Vitamin B12 deficiency and gastric histopathology in older patients

AIM: To compare upper gastric endoscopic and histopathologic findings in older adults in the presence and absence of B12 deficiency.METHODS: A prospective analysis of upper gastric endoscopic and gastric histopathologic findings from 30 newly identified B12-deficient patients (11 males,19 females) and 16 controls with normal B12 status (6males, 10 females) was performed. For all subjects, the indication for upper endoscopy and gastric biopsy were unrelated to B12 status. A single pathologist, blinded to B12 status, processed and interpreted the biopsy samples. Endoscopic and histopathologic findings were correlated with age, gender, hematocrit (Hct), MCV and B12 status.RESULTS: The B12-deficient group had significantly lower mean serum B12 levels compared to the controls (P＜0.00005) while their mean Hct, MCV and serum albumin levels were similar. Iron deficiency (ferritinbased) was present in 21% of B12-deficient patients and intrinsic factor antibodies were present in29% (5/17) of B12-deficient patients. The endoscopic findings revealed significantly different rates of gastritis and atrophy between the B12-deficient and control groups (P= 0.017).B12-deficient patients had significantly less superficial gastritis (62% vs 94%) and significantly more atrophic gastritis (28% vs 0%) as compared to the controls (P= 0.039). Intestinal metaplasia was similar in both groups. Helicobacter pyloriinfection rates were similar in the B12-deficient patients and controls (40% vs31%).CONCLUSION: Significantly different endoscopic findings and types of gastritis could often be observed in the presence and absence of B12 deficiency. Atrophy,based on endoscopy, and atrophic gastritis, based on histopathology, suggest the presence of B12 deficiency.Gastric histopathology is not influenced by the age,gender, Hct or MCV of the patients.

Vitamin B12 deficiency in dialysis patients:risk factors,diagnosis,complications,and treatment:A comprehensive review

Vitamin B12 deficiency is a significant concern among patients with end-stage renal disease undergoing dialysis.However,there hasn’t been extensive research conducted on this particular patient group.The reported incidence rates vary widely,ranging from 20%to 90%,reflecting the complexity of its diagnosis.Dialysis patients often face multiple nutritional deficiencies,including a lack of essential vitamins,due to factors such as dietary restrictions,impaired absorption,and nutrient loss during dialysis.Diagnosing vitamin B12 deficiency in these patients is challenging,and addressing it is crucial to prevent complications and improve their overall quality of life.This review paper delves into the available body of evidence on vitamin B12 deficiency in dialysis patients,examining the contributing risk factors,diagnostic challenges,potential complications,and available treatment options.It provides a well-rounded perspective on the topic,making it a valuable resource for researchers,healthcare practitioners,and policymakers interested in addressing the nutritional needs of dialysis patients.

The Impact of Third Trimester Maternal Serum Vitamin B12 and Folate Status on Fetal Birth Weight. Is Maternal Serum Homocysteine a Predictor of Low Birth Weight Infants?

Objective: The aim of this study is to evaluate vitamin B12, folate, and homocysteine status in pregnant women in the third trimester of pregnancy and their relationship to fetal birth weight and their correlation to corresponding neonatal cord blood levels, and in addition, to evaluate the possibility of maternal serum homocysteine level as a predictor of low birth weight infants. Subjects and Methods: In this cross-sectional study, a total of two hundred pregnant women in third trimester (≥28 weeks) were recruited. After a detailed obstetrical and medical history, and clinical assessment, participants were subdivided into two groups: Group (A)—pregnant women who delivered average birth weight (ABW) infants and Group (B) for those who delivered low birth weight (LBW) infants between completed 37 and 42 weeks. Results: Vitamin B12 deficiency was observed in 24.1% of the total cohort. The mean vitamin B12 level was significantly lower in group (B) compared to group (A) (195.2 ± 38.9 vs. 225.9 ± 66.59 respectively P = 0.008). The mean level of homocysteine for women in group (B) was significantly higher than those determined from women in group (A) (9.10 ± 5.9 vs. 7.6 ± 3.83 respectively, P = 0.042). On the other hand, the mean folate levels showed statistically insignificant differences between both groups. The mean cord vitamin B12 level was significantly lower in LBW infants in comparison to ABW infants (277 ± 61.93 vs. 312.03 ± 81.87 respectively, P = 0.015), while the mean level of cord homocysteine for LBW infants was significantly higher than those levels determined from ABW infants (7.9 ± 3.79 vs. 6.6 ± 2.09 respectively P = 0.0049). Conclusion: Maternal micronutrients particularly cobalamin deficiency could be significant risk for LBW infants. Hyperhomocysteinemia has been shown to be a predictor for adverse pregnancy outcomes particularly LBW.

Influence of folic acid and vitamin B12 combined therapy on plasma Hcy, inflammatory factor levels and blood vessels endothelial function in patients with vascular dementia and type H hypertension

Objective:To investigate influence of folic acid and vitamin B12 combined therapy on plasma homocysteine (Hcy) level, blood vessels endothelial function and inflammatory factors in patients with vascular dementia and type H hypertension.Methods:100 cases of patients with vascular dementia and type H hypertension accorded with the inclusion criteria were selected as research objects. They were randomly divided as the control group and the therapeutic group, 50 cases each. For control group, Enalapril tablets were administered by mouth for treatment. For therapeutic group, folic acid and vitamin B12 treatment were provided on the basis of treatment for control group. Treatments were continued for 12 weeks. Plasma Hcy levels, inflammatory factors [(interleukin-6 (IL-6), interleukin-8 (IL-8) and hypersensitive C reaction protein (hs-CRP)], blood vessels endothelial function indexes variation in patients before and after treatment were observed and detected.Results:Plasma Hcy, IL-6, IL-8 and hs-CRP levels in two groups of patients after treatment were significantly decreased comparing with the same group before treatment, and the above index levels in therapeutic group after treatment were significantly lower than control group (P<0.05);For comparison of blood vessels endothelial function indexes in the patients, NO levels in two groups after treatment were increased in various degrees, and endothelin-1 (ET-1) were decreased. The differences between levels of the two indexes in therapeutic group before and after treatment were significant, and levels after treatment in therapeutic group were significantly better than in control group (P<0.05). While variations of the differences in control group before and after treatment were not significant (P>0.05);After treatment, diastolic pressure and systolic pressure in the two groups of patients were significantly improved comparing with before treatment (P<0.05). However, after treatment, the differences of levels between therapeutic group and control group were not significant (P>0.05). MMSE score in therapeutic group after treatment was significantly higher than before treatment, and significantly higher than in control group (P<0.05).Conclusions: Combined therapy of folic acid and vitamin B12 for treating vascular dementia with type H hypertension could effectively decrease plasma Hcy and inflammatory factor levels, and improve blood vessels endothelial function and dementia degree on patients. It has certain clinical value which deserves to be promoted.

Effects of folic acid and vitamin B12 adjuvant therapy on serum inflammatory cytokines, Hcy and NT-proBNP in elderly patients with coronary heart disease and chronic heart failure

Objective:To investigate the effect of folic acid combined with vitamin B12 supplementation with conventional drugs on the levels of serum inflammatory factors, Hcy and NT-proBNP in elderly patients with chronic heart failure.Methods:89 elderly patients with chronic heart failure were randomly divided into control group (n=47) and observation group (n=42) based on the random data table. The control group was given diuretics, ACEI andβ receptor inhibitor group of three categories of drugs combined treatment, on this basis, the observation group supplemented by folic acid tablets and vitamin B12 treatment, both groups were treated for 8 weeks. The levels of TNF-α, hs-CRP and visfatin, Hcy and NT-proBNP were measured before and after treatment in both groups.Results: There was no significant difference in TNF-α, hs-CRP, visfatin, Hcy and NT-proBNP between the control group and the observation group before treatment. After treatment, the levels of TNF-α, hs-CRP, visfatin, Hcy and NT-proBNP in the two groups decreased significantly ,the difference was significant, the level of the above indexes of the observation group after treatment was significantly lower than that of the control group ,the difference was statistically significant.Conclusion: Folic acid combined with vitamin B12 can reduce the levels of serum inflammatory factors, Hcy and NT-proBNP in elderly patients with coronary heart disease and heart failure, which has certain clinical value.

Serum Vitamin B12 and Homocysteine Levels in Type 2 Diabetic Patients with and without Metformin Therapy

Background: Vitamin B12 (cobalamin) is an essential micronutrient necessary for DNA methylation and plays role in lipid metabolic reactions. Metformin is the first therapeutic choice for T2DM management. Prolonged use of metformin causes vitamin B12 deficiency due to poor absorption by interfering with calcium-based vitamin B12 absorption. Vitamin B12 deficiency leads to elevated homocysteine levels. The aim of this study was to evaluate serum vitamin B12 and homocysteine levels in type 2 diabetic patients with and without metformin therapy. Methods: A cross-sectional study was conducted on two hundred and thirty diabetic patients (180 males and 50 females). Their ages ranged from (30 - 60 years) living in Saudia Arabia at Al-Madinah Al-Monawarah. Patients were selected at outpatients clinics of Islamic University Medical Center during follow up at internal medicine and endocrinology clinic. The included patients were diagnosed with type 2 diabetes mellitus according to American Diabetes Association (ADA) Criteria. The included patients were categorized into two groups according to treatment with metformin drug. Laboratory measurements included serum level of vitamin B12, serum total homocysteine, serum fasting glucose and serum folate. Blood EDTA samples were used to measure HbA1c and MCV. Neurological examinations were performed to detect presence of peripheral neuropathy using Toronto Clinical Neuropathy Score (TCSS), which is a validated and reliable scale for the diagnosis and staging of diabetic polyneuropathy. Results: There were no statistical differences between the two groups as regard (age, sex, smoking, weight, BMI, systolic blood pressure, diastolic blood pressure, fasting blood glucose, Folate and MCV). There were statistical differences between the two groups as regard (duration of diabetes, duration of metformin therapy, dose of metformin, Serum homocystein and HbA1c). The mean of vitamin B12 (pg/mL) of group 1 (312.65 ± 92.28) was lower than that of group 2 (381.55 ± 88.04). In group 1 number of patients with normal vitamin B12 was 116 out of 150 (77.3%) and number of patients with deficient vitamin B12 was 34 out of 150 (22.7%). In group 2 number of patients with normal vitamin B12 was 72 out of 80 (90%) and number of patients with deficient vitamin B12 was 8 out of 80 (10%). Regarding neuropathy;in group 1 113 patients (75.3%) had no neuropathy, 24 patients (16%) had mild neuropathy and 13 patients (8.7%) had moderate neuropathy. In group 2, 71 patients (88.8%) had no neuropathy, 7 patients (8.7%) had mild neuropathy and 2 patients (2.5%) had moderate neuropathy. In conclusion, in our study, the prevalence of vitamin B12 deficiency was higher in metformin users than in non-metformin users. There was an association between vitamin B12 deficiency and the dose and duration of metformin use. There was also an increase in homocysteine level due to vitamin B12 deficiency. Therefore, we recommend routine screening for serum vitamin B12 and homocysteine in individuals with T2DM who take daily metformin doses higher than 2000 mg, or for a duration exceeding 4 years.

Relationship of serum folic acid and vitamin B12 contents with maternal endothelial injury and placental ischemia hypoxia in patients with preeclampsia

Objective:To investigate the relationship of serum folic acid and vitamin B12 contents with maternal endothelial injury and placental ischemia hypoxia in patients with preeclampsia. Methods:A total of 76 puerperae with preeclampsia who gave birth in this hospital between March 2016 and October 2017 were selected as the preeclampsia group, and 100 healthy puerperae who gave birth in this hospital during the same period were selected as the normal control group. The differences in serum contents of folic acid, vitamin B12, endothelial injury indexes and oxidative stress indexes were compared between the two groups 24 h before delivery. Pearson test was used to assess the intrinsic relationship of serum folic acid and vitamin B12 contents with the disease severity in puerperae with preeclampsia.Results:Serum folic acid and vitamin B12 contents of preeclampsia group were lower than those of control group;endothelial injury markers sEng, sFlt-1, ET-1 and TM contents were higher than those of control group whereas ADM content was lower than that of control group;oxidative stress indexes AOPPs and LHP contents were higher than those of normal control group whereas T-AOC content was lower than that of control group. The Pearson test showed that serum folic acid and vitamin B12 contents in puerperae with preeclampsia were directly correlated with vascular endothelial injury and placental ischemia hypoxia.Conclusion: There is folic acid and vitamin B12 deficiency in patients with preeclampsia, and it can aggravate the vascular endothelial injury and placental ischemia hypoxia.

Effects of donepezil combined with folic acid and vitamin B12 on serum levels of inflammatory factors, HCY, NSE and neurotransmitters in elderly patients with Alzheimer's disease complicated with hyperhomocysteinemia

Objective: To investigate the effects of donepezil combined with folic acid and vitamin B12 on the levels of serum inflammatory factors, Hcy, NSE and neurotransmitters in elderly patients with Alzheimer's disease (AD) complicated with hyperhomocysteinemia. Methods: A total of 98 elderly patients with AD complicated with hyperhomocysteinemia were randomly divided into control group (n=48) and observation group (n=50) according to the random data table method. Patients in the control group were treated with donepezil. On this basis, the patients in the observation group were treated with folic acid and vitamin B12, all patients were treated for 3 months. Before and after treatment, the levels of serum inflammatory factors (TNF-α, IL-6 and hs-CRP), Hcy, NSE and brain neurotransmitter (5-HT, NE and DA) were compared between the two groups. Results: Before treatment, the levels of TNF-α, IL-6, hs-CRP, Hcy, NSE, 5-HT, NE and DA of the control group and the observation group were not statistically significant. Compared with the group before treatment, the levels of TNF-α, IL-6, hs-CRP, Hcy and NSE in the two groups were significantly lower, and the level of the observation group was significantly lower than those of the control group, the difference was statistically significant;Compared with the group before treatment, the levels of 5-HT, NE and DA in the two groups were significantly increased, and the observation group was significantly higher than that of the control group, the difference was statistically significant. Conclusion: Donepezil combined folic acid and vitamin B12 in treatment of AD with hyperhomocysteinemia, which can effectively reduce the body's inflammatory response, reduced Hcy and NSE levels, elevated levels of brain neurotransmitters, has important clinical significance.

Correlation of folic acid, vitamin B12 and homocysteine metabolism with lipid levels and inflammatory response in patients with cerebral infarction

Objective:To study the correlation of folic acid, vitamin B12 and homocysteine metabolism with lipid level and inflammatory response in patients with cerebral infarction.Methods:86 patients with cerebral infarction treated in our hospital between January 2015 and June 2016 were collected as cerebral infarction group and 70 healthy subjects receiving physical examination in our hospital during the same period were selected as normal control group. Immediately after admission, RIA method was used to detect peripheral blood folic acid, Vit12 and Hcy levels;automatic biochemical analyzer was used to determine lipid level;enzyme-linked immunosorbent assay (ELISA) was used to detect serum inflammatory factor levels. Results:Serum folic acid and VitB12 levels of cerebral infarction group were lower than those of normal control group while Hcy level was higher than that of normal control group (P<0.05);serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein A1 (ApoA1) levels of cerebral infarction group were higher than those of normal control group while high-density lipoprotein cholesterol (HDL-C) level was lower than that of normal control group (P<0.05);serum interleukin-4 (IL-4) and interleukin-10 (IL-10) levels of cerebral infarction group were lower than those of normal control group while interleukin-8 (IL-8), C-reactive protein (CRP) and tumor necrosis factorα (TNF-α) levels were higher than those of normal control group (P<0.05). The Spearman correlation analysis showed that the folic acid, VitB12 and Hcy levels in patients with cerebral infarction were directly correlated with lipid levels and inflammatory response.Conclusions:Folic acid, vitamin B12 and homocysteine metabolism can directly affect the lipid levels and inflammatory response in patients with cerebral infarction, and are the reliable indexes to early judge the disease severity and guide clinical treatment.

Effects of adjuvant folic acid + vitamin b12 therapy on Hcy metabolism, neurotrophy and nerve injury in patients with Alzheimer's disease

Objective: To explore the effects of adjuvant folic acid + vitamin b12 therapy on Hcy metabolism, neurotrophy and nerve injury in patients with Alzheimer's disease (AD). Methods:A total of 104 patients with Alzheimer's disease were divided into control group (n=52) and study group (n=52) by random number table. Control group received clinical routine treatment, and study group received routine treatment combined with adjuvant folic acid and vitamin b12 therapy. The differences in Hcy metabolism, neurotrophy and nerve injury were compared between the two groups before and after treatment. Results: Before treatment, there was no statistically significant difference in serum contents of Hcy, neurotrophy indexes and nerve injury indexes between the two groups. After 3 months of treatment, serum Hcy of study group was lower than that of control group;serum neurotrophy indexes nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), glial cell-derived neurotrophic factor (GDNF), insulin-like growth factor 1 (IGF-1) and insulin-like growth factor 2 (IGF-2) contents were higher than those of control group;serum nerve injury indexes myelin basic protein (MBP), neuron-specific enolase (NSE), neurofilament heavy (NfH) and S100 calcium-binding protein B (S100B) contents were lower than those of control group. Conclusion: Adjuvent folic acid and vitamin b12 therapy can effectively reduce Hcy content, increase neurotrophy and relieve nerve injury in patients with Alzheimer's disease.

Role of vitamin B12 deficiency in ischemic stroke risk and outcome

Currently,ischemic stroke is the most prevalent form of stroke compared to hemorrhagic and there is a high incidence in older adults.Nutrition is a modifiable risk factor for stroke.B-vitamins are part of a metabolic network that integrates nutritional signals with biosynthesis,redox homeostasis,and epigenetics.These vitamins play an essential role in the regulation of cell proliferation,stress resistance,and embryo development.A deficiency in vitamin B12 is common in older adults and has been reported to be implicated in ischemic stroke.The aim of this review was to investigate whether vitamin B12 deficiencies impact the risk and outcome of ischemic stroke.Clinical data from our literature review strongly suggest that a deficiency in vitamin B12 is a risk factor for ischemic stroke and possible outcome.Our survey of the literature has identified that there is a gap in the understanding of the mechanisms through which a vitamin B12 deficiency leads to an increased risk of stroke and outcome.A vitamin B12 deficiency can increase homocysteine levels,which are a well-established risk factor for ischemic stroke.Another potential mechanism through which vitamin B12 deficient may impact neurological function and increase risk of stroke,is changes in myelination,however this link requires further investigation.Further studies are required in model systems to understand how a vitamin B12 deficiency changes the brain.

Vitamin B complex and vitamin B12 levels after peripheral nerve injury

The aim of the present study was to evaluate whether tissue levels of vitamin B complex and vitamin B12 were altered after crush-induced peripheral nerve injury in an experimental rat model. A total of 80 male Wistar rats were randomized into one control（n = 8） and six study groups（1, 6, 12, 24 hours, 3, and 7 days after experimental nerve injury; n = 12 for each group）. Crush-induced peripheral nerve injury was performed on the sciatic nerves of rats in six study groups. Tissue samples from the sites of peripheral nerve injury were obtained at 1, 6, 12, 24 hours, 3 and 7 days after experimental nerve injury. Enzyme-linked immunosorbent assay results showed that tissue levels of vitamin B complex and vitamin B12 in the injured sciatic nerve were significantly greater at 1 and 12 hours after experimental nerve injury, while they were significantly lower at 7 days than in control group. Tissue level of vitamin B_（12） in the injured sciatic nerve was significantly lower at 1, 6, 12 and 24 hours than in the control group. These results suggest that tissue levels of vitamin B complex and vitamin B12 vary with progression of crush-induced peripheral nerve injury, and supplementation of these vitamins in the acute period may be beneficial for acceleration of nerve regeneration.

Long-term metformin therapy and vitamin B12 deficiency: An association to bear in mind

To date,metformin remains the first-line oral glucose-lowering drug used for the treatment of type 2 diabetes thanks to its well-established long-term safety and efficacy profile.Indeed,metformin is the most widely used oral insulinsensitizing agent,being prescribed to more than 100 million people worldwide,including patients with prediabetes,insulin resistance,and polycystic ovary syndrome.However,over the last decades several observational studies and meta-analyses have reported a significant association between long-term metformin therapy and an increased prevalence of vitamin B12 deficiency.Of note,evidence suggests that long-term and high-dose metformin therapy impairs vitamin B12 status.Vitamin B12(also referred to as cobalamin)is a water-soluble vitamin that is mainly obtained from animal-sourced foods.At the cellular level,vitamin B12 acts as a cofactor for enzymes that play a critical role in DNA synthesis and neuroprotection.Thus,vitamin B12 deficiency can lead to a number of clinical consequences that include hematologic abnormalities(e.g.,megaloblastic anemia and formation of hypersegmented neutrophils),progressive axonal demyelination and peripheral neuropathy.Nevertheless,no definite guidelines are currently available for vitamin B12 deficiency screening in patients on metformin therapy,and vitamin B12 deficiency remains frequently unrecognized in such individuals.Therefore,in this“field of vision”article we propose a list of criteria for a cost-effective vitamin B12 deficiency screening in metformin-treated patients,which could serve as a practical guide for identifying individuals at high risk for this condition.Moreover,we discuss additional relevant topics related to this field,including:(1)The lack of consensus about the exact definition of vitamin B12 deficiency;(2)The definition of reliable biomarkers of vitamin B12 status;(3)Causes of vitamin B12 deficiency other than metformin therapy that should be identified promptly in metformin-treated patients for a proper differential diagnosis;and(4)Potential pathophysiological mechanisms underlying metformin-induced vitamin B12 deficiency.Finally,we briefly review basic concepts related to vitamin B12 supplementation for the treatment of vitamin B12 deficiency,particularly when this condition is induced by metformin.

Folate and vitamin B12 in idiopathic male infertility

Although methylenetetrahydrofolate reductase, a folate enzyme gene, has been associated with idiopathic male infertility, few studies have examined other folate-related metabolites and genes. We investigated whether idiopathic male infertility is associated with variants in folate, vitamin B12 （B12） and total homocysteine （tHcy）-related genes and measured these metabolites in blood. We conducted a case-control study that included 153 men with idiopathic infertility and 184 fertile male controls recruited at the Fertility Center and Antenatal Care Center, University Hospital, Malmo and Lund, Sweden. Serum folate, red cell folate （RCF）, serum B12, plasma tHcy and semen quality were measured. Subjects were genotyped for 20 common variants in 12 genes related to folate/B12/ homocysteine metabolism. Metabolite concentrations and genotype distributions were compared between cases and controls using linear and logistic regression with adjustment for covariates. The phosphatidylethanolamine N-methyltransferase （PEMT） M 175V and TCblR rs173665 polymorphisms were significantly associated with infertility （P=0.01 and P=0.009, respectively）, but not with semen quality. Among non-users of supplements, infertile men had lower serum folate concentrations than fertile men （12.89 vs. 14.73 nmoll^- 1 P=0.02）, but there were no significant differences in RCF, B 12 or tHcy. Folate, B 12 and tHcy concentrations were not correlated with any semen parameters. This study provides little support for low folate or B12 status in the pathogenesis of idiopathic male infertility. Although additional data are needed to confirm these initial findings, our results suggest that PEMTand TCbIR, genes involved in choline and B12 metabolism, merit further investigation in idiopathic male infertility.

Association between metformin and vitamin B12 deficiency in patients with type 2 diabetes

Diabetes mellitus(DM)is still one of the most common diseases worldwide,and its prevalence is still increasing globally.According to the American and European recommendations,metformin is considered a first-line oral hypoglycemic drug for controlling type 2 DM(T2DM)patients.Metformin is the ninth most often prescribed drug in the world,and at least 120 million diabetic people are estimated to receive the drug.In the last 20 years,there has been increasing evidence of vitamin B12 deficiency among metformin-treated diabetic patients.Many studies have reported that vitamin B12 deficiency is related to the malabsorption of vitamin B12 among metformin-treated T2DM patients.Vitamin B12 deficiency may have a very bad complication for the T2DM patient.In this review,we will focus on the effect of metformin on the absorption of vitamin B12 and on its proposed mechanisms in hindering vitamin B12 absorption.In addition,the review will describe the clinical outcomes of vitamin B12 deficiency in metformintreated T2DM.

Neurological Manifestations of Vitamin B12 Deficiency: About a Case

The authors report a case of deficient sensory neuropathy secondary to vitamin B12 deficiency, diagnosed in the neurology department of the Sino-Central African Friendship University Hospital in Bangui. The diagnosis was made possible by electroneuromyography which showed subclinical neurological damage associated with hematological damage (anemia). Through this observation, we recall the diagnostic criteria of the disease in a context of difficult medical practice. .

Determination of Vitamin B12 Using Differential Pulse Polarography

Vitamin B12 is a type of vitamin also known by the name cobalamin. B12 is involved in many metabolism activities, including DNA synthesis, nervous system, red blood formation and immune system. Therefore, we chose the Differential Pulse Polarography (DPP) method is that has a high sensitivity for the determination of vitamin B12. This determination was possible with cobalt present in vitamin B12 structure. Since Co(III) is formed from the oxidation of the vitamin, its polarographic behavior had to be determined in various electrolytes such as acetate, borate, phosphate and ammonia. The polarograms of Co(III) were taken in these electrolytes in which 1.0 M NH3/ (pH = 9.8) and 1.0 M AcOH/AcO- (pH = 4.0) were found as the most suitable electrolytes. This method was successfully applied vitamin of B12 determination in a 1 mL ampoule with high precision. The LOD was found as 3.7 × 10-7 for instead of (S/N = 3). Besides Co(III), interference effects of Zn(II), Ni(II), Cr(III), Fe(III), Cu(II), Cd(II) and Se(IV) were also studied. It was found that only Zn(II) peak had an overlap Co(III) peak in ammonium buffer. This problem could be solved by working in 1.0 M AcOH/AcO- (pH = 4.0) buffer. B12, which is 1000 μg in 1 mL vitamin ampoule, was found for 4 measurements as 999 ± 15 μg as a result of 95% confidence interval.

Hcy相关酶基因MS A2756G、MTRR A66G多态性及Vitamin B12与脑梗死相关性的临床探讨

目的探讨同型半胱氨酸(Hcy)相关酶基因甲硫氨酸合成酶(methioninesynthase,MS)基因A2756G和甲硫氨酸合成酶还原酶(MTRR)基因A66G多态性对维生素B12和Hcy代谢的影响以及与脑梗死的关系,为寻找脑血管病易感基因提供理论依据。方法选取2014年2月-2016年2月在中日友好医院神经内科确诊为急性脑梗死患者100例作为病例组,选取同期的健康体检者100例为对照组,检测血浆Hcy水平和维生素B12的水平,聚合酶链反应-限制片段长度多态性(PCR-RFLP)技术分析基因型的多态性。在维生素B12干预试验中,100例急性脑梗死患者随机分为两组,每组50例,在常规治疗的基础上,试验组予以每天摄入0.5～1 mg维生素B12,而非试验组不服用,1 w后,检测患者血浆中Hcy指标。结果病例组血浆中Hcy的水平明显高于对照组;MS 2756AG、2756GG、MTRR 66AG、66GG型研究对象血浆中Hcy水平明显高于MS 2756AA、MTRR 66AA型研究对象;两组研究对象MS A2756G和MTRR A66G的基因型频率分布有显著性差异;病例组血浆中维生素B12的水平明显低于对照组,血浆中维生素B12的水平与Hcy的水平呈显著负相关;腺苷钴胺干预可明显降低脑梗死患者血浆中的Hcy水平。结论 MS基因A2756G突变和MTRR基因A66G突变是血浆中Hcy升高的重要因素,与脑梗死密切相关,可作为诊断和治疗的分子靶标;腺苷钴胺干预治疗可降低脑梗死患者血浆中Hcy水平。

Correlation between serum vitamin B12 level and peripheral neuropathy in atrophic gastritis

AIM To explore the correlation between serum vitamin B12 level and peripheral neuropathy in patients with chronic atrophic gastritis(CAG). METHODS A total of 593 patients diagnosed with chronic gastritis by gastroscopy and pathological examination fromSeptember 2013 to September 2016 were selected for this study. The age of these patients ranged within 18-to 75-years-old. Blood pressure, height and weight were measured in each patient, and the body mass index value was calculated. Furthermore, gastric acid, serum gastrin, serum vitamin and serum creatinine tests were performed, and peripheral nerve conduction velocity and Helicobacter pylori(H. pylori) were detected. In addition, the type of gastritis was determined by gastroscopy. The above factors were used as independent variables to analyze chronic gastritis with peripheral neuropathy and vitamin B12 deficiency risk factors, and to analyze the relationship between vitamin B12 levels and peripheral nerve conduction velocity. In addition, in the treatment of CAG on the basis of vitamin B12, patients with peripheral neuropathy were observed. RESULTS Age, H. pylori infection, CAG, vitamin B9 and vitamin B12 were risk factors for the occurrence of peripheral nerve degeneration.Furthermore,CAG and H. pylori infection were risk factors for chronic gastritis associated with vitamin B12 deficiency. Serum vitamin B12 level was positively correlated with sensory nerve conduction velocity in the tibial nerve(R = 0.463). After vitamin B12 supplementation, patients with peripheral neuropathy improved. CONCLUSION Serum vitamin B12 levels in patients with chronic gastritis significantly decreased, and the occurrence of peripheral neuropathy had a certain correlation. CAG and H. pylori infection are risk factors for vitamin B12 deficiency and peripheral neuropathy. When treating CAG, vitamin B12 supplementation can significantly reduce peripheral nervous system lesions. Therefore, the occurrence of peripheral neuropathy associated with vitamin B12 deficiency may be considered in patients with CAG. Furthermore, the timely supplementation of vitamin B12 during the clinical treatment of CAG can reduce or prevent peripheral nervous system lesions.

Methylmalonic acid as an indicator of vitamin B12 deficiency in patients on metformin

Context: Metformin is frequently prescribed for the treatment of type 2 diabetes mellitus. It is recommended as a first line agent by the American Diabetes Association. Vitamin B12 deficiency has been suggested as a side effect of metformin therapy;however, previous studies have not assessed the utility of methylmalonic acid levels as an indicator of vitamin B12 status. Objective: To investigate the prevalence of vitamin B12 deficiency in patients on metformin therapy for diabetes by utilizing both vitamin B12 and methylmalonic acid levels. Design, Setting, and Patients: Eighty-eight patients with diabetes, who were either on or off metformin therapy for at least thirty days, were enrolled in a case-controlled study. Blood work and questionnaires were used for analysis. Main Outcome Measures Study: Aims were to detect a clinically significant difference in the prevalence of vitamin B12 deficiency between metformin users and non-users, where such deficiency is defined by both low vitamin B12 and elevated methylmalonic acid levels. Results: Two Sample Equal Variance T-Tests were used to compare averages of measured values and the Chisquare test was used to determine the significance of calculated vitamin B12 deficiency rates between the two groups of patients. Two separate methods for defining vitamin B12 deficiency were utilized. There was no difference in the prevalence of vitamin B12 deficiency in metformin users compared with non-users by either method. Average homocysteine levels were higher in those not on metformin therapy. Conclusion: Vitamin B12 deficiency as defined by an elevated methylmalonic acid level was no greater in patients with diabetes on metformin therapy versus those patients not on metformin treatment.