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. .

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.

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.

Impact of increasing one-carbon metabolites on traumatic brain injury outcome using pre-clinical models

Traumatic brain injury is a major cause of death and disability worldwide,affecting over 69 million individuals yearly.One-carbon metabolism has been shown to have beneficial effects after brain damage,such as ischemic stroke.However,whether increasing one-carbon metabolite vitamins impacts traumatic brain injury outcomes in patients requires more investigation.The aim of this review is to evaluate how one-carbon metabolites impact outcomes after the onset of traumatic brain injury.PubMed,Web of Science,and Google Scholar databases were searched for studies that examined the impact of B-vitamin supplementation on traumatic brain injury outcomes.The search terms included combinations of the following words:traumatic brain injury,dietary supplementation,one-carbon metabolism,and B-vitamins.The focus of each literature search was basic science data.The year of publication in the literature searches was not limited.Our analysis of the literature has shown that dietary supplementation of B-vitamins has significantly improved the functional and behavioral recove ry of animals with traumatic brain injury compared to controls.Howeve r,this improvement is dosage-dependent and is contingent upon the onset of supplementation and whether there is a sustained or continuous delive ry of vitamin supplementation post-traumatic brain injury.The details of supplementation post-traumatic brain injury need to be further investigated.Overall,we conclude that B-vitamin supplementation improves behavioral outcomes and reduces cognitive impairment post-traumatic brain injury in animal model systems.Further investigation in a clinical setting should be stro ngly considered in co njunction with current medical treatments for traumatic brain injury-affected individuals.

Association of Serum Folate and Vitamin B_(12) Concentrations with Obesity in Chinese Children and Adolescents

Objective This study aimed to evaluate the associations of serum folate and/or vitamin B12 concentrations with obesity among Chinese children and adolescents.Methods A cross-sectional study was conducted including 3,079 Chinese children and adolescents,aged 6 to 17 years,from Jiangsu,China.Anthropometric indices,such as,children's body mass index(BMI),BMI z-scores,waist circumference,and waist-to-height ratio were utilized.Multivariable linear regression and generalized additive models were used to investigate the associations of serum folate and vitamin B12 levels with anthropometric indices and odds of obesity.Results We observed that serum vitamin B12 concentrations were inversely associated with all anthropometric indices and the odds of general obesity[odds ratio(OR)=0.68;95%confidence interval(CI)=0.59,0.78]and abdominal obesity(OR=0.68;95%CI=0.60,0.77).When compared to participants with both serum vitamin levels in the two middle quartiles,those with both serum folate and vitamin B12 levels in the highest quartile were less prone to general(OR=0.31,95%CI=0.19,0.50)or abdominal obesity(OR=0.46,95%CI=0.31,0.67).Conversely,participants with vitamin B12 levels in the lowest quartile alongside folate levels in the highest quartile had higher odds of abdominal obesity(OR=2.06,95%CI=1.09,3.91).Conclusion Higher serum vitamin B12 concentrations,but not serum folate concentrations,were associated with lower odds of childhood obesity.Children and adolescents with high levels of vitamin B12 and folate were less likely to be obese.

BIERMER’s Disease: About 4 Cases Diagnosed at Regional University Hospital of Ouahigouya (Chur/Ohg) and Literature Review

Megaloblastic pernicious anemia is an autoimmune disorder, considered rare in African context. The objective of this study was to report four clinical cases collected at the CHUR/OHG, and to review the literature. The study population consisted of two men and two women. The clinical manifestations were mainly neurological and hematological. The neurological signs were mainly paresthesia. One patient presented memory problems. On the biological level, macrocytic anemia and vitamin B12 deficiency were reported in two cases prior to treatment while the other two without serological assay of vitamin B12 were put on trial treatment. Anti-intrinsic factor antibodies were positive in three patients. The Schilling test was not used. Upper gastrointestinal endoscopy revealed atrophic fundic gastritis in all four patients who received treatment through intramuscular injection of hydroxocobalamin (vitamin B12). The evolution was favorable after one month of treatment in all cases. The literature review is dominated by clinical case reports, the largest cohorts of which are from the Maghreb.

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.

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.

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.

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.

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.

Effect of vitamin B12 deficiency anemia on peripapillary retinal nerve fiber layer

AIM:To evaluate the effect of vitamin B12 deficiency anemia(BDA)on peripapillary retinal nerve fiber layer thickness(RNFLT)using spectral domain optical coherence tomography(SD-OCT),and to determine any correlation arising thereof.METHODS:In this cross-sectional observational study,99 eyes of 50 BDA patients of age 18-65 y were compared with 100 eyes of 50 healthy control subjects.All subjects underwent comprehensive clinical,ophthalmic,and hematological evaluation,followed by peripapillary RNFLT assessment using SD-OCT.RESULTS:The mean total,inferior,nasal,and temporal RNFLT were significantly lower in BDA group as compared to control group(P<0.05).The mean total,inferior and nasal RNFLT correlated significantly(P<0.05)with serum Hb%,B12 and mean corpuscular volume(MCV)level(r=0.310,0.435,-0.386 for total;r=0.932,0.481,-0.513 for inferior;r=0.344,0.254,-0.233 for nasal;respectively),while temporal and superior RNFLT quadrant did not show any correlation with any of the hematological parameters(r=0.144,0.167,-0.096;r=0.111,0.070,-0.099;respectively).The mean total RNFLT showed progressive thinning at par with the progression of anemia,except in very severe BDA,where an inverse relationship was documented.CONCLUSION:The mean total,inferior,nasal,and temporal peripapillary RNFLT was significantly thinner in BDA patients.Peripapillary RNFLT thinning seemed to proceed at par with the progression of severity of anemia,except in very sever grade.Early assessment of peripapillary RNFLT may be crucial in BDA patients to prevent potential blinding sequelae.Peripapillary RNFLT thinning in BDA patients should be considered in the differential diagnosis of other non-glaucomatous optic neuropathies,as well.

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.

Effects of ethanol and sex on propionate metabolism evaluated via a faster ^(13)C-propionate breath test in rats

BACKGROUND Alcoholism is regarded as a risk factor for vitamin B_(12)(VB_(12))deficiency.Because V B_(12) serves as a coenzyme of methylmalonyl-CoA mutase,a key enzyme in propionate metabolism,the ^(13)C-propionate breath test(PBT)has been studied as a non-invasive diagnostic modality for VB_(12) deficiency.However,the conventional PBT requires 2 h,which is inconvenient in clinical practice.We hypothesized that a faster PBT can be used to evaluate propionate metabolism and is more easily adaptable for clinical practice.AIM To evaluate a faster PBT for assessing the effects of long-term ethanol consumption on propionate metabolism in ethanol-fed rats(ERs).METHODS ERs were obtained by replacing standard drinking water(for control rats,CRs)with 16%ethanol solution in descendants of F344/DuCrj rats.Faster PBT was performed by administering ^(13)C-propionate aqueous solution to male and female ERs and CRs by inserting a metal tubule from the mouth to the stomach;exhaled gas was collected in a bag to measure its ^(13)CO_(2)/12CO_(2) isotope ratio via infrared isotope spectrometry.Serum VB_(12) and alanine transaminase(ALT)levels were measured via chemiluminescence immunoassay and the lactate dehydrogenaseultraviolet method,respectively.We evaluated statistical differences in mean body weight,change in ^(13)CO_(2)(Δ^(13)CO_(2)‰),peakΔ^(13)CO_(2)‰,and serum VB_(12) and ALT,between males and females and between ERs and CRs using the t-test and Mann-Whitney U test for normally and non-normally distributed variables,respectively.RESULTS Males weighed significantly more than females(P<0.001);CRs weighed significantly more than ERs(P<0.008).Δ^(13)CO_(2) reached a peak(C_(max))at 20 min and 30 min in females and males,respectively,decreasing after 20-30 min without rebound in all groups.Males had significantly higher C_(max) andΔ^(13)CO_(2) at 15-45 min than females(P<0.05;for all pairs).Propionate metabolism was enhanced in male ERs relative to male CRs,whereas metabolism did not differ markedly between ERs and CRs for females.Males had higher serum VB_(12) levels than females,without prominent differences between the ER and CR groups.Male CRs had notably higher ALT levels than male ERs.Thus,chronic ethanol consumption may trigger fatty acid production via intestinal bacteria and changes in gut microbiome composition.CONCLUSION Faster PBT shows that 16%ethanol consumption promotes propionate metabolism without inducing liver injury.This PBT may be used clinically to evaluate gut flora status.

Micronutrient deficiencies in patients with chronic atrophic autoimmune gastritis: A review

Chronic atrophic autoimmune gastritis (CAAG) is an organ-specific autoimmune disease characterized by an immune response, which is directed towards the parietal cells and intrinsic factor of the gastric body and fundus and leads to hypochlorhydria, hypergastrinemia and inadequate production of the intrinsic factor. As a result, the stomach&#x02019;s secretion of essential substances, such as hydrochloric acid and intrinsic factor, is reduced, leading to digestive impairments. The most common is vitamin B12 deficiency, which results in a megaloblastic anemia and iron malabsorption, leading to iron deficiency anemia. However, in the last years the deficiency of several other vitamins and micronutrients, such as vitamin C, vitamin D, folic acid and calcium, has been increasingly described in patients with CAAG. In addition the occurrence of multiple vitamin deficiencies may lead to severe hematological, neurological and skeletal manifestations in CAAG patients and highlights the importance of an integrated evaluation of these patients. Nevertheless, the nutritional deficiencies in CAAG are largely understudied. We have investigated the frequency and associated features of nutritional deficiencies in CAAG in order to focus on any deficit that may be clinically significant, but relatively easy to correct. This descriptive review updates and summarizes the literature on different nutrient deficiencies in CAAG in order to optimize the treatment and the follow-up of patients affected with CAAG.

Anemia after gastrectomy for early gastric cancer:Long-term follow-up observational study

AIM:To identify the incidence and etiology of anemia after gastrectomy in patients with long-term follow-up after gastrectomy for early gastric cancer.METHODS:The medical records of those patients with early gastric adenocarcinoma who underwent curative gastrectomy between January 2006 and October 2007 were reviewed.Patients with anemia in the preoperative workup,cancer recurrence,undergoing systemic chemotherapy,with other medical conditions that can cause anemia,or treated during follow up with red cell transfusions or supplements for anemia were excluded.Anemia was defined by World Health Organization criteria(Hb < 12 g/dL in women and < 13 g/dL in men).Iron deficiency was defined as serum ferritin < 20 g/dL.Vitamin B12 deficiency was defined as serum vitamin B 12 < 200 pg/mL.Iron deficiency anemia was defined as anemia with concomitant iron deficiency.Anemia from vitamin B 12 deficiency was defined as megaloblastic anemia(mean cell volume > 100 fL) with vitamin B 12 deficiency.The profile of anemia over 48 mo of follow-up was analyzed.RESULTS:One hundred sixty-one patients with gastrectomy for early gastric cancer were analyzed.The incidence of anemia was 24.5% at 3 mo after surgery and increased up to 37.1% at 48 mo after surgery.The incidence of iron deficiency anemia increased during the follow up and became the major cause of anemia at 48 mo after surgery.Anemia of chronic disease and megaloblastic anemia were uncommon.The incidence of anemia in female patients was significantly higher than in male patients at 12(40.0% vs 22.0%,P = 0.033),24(45.0% vs 25.0%,P = 0.023),36(55.0% vs 28.0%,P = 0.004),and 48 mo(52.0% vs 31.0%,P = 0.022) after surgery.Patients with total gastrectomy showed significantly higher incidence of anemia than patients with subtotal gastrectomy at 48 mo after surgery(60.7% vs 31.3%,P = 0.008).The incidence of iron deficiency was significantly higher in female patients than in male patients at 6(35.4% vs 13.3%,P = 0.002),12(45.8% vs 16.8%,P < 0.001),18(52.1% vs 22.3%,P < 0.001),24(60.4% vs 20.9%,P < 0.001),36(62.5% vs 29.2%,P < 0.001),and 48 mo(66.7% vs 34.7%,P = 0.001) after surgery.CONCLUSION:Anemia was frequent after gastrectomy for early gastric cancer,with iron deficiency being the major cause.Evaluation for anemia including iron status should be performed after gastrectomy and appropriate iron replacement should be considered.

Pernicious anemia: New insights from a gastroenterological point of view

Pernicious anemia （PA） is a macrocytic anemia that is caused by vitamin B12 deficiency, as a result of intrinsic factor deficiency. PA is associated with atrophic body gastritis （ABG）, whose diagnosis is based on histological confirmation of gastric body atrophy. Serological markers that suggest oxyntic mucosa damage are increased fasting gastrin and decreased pepsinogen I. Without performing Schilling＇s test, intrinsic factor deficiency may not be proven, and intrinsic factor and parietal cell antibodies are use- ful surrogate markers of PA, with 73% sensitivity and 100% specificity. PA is mainly considered a disease of the elderly, but younger patients represent about 15% of patients. PA patients may seek medical advice due to symptoms related to anemia, such as weak-ness and asthenia. Less commonly, the disease is suspected to be caused by dyspepsia. PA is frequently associated with autoimmune thyroid disease （40%） and other autoimmune disorders, such as diabetes mellitus （10%）, as part of the autoimmune polyen-docrine syndrome. PA is the end-stage of ABG. Long- standing Helicobacter pylori infection probably plays a role in many patients with PA, in whom the active infectious process has been gradually replaced by an autoimmune disease that terminates in a burned-out infection and the irreversible destruction of the gastric body mucosa. Human leucocyte antigen-DR genotypes suggest a role for genetic susceptibility in PA. PA patients should be managed by cobalamin replacement treatment and monitoring for onset of iron deficiency. Moreover, they should be advised about possible gastrointestinal long-term consequences, such as gastric cancer and carcinoids.

Restorative effect and mechanism of mecobalamin on sciatic nerve crush injury in mice

Mecobalamin, a form of vitamin B12 containing a central metal element （cobalt）, is one of the most important mediators of nervous system function. In the clinic, it is often used to accelerate recovery of peripheral nerves, but its molecular mechanism remains unclear. In the present study, we performed sciatic nerve crush injury in mice, followed by daily intraperitoneal administra-tion of mecobalamin （65 μg/kg or 130 μg/kg） or saline （negative control）. Walking track analysis, histomorphological examination, and quantitative real-time PCR showed that mecobalamin signiifcantly improved functional recovery of the sciatic nerve, thickened the myelin sheath in myelinated nerve ifbers, and increased the cross-sectional area of target muscle cells. Further-more, mecobalamin upregulated mRNA expression of growth associated protein 43 in nerve tissue ipsilateral to the injury, and of neurotrophic factors （nerve growth factor, brain-derived nerve growth factor and ciliary neurotrophic factor） in the L4–6 dorsal root ganglia. Our ifndings indicate that the molecular mechanism underlying the therapeutic effect of mecobalamin after sciatic nerve injury involves the upregulation of multiple neurotrophic factor genes.

Increased levels of homocysteine in patients with ulcerative colitis

AIM: To investigate serum levels of homocysteine (Hcys) and the risk that altered levels carry for thrombosis development in ulcerative colitis (UC) patients. METHODS: 55 UC patients and 45 healthy adults were included. Hcys, vitamin B12 and folic acid levels were measured in both groups. Clinical history and thrombo- embolic events were investigated. RESULTS: The average Hcys level in the UC patients was 13.3 ± 1.93 μmmol/L (range 4.60-87) and was higher than the average Hcys level of the control group which was 11.2 ± 3.58 μmmol/L (range 4.00-20.8) (P < 0.001). Vitamin B12 and folic acid average values were also lower in the UC group (P < 0.001). Whenmultivariate regression analysis was performed, it was seen that folic acid deficiency was the only risk factor for hyperhomocysteinemia. Frequencies of thromboembolic complications were not statistically significantly different in UC and control groups. When those with and without a thrombosis history in the UC group were compared according to Hcys levels, it was seen that there were no statistically significant differences. A negative linear relationship was found between folic acid levels and Hcys. CONCLUSION: We could not find any correlations between Hcys levels and history of prior thromboembolic events.

A preliminary study on the teratogenesis of dexamethasone and the preventive effect of vitamin B_(12 )on murine embryonic palatal shelf fusion in vitro

Excessive dexamethasone (Dex) administrated into pregnant mice during critical periods of palatal development can produce a high incidence of cleft palate. Its mechanisms remain unknown. Vitamin B12 has been shown to antagonize the tera- togenic effects of Dex, which, however, remains controversial. In this study, we investigated the effects of Dex and vitamin B12 on murine embryonic palatal shelf fusion using organ culture of murine embryonic shelves. The explanted palatal shelves on em- bryonic day 14 (E14) were cultured for 24, 48, 72 or 96 h in different concentrations of Dex and/or vitamin B12. The palatal shelves were examined histologically for the morphological alterations on the medial edge epithelium (MEE) and fusion rates among different groups. It was found that the palatal shelves were not fused at 72 h or less of culture in Dex group, while they were completely fused in the control and vitamin B12-treated groups at 72 and 96 h, respectively. The MEE still existed and proliferated. In Dex+vitamin B12 group the palatal shelves were fused at each time point in a similar rate to controls. These results may suggest that Dex causes teratogenesis of murine embryonic palatal shelves and vitamin B12 prevents the teratogenic effect of Dex on palatogenesis on murine embryos in vitro.