statistically analyzed using the Student's T-test, and the correlation between vitamin B12 and Hb was analyzed using the Spearmen test. Data that cannot use by Independent T-test were tested using the Mann Whitney test.&#x0D; Results/Conclusion. There was no significant difference between the control and treatment groups on plasma Nrf2 levels (4.02 ± 0.59 pg/ml vs 3.34 ± 0.55 pg/ml; p = 0.07) and tissue vitamin B12 (0.0035 ± 0.0016 µg/ml vs 0.0030 ± 0.0006 µg/ml ; p = 0.8).&#x0D; Keywords: Nrf2 Plasma, Defisiensi, Vitamin B12

Vitamin B12 Deficiency Presenting as Pancytopenia with Hepatosplenomegaly in an Infant

Deficiency of vitamin B12 due to nutritional insufficiency is common in developing part of world. Serum vitamin B12 level in infants is determined by the foetal storage during pregnancy. Therefore, evaluation on vitamin B12 level during pregnancy is essential for prevention of vitamin B12 deficiency in infancy. Here we report a vitamin B12 deficient infant who presented with hepatosplenomegaly with pancytopenia including normocytic anaemia and circulating atypical cells. It is also a reminder to clinicians about the uncommon manifestation of vitamin B12 deficiency which mimics haematological malignancy.

Burning Erythematous Oral Macules as the Presenting Manifestation of Vitamin B12 Deficiency

Burning Erythematous Oral Macules as the Presenting Manifestation of Vitamin B12 Deficiency

Vitamin B12 deficiency as a cause of severe neurological symptoms in breast fed infant \u2013 a case report

BackgroundVitamin B12 (cobalamin, cbl) deficiency in children is rare and may occurs in exclusively breast fed infants of mothers on vegetarian or vegan diet with lack of appropriate supplementation. The clinical manifestation of vitamin B12 deficiency include neurological disorders, megaloblastic anemia and failure to thrive. Routine and commonly used laboratory tests such as cell blood count (CBC) or serum vitamin B12 level are sufficient for appropriate diagnosis. Typical therapy is based on intramuscular cobalamin injections. Early diagnosis and early onset of treatment are crucial factors for long-term prognosis of patients as the duration of deficiency may be correlated with the development of long lasting changes in the nervous system.The purpose of this article is to present influence of maternal vitamin B12 deficiency as a cause of infant psychomotor retardation.Case presentationWe report the case of a 7 months old girl whose parents sought medical advice due to pathological somnolence and developmental regression of their daughter with onset approximately 2 months prior to the visit. Following several diagnostic tests it was determined that the infant’s symptoms were due to vitamin B12 deficiency which was secondary to the mother’s latent Addison-Biermer disease. Apart from neurological symptoms the infant also showed megaloblastic anemia which is typical to cobalamin deficiencies. Intramuscular vitamin B12 supplementation resulted in instant improvement of the patient’s general condition and blood morphology. Unfortunately, psychological examination indicated long-term psychomotor retardation due to delayed diagnosis of B12 deficiency.ConclusionsVitamin B12 levels should be considered during differential diagnosis of neurological symptoms in exclusively breast-fed infants especially if they co-exist with megaloblastic anemia and psychomotor retardation.

Máculas eritematosas urentes orales como manifestación inicial de deficiencia de la vitamina B12

Máculas eritematosas urentes orales como manifestación inicial de deficiencia de la vitamina B12