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Pavlov, Ch S., I. V. Damulin, Yu O. Shulpekova, and E. A. Andreev. "Neurological disorders in vitamin B12 deficiency." Terapevticheskii arkhiv 91, no. 4 (April 15, 2019): 122–29. http://dx.doi.org/10.26442/00403660.2019.04.000116.
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The review discusses thesteps of vitamin B12 metabolism and its role in maintaining of neurological functions. The term "vitamin B12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the peripherу cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as “holotranscobalamin”). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B12 - only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxyadenosylcobalamin (in mitochondria). The main causes of cobalamin deficiency are related to inadequate intake of animal products, autoimmune gastritis, pancreatic insufficiency, terminal ileum disease, syndrome of intestinal bacterial overgrowth. Relative deficiency may be seen in excessive binding of vitamin B12 to transcobalamin I. Cobalamin deficiency most significantly affects functions of blood, nervous system and inflammatory response. Anemia occurs in 13-15% of cases; macrocytosis is an early sign. The average size of neutrophils and monocytes is the most sensitive marker of megaloblastic hematopoiesis. The demands in vitamin B12 are particularly high in nervous tissue. Hypovitaminosis is accompanied by pathological lesions both in white and gray brain matter. Several types of neurological manifestations are described: subacute combined degeneration of spinal cord (funicular myelinosis), sensomotor polyneuropathy, optic nerve neuropathy, cognitive disorders. The whole range of neuropsychiatric disorders with vitamin B12 deficiency has not been studied well enough. Due to certain diagnostic difficulties they are often regarded as "cryptogenic", "reactive", "vascular» origin. Normal or decreased total plasma cobalamin level could not a reliable marker of vitamin deficiency. In difficult cases the content of holotranscobalamin, methylmalonic acid / homocysteine, and folate in the blood serum should be investigated besides carefully analysis of clinical manifestations.
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Shaikh, Shumaila, Azhar Memon, Muhammad Atif Ata, and Haji Khan Khoharo. "COBALAMIN DEFICIENCY." Professional Medical Journal 23, no. 02 (February 10, 2016): 176–81. http://dx.doi.org/10.29309/tpmj/2016.23.02.1064.
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Objectives: The present study aims to evaluate the serum cobalamin inHelicobacter pylori (H. pylori) infected patients. Study Design: Case control study. Place andDuration: Department of Medicine, Isra University Hospital Hyderabad from March 2013- April2014. Methodology: A sample of 109 subjects including Helicobacter pylori positive subjectsand controls were selected according to study criteria. Centrifugation of blood was performedat 4000 rpm for 10 minutes and sera were stored at -20oC. Blood sera were used for H. pyloriserological testing. Blood counting was performed on hematoanalyzer. Cobas e411 analyzerwas used for detection of cobalamin. 64 kD H. pylori antigens was detected by ELISA. Thedata was entered into SPSS version 21.0. (IBM, Incorporation, USA) A 2-tailed p-value of ≤0.05was considered significant for statistical analysis. Results: Of total 109, 54.1% (n=59) wereH. pylori seropositive cases and others were controls i.e. 45.9% (n=50). Cases and controlsshowed cobalamin levels of 290±49.3 vs. 351±32.9 pg/ml respectively (p=0.0001). Red bloodcell indices were found to show statistically significant difference between cases and controls(p=0.001). Conclusion: Serum cobalamin deficiency was noted in both Helicobacter pyloripositive and controls, however deficiency was more pronounced in Helicobacter pylori positivesubjects.
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Norman, E. J., and C. Cronin. "Cobalamin deficiency." Neurology 47, no. 1 (July 1, 1996): 310. http://dx.doi.org/10.1212/wnl.47.1.310.
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Shevell, Michael I., and David S. Rosenblatt. "The Neurology of Cobalamin." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 19, no. 4 (November 1992): 472–86. http://dx.doi.org/10.1017/s0317167100041676.
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ABSTRACT:The following review indicates that the impact of cobalamin on neurologic disease extends far beyond the traditional myelopathy of classical pernicious anemia. The delineation of a broad spectrum of inherited disorders of cobalamin processing has served to illustrate and precisely define each step in the normal absorption, transport and intracellular metabolism of this essential vitamin. Recent clinical work has extended the boundaries of acquired cobalamin deficiency to encompass a variety of neuropsychiatric disturbances without identifiable concomitant hematologic derangements and emphasized the utility and sensitivity of new laboratory tests. These findings will demand increased vigilance from clinicians so that atypical and subtle cobalamin deficiency states will be readily diagnosed. The wide range of neurologic dysfunction observed in both inherited and acquired disorders of cobalamin metabolism challenges basic scientists to delineate cobalamin’s presumed important role in the normal development and homeostasis of the nervous system.
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Carmel, Ralph. "Subclinical cobalamin deficiency." Current Opinion in Gastroenterology 28, no. 2 (March 2012): 151–58. http://dx.doi.org/10.1097/mog.0b013e3283505852.
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Carmel, Ralph. "Subtle Cobalamin Deficiency." Annals of Internal Medicine 124, no. 3 (February 1, 1996): 338. http://dx.doi.org/10.7326/0003-4819-124-3-199602010-00010.
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van Asselt, Dieneke Z. B., Chris M. G. Thomas, Martin F. G. Segers, Henk J. Blom, Ron A. Wevers, and Willibrord H. L. Hoefnagels. "Cobalamin-binding proteins in normal and cobalamin-deficient older subjects." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 40, no. 1 (January 1, 2003): 65–69. http://dx.doi.org/10.1258/000456303321016187.
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Background: The causes of cobalamin (vitamin B12) deficiency in older people are only partly understood. We investigated the role of the cobalamin-binding proteins and tested the hypothesis that low saturated transcobalamin concentration is an early marker of cobalamin deficiency. Methods: We measured saturated (holo) and unsaturated (apo) transcobalamin and haptocorrin concentrations in healthy middle-aged volunteers, healthy older volunteers, cobalamin-deficient older volunteers and cobalamin-deficient older patients. Results: Holo and apo concentrations of transcobalamin and haptocorrin were similar in healthy middle-aged and older subjects. Holotranscobalamin concentrations were significantly decreased in cobalamin-deficient subjects but did not differ between healthy volunteers and patients. Furthermore, the relative amount of cobalamin on transcobalamin (i.e. holotranscobalamin/holotranscobalamin + holohaptocorrin) was similar in all four groups. Conclusions: Abnormalities of the cobalamin-binding proteins are not a cause of cobalamin deficiency in the aged. Plasma holotranscobalamin concentration did not differ between stages of cobalamin deficiency in older persons. Therefore, plasma holotranscobalamin is not an early marker of cobalamin deficiency in older people and has no additional value in the diagnostic work-up of reduced plasma cobalamin concentrations in older people.
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Bolann, Bjørn J., Jan Dag Solli, Jörn Schneede, Kjell A. Grøttum, Arne Loraas, Morgan Stokkeland, Asbjørn Stallemo, et al. "Evaluation of Indicators of Cobalamin Deficiency Defined as Cobalamin-induced Reduction in Increased Serum Methylmalonic Acid." Clinical Chemistry 46, no. 11 (November 1, 2000): 1744–50. http://dx.doi.org/10.1093/clinchem/46.11.1744.
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Abstract Background: Early detection of cobalamin deficiency is clinically important, and there is evidence that such deficiency occurs more frequently than previously anticipated. However, serum cobalamin and other commonly used tests have limited ability to diagnose a deficiency state. Methods: We investigated the ability of hematological variables, serum cobalamin, plasma total homocysteine (tHcy), serum and erythrocyte folate, gastroscopy, age, and gender to predict cobalamin deficiency. Patients (n = 196; age range, 17–87 years) who had been referred from general practice for determination of serum cobalamin were studied. Cobalamin deficiency was defined as serum methylmalonic acid (MMA) >0.26 μmol/L with at least 50% reduction after cobalamin supplementation. ROC and logistic regression analyses were used. Results: Serum cobalamin and tHcy were the best predictors, with areas under the ROC curve (SE) of 0.810 (0.034) and 0.768 (0.037), respectively, but age, intrinsic factor antibodies, and gastroscopy gave additional information. Conclusions: When cobalamin deficiency is suspected in general practice, serum cobalamin should be the first diagnostic test, and the result should be interpreted in relation to the age of the patient. When a definite diagnosis cannot be reached, MMA and tHcy determination will provide additional discriminative information, but MMA, being more specific, is preferable for assessment of cobalamin status.
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Andrès, Emmanuel, Thomas Vogel, Laure Federici, Jacques Zimmer, Ecaterina Ciobanu, and Georges Kaltenbach. "Cobalamin Deficiency in Elderly Patients: A Personal View." Current Gerontology and Geriatrics Research 2008 (2008): 1–7. http://dx.doi.org/10.1155/2008/848267.
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Cobalamin (vitamin B12) deficiency is particularly common in the elderly (>65 years of age) but is often unrecognized because its clinical manifestations are subtle; however, they are also potentially serious, particularly from a neuropsychiatric and hematological perspective. In the elderly, the main causes of cobalamin deficiency are pernicious anemia and food-cobalamin malabsorption. Food-cobalamin malabsorption syndrome is a disorder characterized by the inability to release cobalamin from food or its binding proteins. This syndrome is usually caused by atrophic gastritis, related or unrelated toHelicobacter pyloriinfection, and long-term ingestion of antacids and biguanides. Management of cobalamin deficiency with cobalamin injections is currently well documented but new routes of cobalamin administration (oral and nasal) are being studied, especially oral cobalamin therapy for food-cobalamin malabsorption.
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Rzepka, Zuzanna, Jakub Rok, Mateusz Maszczyk, Artur Beberok, Justyna Magdalena Hermanowicz, Dariusz Pawlak, Dorota Gryko, and Dorota Wrześniok. "Response of Human Glioblastoma Cells to Vitamin B12 Deficiency: A Study Using the Non-Toxic Cobalamin Antagonist." Biology 10, no. 1 (January 19, 2021): 69. http://dx.doi.org/10.3390/biology10010069.
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The most important biological function of vitamin B12 is to accomplish DNA synthesis, which is necessary for cell division. Cobalamin deficiency may be especially acute for rapidly dividing cells, such as glioblastoma cells. Therefore, cobalamin antagonists offer a medicinal potential for developing anti-glioma agents. In the present study, we developed an in vitro model of cobalamin deficiency in glioblastoma cells. Long-term treatment of cells with the cobalamin analogue, hydroxycobalamin [c-lactam] (HCCL) was applied to induce an increase of hypocobalaminemia biomarker. Cytometric assays demonstrated that vitamin B12 promoted glioblastoma cells proliferation, whereas the treatment of cells with HCCL caused a dramatic inhibition of cell proliferation and an induction of cell cycle arrest at the G2/M phase. Vitamin B12 counteracted all the observed effects of HCCL. In the in silico study, we characterized the molecular interactions between HCCL and transcobalamin II (TCII). We have demonstrated that HCCL shares similar interactions with TCII as naturally occurring cobalamins and therefore may act as a competitive inhibitor of this key transporter protein. We assessed the impact of HCCL on the mortality or developmental malformations of zebrafish embryos. Collectively, our findings suggest that the use of cobalamin transport antagonists as potential anti-glioma agents would be worth exploring further.
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Carmel, Ralph. "Mild Transcobalamin I (Haptocorrin) Deficiency and Low Serum Cobalamin Concentrations." Clinical Chemistry 49, no. 8 (August 1, 2003): 1367–74. http://dx.doi.org/10.1373/49.8.1367.
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Abstract Background: Low cobalamin concentrations are common, but their causes are often unknown. Transcobalamin I/haptocorrin (TC I/HC) deficiency, viewed as a rare cause, has not been examined systematically in patients with unexplained low serum cobalamin. Methods: Total TC I/HC was measured by RIA in three subgroups of 367, 160, and 38 patients with different categories of low cobalamin concentrations and three comparison subgroups of 112, 281, and 119 individuals with cobalamin concentrations within the reference interval. Additional studies, including family studies, were done in selected patients found to have low TC I/HC concentrations. Results: Low TC I/HC concentrations suggestive of mild TC I/HC deficiency occurred in 54 of 367 (15%) patients with low cobalamin identified by clinical laboratories and 24 of 160 (15%) patients whose low cobalamin was unexplained after absorption and metabolic evaluation, but in only 2 of 38 patients with malabsorptive causes of low cobalamin concentrations (5%). The prevalence was only 3% (8 of 281 plasma samples) to 5% (6 of 112 sera) in patients with cobalamin concentrations within the reference interval and 3% (4 of 119) in healthy volunteers. Three patients with low cobalamin (0.6%) had severe TC I/HC deficiency with undetectable TC I/HC. Presumptive heterozygotes for severe TC I/HC deficiency in two families had the findings of mild TC I/HC deficiency; mild deficiency was also found in at least three of seven studied families of patients with mild TC I/HC deficiency. Conclusions: Mild TC I/HC deficiency is frequently associated with low cobalamin, is often familial, and its biochemical phenotype appears identical to the heterozygous state of severe TC I/HC deficiency. Severe TC I/HC deficiency also appears to be more common than suspected. Both diagnoses should be considered in all patients with unexplained low serum cobalamin.
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Owens, Julie A., J. S. D. Scott, and W. G. E. Cooksley. "The retention of cobalamin by the liver in the cobalamin-deficient rat." Clinical Science 68, no. 5 (May 1, 1985): 553–60. http://dx.doi.org/10.1042/cs0680553.
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1. The effect of cobalamin deficiency on whole body cobalamin content and its turnover was examined in the rat. Quantitative and qualitative changes in hepatic cobalamin were also followed and the effect of deficiency on the turnover of this cobalamin was determined in the isolated perfused liver. 2. As cobalamin deficiency developed after total gastrectomy, whole body cobalamin content declined at a constant rate, indicating no attempt to conserve total body cobalamin stores even when depleted (5% of normal). 3. In contrast, the cobalamin concentration of liver declined more slowly, indicating conservation of hepatic cobalamin. Furthermore, the methylcobalamin (Me Cbl) content of liver was maintained or even increased. 4. Measurement of the rate of release of cobalamin by the isolated perfused liver at varying times after gastrectomy showed that as depletion of whole body and hepatic cobalamin stores proceeded, the rates of release of hepatic cobalamin into plasma and bile decreased. Regression analysis showed that the fractional rates of release of hepatic cobalamin into plasma (r = 0.9, P < 0.001, n = 15) and bile (r = 0.65, P<0.01, n = 15) were significantly correlated with hepatic cobalamin content. 5. It is concluded that conservation of hepatic cobalamin in deficiency is achieved, at least in part, by a specific decrease in the rate of release of hepatic cobalamin.
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Kaya, Hamza, Tuba Taslamacioglu Duman, Gizem Kahveci, Elif Basaran, and Gulali Aktas. "An Exceptional Case of Cobalamin Deficiency that Presented with Extremely High Indirect Bilirubin Levels." National Journal of Health Sciences 6, no. 3 (December 19, 2022): 140–41. http://dx.doi.org/10.21089/njhs.63.0140.
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Cobalamin deficiency anemia is a type of anemia that present with weakness, fatigue, icteric sclera and neuropathy. Main causes of cobalamin deficiency are low intake or decreased absorption (gastric and intestinal causes). In present case, we report a 65-year-old male who presented to the emergency department with signs and symptoms of cobalamin deficiency including bilateral peripheral neuropathy, icteric skin and sclera, and abdominal pain in right upper quadrant. He had low cobalamin and extremely high bilirubin levels (8mg/dL) in serum. After the diagnosis of cobalamin deficiency established, 1mg daily cobalamin treatment initiated for five days which would follow weekly and monthly intramuscular injections consequently. Hemolysis and other causes of elevated indirect bilirubin levels were excluded in differential diagnosis. Clinical and laboratory improvements were achieved after the treatment. In conclusion, physicians should kept in mind cobalamin deficiency even in subjects with unusual high levels of indirect bilirubin.
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Toresson, Linda, Jan S. Suchodolski, Thomas Spillmann, Bruna C. Lopes, Johnathan Shih, Jörg M. Steiner, and Rachel Pilla. "The Intestinal Microbiome in Dogs with Chronic Enteropathies and Cobalamin Deficiency or Normocobalaminemia—A Comparative Study." Animals 13, no. 8 (April 17, 2023): 1378. http://dx.doi.org/10.3390/ani13081378.
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Cobalamin deficiency is a common sequela of chronic enteropathies (CE) in dogs. Studies comparing the intestinal microbiome of CE dogs with cobalamin deficiency to those that are normocobalaminemic are lacking. Therefore, our aim was to describe the fecal microbiome in a prospective, comparative study evaluating 29 dogs with CE and cobalamin deficiency, 18 dogs with CE and normocobalaminemia, and 10 healthy control dogs. Dogs with cobalamin deficiency were also analyzed after oral or parenteral cobalamin supplementation. Overall microbiome composition (beta diversity) at baseline was significantly different in CE dogs with cobalamin deficiency when compared to those with normocobalaminemia (p = 0.001, R = 0.257) and to healthy controls (p = 0.001, R = 0.363). Abundances of Firmicutes and Actinobacteria were significantly increased (q = 0.010 and 0.049), while those of Bacteroidetes and Fusobacteria were significantly decreased (q = 0.002 and 0.014) in CE dogs with cobalamin deficiency when compared to healthy controls. Overall microbiome composition in follow-up samples remained significantly different after 3 months in both dogs receiving parenteral (R = 0.420, p = 0.013) or oral cobalamin supplementation (R = 0.251, p = 0.007). Because cobalamin supplementation, in combination with appropriate therapy, failed to restore the microbiome composition in the dogs in our study, cobalamin is unlikely to be the cause of those microbiome changes but rather an indicator of differences in underlying pathophysiology that do not influence clinical severity but result in a significant aggravation of dysbiosis.
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Feldman, Sydney, Salman Aljarallah, and Shiv Saidha. "Primary progressive multiple sclerosis to be treated with ocrelizumab: a mistaken case of cobalamin deficiency." BMJ Case Reports 12, no. 5 (May 14, 2019): e229080. http://dx.doi.org/10.1136/bcr-2018-229080.
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Cobalamin (vitamin B12) deficiency often manifests with neurologic symptoms and may rarely mimic multiple sclerosis (MS) among other neurological disorders. However, MRI changes associated with cobalamin deficiency are typically spinal predominant and distinct from MS-related changes. We report a case of a patient with cobalamin deficiency who was recommended by her primary neurologist to commence treatment with ocrelizumab, a potent anti-CD20 B-cell depleting monoclonal antibody, after being diagnosed with primary progressive MS. However, cervical spine MRI demonstrated changes classical of cobalamin deficiency including ‘inverted V sign’ signal hyperintensity and following parenteral cobalamin supplementation her neurological symptoms quickly and dramatically improved.
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Carmel, Ralph, James Parker, and Zvi Kelman. "Mutations of TCN1 Cause Transcobalamin I Deficiency with Low Serum Cobalamin Levels That Are Indistinguishable From Cobalamin Deficiency." Blood 114, no. 22 (November 20, 2009): 1989. http://dx.doi.org/10.1182/blood.v114.22.1989.1989.
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Abstract Abstract 1989 Poster Board I-1011 Low serum cobalamin levels have diverse origins. Indeed, in 21-22% of cases low cobalamin levels do not even reflect cobalamin deficiency, as judged by metabolic criteria, and in most of the rest they reflect subclinical, purely biochemical cobalamin insufficiency. These complicate the interpretation of low cobalamin levels and have engendered controversies. Transcobalamin (TC) I deficiency causes spuriously low cobalamin levels because this binding protein normally carries >70% of the cobalamin in the blood, yet cellular cobalamin status remains normal despite the low plasma cobalamin levels. The entity is often misdiagnosed as cobalamin deficiency and incorrectly treated with cobalamin, and it is thought to be rare. Diagnosis is especially elusive if TC I deficiency is mild. We recently described two TCN1 nonsense mutations, 270delG and 315C>T, in 8 affected members of 3 non-Caucasian families, that caused TC I deficiency that was severe (absence of TC I and very low cobalamin) when both alleles are affected or mild (low plasma TC I and low or low-normal cobalamin) when only one allele was affected (Carmel et al, Br J Haematol, in press). We now describe the new association between TC I deficiency and a TCN1 polymorphism known to be more common in Caucasians. Patients and Methods: Plasma total TC I was assayed by radioimmunassay. TCN1 was sequenced as previously described, using 9 primer sets to sequence each of the 9 exons, in 4 unrelated patients with unexplained low cobalamin levels, in all of whom cobalamin deficiency and malabsorption were ruled out by metabolic and absorption studies. Available relatives were similarly tested. Results: All 4 unrelated propositi with mild TC I deficiency (plasma TC I 87-136 pmol/l, normal 165-454; serum cobalamin 94-155 pmol/l, normal 162-664) were found to be heterozygotes for a 999G>T missense mutation that causes substitution of tyrosine, a large hydrophobic amino acid, for the smaller, negatively charged aspartic acid at position 301. These 4 families of Caucasian ancestry also included 3 relatives with equally mild TC I deficiency (TC I 117-185; cobalamin 111-271), all of whom had the same mutation. In contrast, all 4 relatives with normal TC I levels (TC I 205-367; cobalamin 210-345) had no mutations. Conclusions: The association of heterozygosity for 999G>T with mild TC I deficiency in 7 affected members of 4 Caucasian families and its absence in all 4 unaffected members of these families suggest that this common mutation is responsible for TC I deficiency. It also adheres to the association of heterozygosity for our previously identified TCN1 mutations (270delG and 315C>T) with mild TC I-deficiency. The former occurred in non-Caucasian families, particularly of African ancestry, and were often linked in unexplained, possibly indirect ways with Hemoglobin S. The findings also suggest TCN1 mutational diversity among different ethnic groups. The known preponderance of the 999G>T polymorphism in European subjects is compatible with our ethnic findings. It may also explain why whites have significantly lower cobalamin and TC I levels than do blacks. Finally, the relatively high frequency of 999G>T polymorphism (11.6% + 0.02% heterozygosity frequency; NCBI website) resembles the 15% frequency of mild TC I deficiency reported in a TC I survey that suggested that TC I deficiency is a surprisingly common cause of low serum cobalamin levels and may often be hereditary. These TCN1 mutations should expand the ability to diagnose TC I deficiency, which can be a difficult diagnosis to make because TC I immunoassay is rarely available. They should also allow more reliable study of hereditary TC I deficiency and its frequency as a cause of low cobalamin levels. A better understanding of the entity may help clarify the currently mysterious role of TC I. Disclosures: Carmel: Emisphere Biotechnology: Consultancy; New York Methodist Hopital: Patent application pending on work presented here. Kelman:New York Methodist Hospital: Patent application on work presented here.
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Olson, Sven R., Thomas G. Deloughery, and Jason A. Taylor. "Time to Abandon the Serum Cobalamin Level for Diagnosing Vitamin B12 Deficiency." Blood 128, no. 22 (December 2, 2016): 2447. http://dx.doi.org/10.1182/blood.v128.22.2447.2447.
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Abstract B12 deficiency is a common, reversible cause of macrocytic anemia and neurological symptoms. Suspected B12 deficiency can be evaluated both directly and indirectly using a variety of assays. The serum cobalamin level, despite highly variable sensitivity and specificity, is often the sole test relied upon to diagnose B12 deficiency, despite being influenced by many common medical conditions. B12 levels tend to fall late in deficiency, making it less useful in detecting acute fluctuations in body stores. In addition, assay methodology has proven problematic, with high rates of falsely normal cobalamin levels using newer chemi-luminescent technologies. Most assays also tend to measure total serum cobalamin, notwithstanding the fact that 80% of cobalamin circulates in biochemically inert form. These factors make it difficult to establish thresholds for "normal" serum cobalamin. B12 status exist along a continuous spectrum ranging from subclinically low vitamin concentrations, as observed in vegans who maintain a system of enterohepatic circulation, to fulminant deficiency with severe clinical signs and symptoms. Serum cobalamin <200 pg/mL is a threshold commonly used to delineate true deficiency, though such low levels are infrequently observed. Methylmalonic acid (MMA), a molecular intermediate in a unique metabolic pathway requiring cobalamin as a cofactor, can be also be used to assess B12 status. MMA reflects tissue availability of biochemically active cobalamin rather than total cobalamin, with an excellent sensitivity. Fluctuations in MMA occur rapidly, and are detectable in the setting of subtle neurologic, psychiatric or hematologic signs and symptoms when corresponding serum cobalamin levels may remain normal. False positive MMA can be seen in renal dysfunction, though typically to a far milder degree than true deficiency. To explore the operating characteristics of these serum tests in detecting clinical B12 deficiency, we retrospectively identified all MMAs measured at our institution over the 2015 calendar year and compared any elevated values with corresponding serum cobalamin levels drawn within the same week. 34 of 42 (81%) elevated MMAs were associated with a serum cobalamin level within our laboratory's reference range, and six (14%) of these were actually greaterthan the upper limit of normal. Acknowledging the limited size of our data set, this translates to a 19% sensitivity of serum cobalamin for detecting elevations in MMA and, by extrapolation, detecting clinical B12 deficiency. This sensitivity is far lower than that commonly reported in the literature. Despite the superior test characteristics of MMA, serum cobalamin is often the first and only test performed to evaluate B12 status due to "economic" reasons or force of habit. If only the cobalamin level were relied upon, many patients would go untreated for a curable disease. While the cost difference of serum cobalamin and MMA assays at our hospital ($7.00 and $18.00, respectively) is not negligible, the time and expense of repeated cobalamin measurements or other testing necessary to accurately diagnose B12 deficiency is arguably greater. The mass of accumulated data shows that serum cobalamin is an insensitive assay for B12 deficiency and should be abandoned. MMA is superior for detecting diminished functional B12 stores; increased utilization of this test will result in more accurate and cost-efficient diagnosis of true B12 deficiency. Disclosures Taylor: Baxalta/Shire: Consultancy, Research Funding; Novo Nordisk: Research Funding; Kedrion: Research Funding; CSL Behring: Consultancy, Research Funding.
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Carmel, Ralph. "How I treat cobalamin (vitamin B12) deficiency." Blood 112, no. 6 (September 15, 2008): 2214–21. http://dx.doi.org/10.1182/blood-2008-03-040253.
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Abstract The challenges in medical management of cobalamin deficiency lie in attention to the unique pathophysiology that underlies cobalamin deficiency, more than in the mechanics of therapy. The central physiologic principles are that clinically important deficiency is more likely to occur (and progress) when intrinsic factor–driven absorption fails than when diet is poor and that most causes take years to produce clinically obvious deficiency. Transient defects have little clinical impact. The key management principle is the importance of follow-up, which also requires knowing how the deficiency arose. The virtues of these principles are not always fully appreciated. Recent developments have made diagnosis and management more difficult by diminishing the ability to determine cobalamin absorption status. Clinicians must also grapple with premature medicalization of isolated, mild biochemical changes that added many asymptomatic cases of still undetermined medical relevance to their caseload, often expanded by inflated cobalamin level criteria. The potential for misattribution of cobalamin-unrelated presentations to nongermane cobalamin and metabolite abnormalities has grown. Pathophysiologically based management requires systematic attention to each of its individual components: correctly diagnosing cobalamin deficiency, reversing it, defining its underlying cause, preventing relapse, managing the underlying disorder and its complications, and educating the patient.
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Kurnat-Thoma, Emma L., Faith Pangilinan, Amy M. Matteini, Bob Wong, Ginette A. Pepper, Sally P. Stabler, Jack M. Guralnik, and Lawrence C. Brody. "Association of Transcobalamin II (TCN2) and Transcobalamin II-Receptor (TCblR) Genetic Variations With Cobalamin Deficiency Parameters in Elderly Women." Biological Research For Nursing 17, no. 4 (February 5, 2015): 444–54. http://dx.doi.org/10.1177/1099800415569506.
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Cobalamin (vitamin B12) deficiency is a subtle progressive clinical disorder, affecting nearly 1 in 5 individuals > 60 years old. This deficiency is produced by age-related decreases in nutrient absorption, medications that interfere with vitamin B12 absorption, and other comorbidities. Clinical heterogeneity confounds symptom detection for elderly adults, as deficiency sequelae range from mild fatigue and weakness to debilitating megaloblastic anemia and permanent neuropathic injury. A better understanding of genetic factors that contribute to cobalamin deficiency in the elderly would allow for targeted nursing care and preventive interventions. We tested for associations of common variants in genes involved in cobalamin transport and homeostasis with metabolic indicators of cobalamin deficiency (homocysteine and methylmalonic acid) as well as hematologic, neurologic, and functional performance features of cobalamin deficiency in 789 participants of the Women’s Health and Aging Studies. Although not significant when corrected for multiple testing, eight single nucleotide polymorphisms (SNPs) in two genes, transcobalamin II ( TCN2) and the transcobalamin II-receptor ( TCblR), were found to influence several clinical traits of cobalamin deficiency. The three most significant findings were the identified associations involving missense coding SNPs, namely, TCblR G220R (rs2336573) with serum cobalamin, TCN2 S348F (rs9621049) with homocysteine, and TCN2 P259R (rs1801198) with red blood cell mean corpuscular volume. These SNPs may modify the phenotype in older adults who are more likely to develop symptoms of vitamin B12 malabsorption.
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Kuzminski, Antoinette M., Eric J. Del Giacco, Robert H. Allen, Sally P. Stabler, and John Lindenbaum. "Effective Treatment of Cobalamin Deficiency With Oral Cobalamin." Blood 92, no. 4 (August 15, 1998): 1191–98. http://dx.doi.org/10.1182/blood.v92.4.1191.
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Abstract Because cobalamin deficiency is routinely treated with parenteral cobalamin, we investigated the efficacy of oral therapy. We randomly assigned 38 newly diagnosed cobalamin deficient patients to receive cyanocobalamin as either 1 mg intramuscularly on days 1, 3, 7, 10, 14, 21, 30, 60, and 90 or 2 mg orally on a daily basis for 120 days. Therapeutic effectiveness was evaluated by measuring hematologic and neurologic improvement and changes in serum levels of cobalamin (normal, 200 to 900 pg/mL) methylmalonic acid (normal, 73 to 271 nmol/L), and homocysteine (normal, 5.1 to 13.9 μmol/L). Five patients were subsequently found to have folate deficiency, which left 18 evaluable patients in the oral group and 15 in the parenteral group. Correction of hematologic and neurologic abnormalities was prompt and indistinguishable between the 2 groups. The mean pretreatment values for serum cobalamin, methylmalonic acid, and homocysteine were, respectively, 93 pg/mL, 3,850 nmol/L, and 37.2 μmol/L in the oral group and 95 pg/mL, 3,630 nmol/L, and 40.0 μmol/L in the parenteral therapy group. After 4 months of therapy, the respective mean values were 1,005 pg/mL, 169 nmol/L, and 10.6 μmol/L in the oral group and 325 pg/mL, 265 nmol/L, and 12.2 μmol/L in the parenteral group. The higher serum cobalamin and lower serum methylmalonic acid levels at 4 months posttreatment in the oral group versus the parenteral group were significant, with P < .0005 and P < .05, respectively. In cobalamin deficiency, 2 mg of cyanocobalamin administered orally on a daily basis was as effective as 1 mg administered intramuscularly on a monthly basis and may be superior. © 1998 by The American Society of Hematology.
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Kuzminski, Antoinette M., Eric J. Del Giacco, Robert H. Allen, Sally P. Stabler, and John Lindenbaum. "Effective Treatment of Cobalamin Deficiency With Oral Cobalamin." Blood 92, no. 4 (August 15, 1998): 1191–98. http://dx.doi.org/10.1182/blood.v92.4.1191.416k15_1191_1198.
Full textAbstract:
Because cobalamin deficiency is routinely treated with parenteral cobalamin, we investigated the efficacy of oral therapy. We randomly assigned 38 newly diagnosed cobalamin deficient patients to receive cyanocobalamin as either 1 mg intramuscularly on days 1, 3, 7, 10, 14, 21, 30, 60, and 90 or 2 mg orally on a daily basis for 120 days. Therapeutic effectiveness was evaluated by measuring hematologic and neurologic improvement and changes in serum levels of cobalamin (normal, 200 to 900 pg/mL) methylmalonic acid (normal, 73 to 271 nmol/L), and homocysteine (normal, 5.1 to 13.9 μmol/L). Five patients were subsequently found to have folate deficiency, which left 18 evaluable patients in the oral group and 15 in the parenteral group. Correction of hematologic and neurologic abnormalities was prompt and indistinguishable between the 2 groups. The mean pretreatment values for serum cobalamin, methylmalonic acid, and homocysteine were, respectively, 93 pg/mL, 3,850 nmol/L, and 37.2 μmol/L in the oral group and 95 pg/mL, 3,630 nmol/L, and 40.0 μmol/L in the parenteral therapy group. After 4 months of therapy, the respective mean values were 1,005 pg/mL, 169 nmol/L, and 10.6 μmol/L in the oral group and 325 pg/mL, 265 nmol/L, and 12.2 μmol/L in the parenteral group. The higher serum cobalamin and lower serum methylmalonic acid levels at 4 months posttreatment in the oral group versus the parenteral group were significant, with P < .0005 and P < .05, respectively. In cobalamin deficiency, 2 mg of cyanocobalamin administered orally on a daily basis was as effective as 1 mg administered intramuscularly on a monthly basis and may be superior. © 1998 by The American Society of Hematology.
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Norman, E. J. "Screening for cobalamin deficiency." Archives of Family Medicine 4, no. 4 (April 1, 1995): 304a—305. http://dx.doi.org/10.1001/archfami.4.4.304a.
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Yao, Y. "Screening for cobalamin deficiency." Archives of Family Medicine 4, no. 4 (April 1, 1995): 305. http://dx.doi.org/10.1001/archfami.4.4.305.
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Menachem, Yoram, Amos M. Cohen, and Moshe Mittelman. "Cobalamin deficiency and infertility." American Journal of Hematology 46, no. 2 (June 1994): 152. http://dx.doi.org/10.1002/ajh.2830460219.
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Hagelskjaer, L., and K. Rasmussen. "Methylmalonic Acid Concentration in Serum Not Affected in Hepatic Disease." Clinical Chemistry 38, no. 4 (April 1, 1992): 493–95. http://dx.doi.org/10.1093/clinchem/38.4.493.
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Abstract Accumulation of methylmalonic acid may provide an early clue to deficiency of cobalamin (vitamin B12) in tissue. Metabolic abnormalities involving precursors of methylmalonic acid are frequently observed in patients with hepatic diseases. To establish whether methylmalonic acid accumulates and thereby gives false-positive test results for cobalamin deficiency, we measured the concentration of methylmalonic acid in serum of patients with various hepatic diseases. Many of the patients had increased concentrations of cobalamin in serum. In serum from 70 patients, the mean concentration of methylmalonic acid (252, SE 25 nmol/L) did not differ significantly from that found in healthy subjects (211, SE 12 nmol/L). We conclude that the assay of methylmalonic acid in serum may be useful for evaluating cobalamin status in hepatic disease with functional cobalamin deficiency despite an artificially increased normal or high concentration of cobalamin in serum.
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Tazi Mezalek, Zoubida, Wafaa Ammouri, Mouna Maamar, Meriem Bourkia, Hicham Harmouche, Mohammed Adnaoui, Meryem Alaoui, and Nisrine Bouigua. "Vitamine B12 Deficiency Presenting As Severe Pancytopenia in Adult Patients. a Monocentric Study of 104 Cases." Blood 128, no. 22 (December 2, 2016): 4812. http://dx.doi.org/10.1182/blood.v128.22.4812.4812.
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Abstract Vitamin B12 deficiency should be suspected in all patients with unexplained anemia and/or neuropsychiatric symptoms, and special attention should be paid to patients at risk (the elderly, vegetarians, patients with autoimmune thyroiditis or vitiligo, patients receiving proton pump inhibitors or biguanides for prolonged periods). Documented symptomatic pancytopenia related to cobalamin deficiency is very rare representing less than 5% cases in different series. We aim to report an important series of pancytopenia related to cobalamin deficiency to analyze the clinical, biological and outcomes of those patients. Methods : Consecutive patients presented with B12 deficiency and pancytopenia were included. Charts were retrospectively reviewed from an internal medicine department during a period of 15 years (2000-2015). Diagnosis of cobalamine deficiency used the vitamin B12 dosage bellow 200 pg/ml. Assessment included clinical features, blood count and morphological review and a statistical analysis of those parameters comparing pancytopenic and non-pancytopenic patients. Results The medical records of 268 consecutive patients hospitalized for cobalamin deficiency from January 2000 to December 2015 were identified and retrospectively analyzed. Among them, 104 patients had pancytopenia (38.8%). The median age was 55+17 years and the sex ratio : 1. Pancytopenia revealed vitamin B12 deficiency in all cases. Neurological manifestations were associated in 13 cases and digestive involvement in 16 cases. Twenty five patients presented with febrile neutropenia. Fourteen patients (13.4%) presented with "pseudo" thrombotic microangiopathy. The mean hemoglobin level was 58+19 g/L, the neurtophils count was 1188+579/µl and median platelets count was 69.616+34.379/µl. Macrocytosis was present in 80.7% of patient with mean MCV was 106+11 fl, but was normal (<95 fl) in 20 patients. The mean serum vitamine B12 levels was 80+11 pg/ml. The median serum lactate dehydrogenase level was high (3.204 IU/L). The causes of B12 vitamin deficiency were mainly food cobalamin malabsorption (63.4%) and pernicious anemia (28.8%). Correction of the hematological abnormalities was achieved in all patients treated with either intramuscular, subcutaneous or oral cyanocobalamin. Significant differences appears comparing patients with or without pancytopenia. Pancytopenic patients had significantly lower MCV mean (p=0.001), lower polynuclear neutrophils count and lower platelets count. Atrophic gastritis was also significantly associated with pancytopenia (p=0.005). There was no significant difference in mean haemoglobin level (p=0.3), serum cobalamin level (p=0.17). Looking at other variables that could explain the high prevalence of pancytopenia in our series, there were no difference in ferritinemia level or number of patients with of iron deficiency . Conclusion In this study, based a single institution with a large number of consecutive patients with well-documented cobalamin deficiency, we found a high prevalence (38,8%) of severe pancytopenia. We don't find yet an explanation for those findings. Those results can also remind us that severe vitamin B12 deficiency may present with findings mimicking malign hematologic disorder and timely recognition and supplementation lead to resolution of symptoms and blood abnormalities. Disclosures No relevant conflicts of interest to declare.
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Babu, Reshma, Mohamed Yasir. H, and Bincy Babu. "A Brief Review on the Association of Prolonged Metformin Therapy and Vitamin B12 Deficiency." International Journal of Research and Review 10, no. 6 (June 20, 2023): 415–23. http://dx.doi.org/10.52403/ijrr.20230652.
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Type 2 Diabetes Mellitus is a fast-growing health challenge, signaled by hyperglycemia. There are two types of diabetes mellitus, Type 1 and Type 2; both are equally life threatening condition. Type 1 diabetes is a persistent autoimmune disease as a consequence of insulin deficiency, whereas in Type 2 diabetes the body either does not produce enough insulin or develops resistance to insulin. Metformin is the exclusive pharmacologic management for Type 2 diabetes mellitus and frequently prescribed drug either single or in combination with insulin or other hypoglycemic agents. Metformin has immensely improved insulin sensitivity and defend against vascular complications. Vitamin B 12 (cobalamin) has a vital role in DNA synthesis, cellular metabolism and the deficiency will lead to megaloblastic anemia. Several studies state that metformin can cause cobalamin deficiency in doses greater than 2000 mg/ day and for a time period of more than 4 years. Hence, cobalamin and calcium supplementation will reduce the occurrence of cobalamin deficiency in patients with metformin therapy. Keywords: Type 2 diabetes mellitus, Metformin, Vitamin B 12, Vitamin B 12 deficiency, Cobalamin.
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Rasmussen, K., L. Moelby, and M. K. Jensen. "Studies on methylmalonic acid in humans. II. Relationship between concentrations in serum and urinary excretion, and the correlation between serum cobalamin and accumulation of methylmalonic acid." Clinical Chemistry 35, no. 12 (December 1, 1989): 2277–80. http://dx.doi.org/10.1093/clinchem/35.12.2277.
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Abstract Methylmalonic acid (MMA) concentrations are increased in cobalamin (vitamin B12) deficiency, but the relative diagnostic usefulness of determination of MMA in serum vs urine has not yet been assessed. We obtained urine collections and matched serum samples from 28 healthy volunteers and from 20 consecutive patients admitted for clinical and hematological evaluation because of low cobalamin concentrations in serum. Increased concentrations of MMA in serum were found in 12 patients, in all of whom a clinical diagnosis of cobalamin deficiency was established. By contrast, cobalamin deficiency was excluded in seven of the eight remaining patients, who all had normal MMA concentrations. Here we report that linear relationships exist between MMA concentrations in serum (investigated range: 0.05-34.2 mumol/L) and MMA concentrations in urine (r = 0.74), concentrations relative to creatinine (r = 0.98), and MMA excretion rates (r = 0.97) (P less than 0.001 in each instance). Our data are consistent with glomerular filtration and passive reabsorption of MMA by the tubules. We demonstrate, for the first time, a negative correlation between concentrations of cobalamin and MMA in serum in clinical cobalamin deficiency (r = -0.69; P less than 0.01; n = 12); when the values for MMA were log transformed, the correlation with cobalamin was much better (r = -0.84; P less than 0.0005).
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Ibarrola, Patricia, Laura Blackwood, Peter A. Graham, Helen Evans, and Alexander J. German. "Hypocobalaminaemia is uncommon in cats in the United Kingdom." Journal of Feline Medicine and Surgery 7, no. 6 (December 2005): 341–48. http://dx.doi.org/10.1016/j.jfms.2005.02.001.
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Recent work has highlighted the importance of cobalamin deficiency in cats with a range of alimentary tract diseases. The primary aim of our study was to determine the incidence of subnormal cobalamin concentrations in sick cats with and without alimentary system disorders. Firstly, serum cobalamin concentrations were measured in a population of cats, with and without gastrointestinal (GI) disease, evaluated at a referral hospital. In the second part of the study, the incidence of cobalamin deficiency was assessed in samples submitted to a commercial laboratory specifically for cobalamin measurement. For both studies, a validated radioimmunoassay was used to measure serum cobalamin concentrations (reference range: >150 pg/ml). In the first part of the study, 132 cats were included and none of these cats had subnormal cobalamin concentrations (median=1172; range: 278 to >2000). There were no differences in cobalamin concentrations between cats with alimentary system disorders, and those with diseases of other organs. In the second part, 682 samples were submitted for cobalamin assay over a period of 3 years, and only one cat had a result below the reference range (median=794; range: 147 to >2000). Cobalamin deficiency was rare in the population tested and this may suggest that the incidence of this biochemical abnormality is less common than reported in the USA.
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Lane, Lenee A., and Carlos Rojas-Fernandez. "Treatment of Vitamin B12–Deficiency Anemia: Oral versus Parenteral Therapy." Annals of Pharmacotherapy 36, no. 7-8 (July 2002): 1268–72. http://dx.doi.org/10.1345/aph.1a122.
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OBJECTIVE: To evaluate the use of oral cyanocobalamin therapy in the treatment of cobalamin (vitamin B12)–deficient anemia. DATA SOURCES: Primary and review articles were identified by MEDLINE search (1966–May 2000) and through secondary sources. DATA SYNTHESIS: Cobalamin-deficient anemia is among the most common diagnoses in older populations. Cobalamin-deficient anemia may be diagnosed as pernicious anemia, resulting from the lack of intrinsic factor required for cobalamin absorption or as protein malabsorption from the inability to displace cobalamin from protein food sources. Several studies provide evidence that daily oral cyanocobalamin as opposed to monthly parenteral formulations may adequately treat both types of cobalamin-deficient anemias. CONCLUSIONS: Daily oral cyanocobalamin at doses of 1000–2000 μg can be used for treatment in most cobalamin-deficient patients who can tolerate oral supplementation. There are inadequate data at the present time to support the use of oral cyanocobalamin replacement in patients with severe neurologic involvement.
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Lutz, Sabina, Adrian C. Sewell, Claudia E. Reusch, and Peter H. Kook. "Clinical and Laboratory Findings in Border Collies with Presumed Hereditary Juvenile Cobalamin Deficiency." Journal of the American Animal Hospital Association 49, no. 3 (May 1, 2013): 197–203. http://dx.doi.org/10.5326/jaaha-ms-5867.
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Juvenile cobalamin deficiency is a rare disease in border collies and its diagnosis requires a high level of clinical suspicion. The goal of this study was to increase awareness of this disease by describing the clinical and laboratory findings in four young border collies with inherited cobalamin deficiency. The median age of the dogs was 11.5 mo (range, 8–42 mo), and two of the four dogs were full siblings. Clinical signs included intermittent lethargy (n = 4), poor body condition (n = 4), odynophagia (n = 2), glossitis (n = 1), and bradyarrhythmia (n = 1). Pertinent laboratory abnormalities were mild to moderate normocytic nonregenerative anemia (n = 3), increased aspartate aminotransferase (AST) activity (n = 3), and mild proteinuria (n = 3). All of the dogs had serum cobalamin levels below the detection limit of the assay, marked methylmalonic aciduria, and hyperhomocysteinemia. Full clinical recovery was achieved in all dogs with regular parenteral cobalamin supplementation, and laboratory abnormalities resolved, except the proteinuria and elevated AST activity persisted. This case series demonstrates the diverse clinical picture of primary cobalamin deficiency in border collies. Young border collies presenting with ambiguous clinical signs should be screened for cobalamin deficiency.
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Cherdak, M. A., and E. A. Mkhitaryan. "Vitamin B12 Deficiency in Neurological Disorders of Older Adults: Etiology, Diagnostics, Treatment." Russian Journal of Geriatric Medicine, no. 2 (June 30, 2024): 100–107. http://dx.doi.org/10.37586/2686-8636-2-2024-100-107.
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One of the common problems associated with aging is vitamin B12 (cobalamin) deficiency. According to some reports, it is present in every third person over the age of 60. Cobalamin is involved in numerous biologically important reactions, and its deficiency manifests itself in a range of disorders, including hematological and gastrointestinal symptoms, as well as pathology in various parts of the nervous system. The article discusses clinical variants of neurological disorders related to vitamin B12 deficiency, such as damage to both the peripheral and the central nervous systems. The relationship between cobalamin deficiency and the development of cognitive and other neuropsychiatric disorders in older individuals is discussed. Data on specific causes of vitamin B12 deficiencies in older individuals, including iatrogenic factors, are presented. Modern approaches to the diagnosis and correction of cobalamin deficiency are outlined, taking into account the characteristics of the geriatric population.
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Khera, Sanjeev, Suman Kumar Pramanik, and Saroj Kumar Patnaik. "Transcobalamin deficiency: vitamin B12 deficiency with normal serum B12 levels." BMJ Case Reports 12, no. 10 (October 2019): e232319. http://dx.doi.org/10.1136/bcr-2019-232319.
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Transcobalamin (TC) deficiency is a rare autosomal recessive inborn error of cobalamin transport which clinically manifests in early infancy. We describe a child with TC deficiency who presented with classical clinical and lab stigmata of inborn error of vitamin B12 metabolism except normal serum B12 levels. He was started on empirical parenteral cobalamin supplements at 2 months of age; however, the definitive diagnosis could only be established at 6 years of age when a genetic evaluation revealed homozygous nonsense variation in exon 8 of the TCN2 gene (chr22:g.31019043C>T).
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Khan, Salman, Javaria Amil, Husnain Hashim, Amanullah Khokhar, Dur E. Huma, and Tahir Mukhtar Syed. "Frequency of Vitamin Cobalamin Deficiency in Macrocystic Anemia Cases Reporting at Tertiary Care Hospital." Pakistan Journal of Medical and Health Sciences 16, no. 6 (June 30, 2022): 1074–76. http://dx.doi.org/10.53350/pjmhs221661074.
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Objective: The purpose of this study is to determine the frequency of vitamin cobalamin deficiency in macrocystic anemia cases reporting at tertiary care Hospital. Study Design: Cross-sectional Place and Duration: In Medicine department of DHQ Teaching Hospital, Sargodha and DHQ Hospital, Dera Ismail Khan for the duration of six months from August 2021 to January 2022. Methods: Total 210 cases of macrocytic anemia of both genders with ages 18-62 years were presented. Age, sex, and body mass index were among the specific demographics of the enrolled cases that were documented after receiving informed written consent. Ante-cubital fossa blood was sampled for 5 mL. To estimate the amount of vitamin cobalamin using an ELISA test kit, samples were centrifuged and sera were collected. SPSS 24.0 was used to analyze all data. Results: Among 210 cases, 130 (61.9%) were males and 80 (38.1%) females in this study. 70 (33.3%) cases had ages 18-35 years, 90 (42.9%) had ages 36-50 years and 50 (23.9%) had ages >50 years. Mean BMI of the presented cases was 24.66±14.49 kg/m2. We found that 180 (85.7%) patients had deficiency of cobalamin and 30 (14.3%) cases had normal cobalamin. Among 180 cases of cobalamin deficiency, 70 (38.9%) patients were severe, border line was found in 45 (25%) cases and deficient cases were 65 (36.1%). Conclusion: We concluded in this study that patients with macrocystic anemia had higher number of vitamin cobalamin deficiency found in 85.7% cases. Majority of the patients were deficient and had severe deficiency of cobalmin. Keywords: Vitamin Cobalamin, Macrocystic Anemia, Severe Deficiency
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Kotilea, Kallirroi, Stefanie Quennery, Valérie Decroës, and Dominique A. Hermans. "Successful Sublingual Cobalamin Treatment in a Child with Short-Bowel Syndrome." Journal of Pediatric Pharmacology and Therapeutics 19, no. 1 (January 1, 2014): 60–63. http://dx.doi.org/10.5863/1551-6776-19.1.60.
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Vitamin B12 (B12) is essential for deoxyribonucleic acid synthesis, to maintain normal hematologic and neurologic functions. Studies suggest that cobalamin deficiency in children is more common than previously recognized. Main causes are decreased intake, abnormal absorption, and inborn errors of metabolism. The classic treatment for cobalamin deficiency is intramuscular administration of B12. There are no data concerning the use of alternative routes of cobalamin administration in children. This report shares the experience of sublingual administration of B12 to a patient with short-bowel syndrome and B12 malabsorption. We report the case of successful treatment of cobalamin deficiency by sublingual administration in a 9-year-old patient who had undergone intestinal resection and jejunum-colon, with anastomosis of 32 cm of residual small intestine and absence of distal jejunum and ileocecal junction. We determined a B12 deficiency because low serum cobalamin levels (<200 pg/mL) were shown in 2 consecutive tests (130 pg/mL and 170 pg/mL). The patient presented with neither clinical nor hematological manifestations. He received sublingual cobalamin preparation, 1000-mcg sublingual nuggets per day for 1 month. Normalization of serum cobalamin was obtained (790 pg/mL) after 1 month of treatment. The sublingual route of administration not only improved the quality of life of this patient by avoiding monthly painful injections but also reduced the cost of treatment and the number of hospital visits.
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Rzepka, Zuzanna, Jakub Rok, Justyna Kowalska, Klaudia Banach, and Dorota Wrześniok. "Cobalamin Deficiency May Induce Astrosenescence—An In Vitro Study." Cells 11, no. 21 (October 28, 2022): 3408. http://dx.doi.org/10.3390/cells11213408.
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Cobalamin (vitamin B12) deficiency is one of the major factors causing degenerative changes in the nervous system and, thus, various neurological and psychiatric symptoms. The underlying cellular mechanism of this phenomenon is not yet fully understood. An accumulation of senescent astrocytes has been shown to contribute to a wide range of pathologies of the nervous system, including neurodegenerative disorders. This study aimed to investigate whether cobalamin deficiency triggers astrosenescence. After inducing cobalamin deficiency in normal human astrocytes in vitro, we examined biomarkers of cellular senescence: SA-β-gal, p16INK4A, and p21Waf1/Cip1 and performed cell nuclei measurements. The obtained results may contribute to an increase in the knowledge of the cellular effects of cobalamin deficiency in the context of astrocytes. In addition, the presented data suggest a potential causative agent of astrosenescence that has not been proven to date.
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Memon, Azhar, Abdul Raqeeb, Mona Humaira, and Haji Khan Khoharo. "TYPE 2 DIABETICS." Professional Medical Journal 23, no. 06 (June 10, 2016): 641–45. http://dx.doi.org/10.29309/tpmj/2016.23.06.1599.
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Objectives: To evaluate serum cobalamin with special reference to dyslipidemiain type 2 Diabetic subjects. Study Design: Observational study Place and Duration:Department of Medicine, Isra University Hyderabad, Sindh from January 2014 to July 2014.Methodology: A sample of 107 type 2 diabetic subjects was selected according to inclusionand exclusion criteria. Cobalamin was measured on Roche Cobas e411 chemistry analyzerand blood lipoproteins by standard laboratory methods. Data was analyzed by SPSS 21.0(IBM, Incorporation, USA) using student t and Chi square tests for continuous and categoricalvariables respectively. P-value of ≤ 0.05 was taken significant. Results: Cobalamin deficiencywas noted in 51 (47.6%) of diabetics and cobalamin deficiency was associated withdyslipidemia. Mean ± SD of cobalamin in normal and reduced cobalamin groups were notedas 355±29.5 and 183±17.5 pg/ml respectively (p=0.0001). Triglycerides, total cholesterol,HDLc, LDLc and VLDLc differed significantly in the normal and reduced cobalamin subjects(p<0.001). Lipoprotein sub fractions showed a negative correlation with serum cobalamin(p≤0.02). Conclusion: Cobalamin deficiency is common in type 2 diabetics and is associatedwith dyslipidemia.
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Achebe, Maureen M., and Anat Gafter-Gvili. "How I treat anemia in pregnancy: iron, cobalamin, and folate." Blood 129, no. 8 (February 23, 2017): 940–49. http://dx.doi.org/10.1182/blood-2016-08-672246.
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AbstractAnemia 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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Hølleland, Geir, Jørn Schneede, Per Magne Ueland, Per Kristian Lund, Helga Refsum, and Sverre Sandberg. "Cobalamin Deficiency in General Practice. Assessment of the Diagnostic Utility and Cost-Benefit Analysis of Methylmalonic Acid Determination in Relation to Current Diagnostic Strategies." Clinical Chemistry 45, no. 2 (February 1, 1999): 189–98. http://dx.doi.org/10.1093/clinchem/45.2.189.
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Abstract Diagnosing cobalamin deficiency is often difficult. We investigated the diagnostic strategies that 224 general practitioners used to assess cobalamin status and the criteria on which they based their decisions to supplement patients. From all serum cobalamin analyses carried out at a single laboratory during 1993, individuals with serum cobalamin concentrations <300 pmol/L were identified, and one patient per general practitioner was included. When serum methylmalonic acid (s-MMA) values >0.376 μmol/L were used as the “reference standard” for cobalamin deficiency, the serum cobalamin assay had a diagnostic sensitivity of 0.40 and a specificity of 0.98. With the same reference standard, the diagnostic accuracy of the physicians’ decision to supplement patients had the same specificity but a higher sensitivity (0.51). Cost-benefit analysis indicated that measurement of s-MMA can be recommended in patients with serum cobalamin >60–90 pmol/L and <200–220 pmol/L, depending on its diagnostic accuracy.
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Nexø, Ebba, Mads Hansen, Karsten Rasmussen, Anders Lindgren, and Ralph Gräsbeck. "How to diagnose cobalamin deficiency." Scandinavian Journal of Clinical and Laboratory Investigation 54, sup219 (January 1994): 61–76. http://dx.doi.org/10.3109/00365519409088580.
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Marchi, Giacomo, Fabiana Busti, Acaynne Lira Zidanes, Alice Vianello, and Domenico Girelli. "COBALAMIN DEFICIENCY IN THE ELDERLY." Mediterranean Journal of Hematology and Infectious Diseases 12, no. 1 (June 28, 2020): e2020043. http://dx.doi.org/10.4084/mjhid.2020.043.
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Older people are at risk for cobalamin (vitamin B12) deficiency because of a number of common disorders (e.g. autoimmune gastritis) and drugs (e.g. antacids) that may alter its absorption and utilization. The prevalence of cobalamin deficiency increases with age, resulting particularly elevated in frail and institutionalized subjects. At variance with common sense, the diagnosis is far from simple and requires a high degree of suspicion, due to heterogeneity and non-specificity of the signs and symptoms, ranging from macrocytosis (with or without anemia) to neuropsychiatric manifestations, that characterize several other aging-related disorders, like hematological malignancies, diabetes, hypothyroidism or vasculopathies. Furthermore, the detection of low levels of serum vitamin B12 appears poorly sensitive and specific. Other biomarkers, like serum homocysteine or methylmalonic acid, have improved the diagnostic possibilities but are expensive, not widely available and may be influenced by some confounders (e.g. folate deficiency, or chronic renal failure). Early recognition and treatment are crucial, since a proportion of patients develop severe complications, such as bone marrow failure and irreversible neurological impairment. High-dose oral treatment has proven to be as effective as the parenteral route even in subjects with malabsorption, ensuring the complete resolution in the majority of cases. In this review, we trace the essential role of cobalamin in humans, the possible causes and impact of deficiency, the diagnostic challenges and the therapeutic options, between old and emerging concepts, with a particular focus on the elderly.
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Carmel, Ralph. "Current Concepts in Cobalamin Deficiency." Annual Review of Medicine 51, no. 1 (February 2000): 357–75. http://dx.doi.org/10.1146/annurev.med.51.1.357.
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Machado, Raquel, Filipa Furtado, Paula Kjöllerström, and Florbela Cunha. "Cutaneous hyperpigmentation and cobalamin deficiency." British Journal of Haematology 174, no. 6 (July 19, 2016): 834. http://dx.doi.org/10.1111/bjh.14242.
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Drinka, Paul, and Ralph Carmel. "Cobalamin Deficiency in the Elderly." Journal of the American Geriatrics Society 41, no. 8 (August 1993): 891–92. http://dx.doi.org/10.1111/j.1532-5415.1993.tb06201.x.
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Winston, Julia L., and Jonathan T. Stewart. "ORAL THERAPY FOR COBALAMIN DEFICIENCY." Journal of the American Geriatrics Society 48, no. 8 (August 2000): 1021–22. http://dx.doi.org/10.1111/j.1532-5415.2000.tb06908.x.
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Chatterjee, A., R. Yapundich, C. A. Palmer, D. C. Marson, and G. W. Mitchell. "Leukoencephalopathy associated with cobalamin deficiency." Neurology 46, no. 3 (March 1, 1996): 832–34. http://dx.doi.org/10.1212/wnl.46.3.832.
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Bodamer, Olaf AF, and Fernando Scaglia. "Sublingual therapy for cobalamin deficiency." Lancet 354, no. 9189 (October 1999): 1562. http://dx.doi.org/10.1016/s0140-6736(05)76599-5.
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Healton, Edward B., David G. Savage, John C. M. Brust, T. J. Garrett, and John Lindenbaum. "Neurologic Aspects of Cobalamin Deficiency." Medicine 70, no. 4 (July 1991): 229–45. http://dx.doi.org/10.1097/00005792-199107000-00001.
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Ray, J. G. "Cobalamin deficiency in elderly patients." Canadian Medical Association Journal 172, no. 4 (February 15, 2005): 448–50. http://dx.doi.org/10.1503/cmaj.1041365.
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Wetterberg, S. P. "Cobalamin deficiency in elderly patients." Canadian Medical Association Journal 172, no. 4 (February 15, 2005): 450. http://dx.doi.org/10.1503/cmaj.1041367.
Full text