Vitamin B6 Deficiency Research Articles

S1469 Prevalence of Helicobacter pylori Infection Among Hispanics Living in Puerto Rico Undergoing Bariatric Surgery

Introduction: Obesity is a public health problem that affects developed and developing countries. Its prevalence is around 33% in the United States and 30-35% in Puerto Rico. Helicobacter pylori (HP) infection in bariatric patients has been linked to post-surgical foregut symptoms, marginal ulcers, and an increased incidence rate of viscus perforation. However, the feco-prevalence of H. pylori infections in this population has not been studied. Therefore, this study aimed to examine the feco-prevalence of HP infection among patients undergoing bariatric surgery in Puerto Rico. Methods: A retrospective cross-sectional chart review was conducted. The Feco-positivity was determined using stool H. pylori antigen immunoassay. Helicobacter pylori feco-prevalence was estimated with 95% confidence using the proportion z-test. Pearson's Chi-Square test was used to determine associations between the variables. Results: A total of 307 medical records of patients undergoing bariatric surgery were reviewed. The mean age of the study population was 42 ± 12 years, of whom 79.1% were female. The overall feco-prevalence of H. pylori was 18.0%, with nausea and belching the most prevalent symptoms reported (P < 0.05). A 90% eradication rate was observed with the first treatment course. The prevalence of vitamin B6 deficiency in patients with HP positive was 32% compared to patients with HP negative 20%, with a P-value of 0.05 (Figure). Conclusion: HP feco-prevalence in bariatric surgery patients is estimated to be 18%, less than the previously estimated prevalence of Helicobacter pylori using seroprevalence of Hispanics in Puerto Rico. However, the seroprevalence of HP infection is less sensitive and specific to disease than the feco-prevalence. Therefore, further investigation is warranted about HP feco-prevalence in the general population of Puerto Rico. There was a statistically significant increase in the prevalence of vitamin B6 deficiency in patients with HP positive that has not previously been reported and warrants further investigation.Figure 1.: Prevalence of H. pylori in patients with Vitamin deficiency

Upregulation of TLR4/MyD88 pathway in alcohol-induced Wernicke’s encephalopathy: Findings in preclinical models and in a postmortem human case

Wernicke’s encephalopathy (WE) is a neurologic disease caused by vitamin B1 or thiamine deficiency (TD), being the alcohol use disorder its main risk factor. WE patients present limiting motor, cognitive, and emotional alterations related to a selective cerebral vulnerability. Neuroinflammation has been proposed to be one of the phenomena that contribute to brain damage. Our previous studies provide evidence for the involvement of the innate immune receptor Toll-like (TLR)4 in the inflammatory response induced in the frontal cortex and cerebellum in TD animal models (animals fed with TD diet [TDD] and receiving pyrithiamine). Nevertheless, the effects of the combination of chronic alcohol consumption and TD on TLR4 and their specific contribution to the pathogenesis of WE are currently unknown. In addition, no studies on TLR4 have been conducted on WE patients since brains from these patients are difficult to achieve. Here, we used rat models of chronic alcohol (CA; 9 months of forced consumption of 20% (w/v) alcohol), TD hit (TDD + daily 0.25 mg/kg i.p. pyrithiamine during 12 days), or combined treatment (CA + TDD) to check the activation of the proinflammatory TLR4/MyD88 pathway and related markers in the frontal cortex and the cerebellum. In addition, we characterized for the first time the TLR4 and its coreceptor MyD88 signature, along with other markers of this proinflammatory signaling such as phospo-NFκB p65 and IκBα, in the postmortem human frontal cortex and cerebellum (gray and white matter) of an alcohol-induced WE patient, comparing it with negative (no disease) and positive (aged brain with Alzheimer’s disease) control subjects for neuroinflammation. We found an increase in the cortical TLR4 and its adaptor molecule MyD88, together with an upregulation of the proinflammatory signaling molecules p-NF-ĸB and IĸBα in the CA + TDD animal model. In the patient diagnosed with alcohol-induced WE, we observed cortical and cerebellar upregulation of the TLR4/MyD88 pathway. Hence, our findings provide evidence, both in the animal model and the human postmortem brain, of the upregulation of the TLR4/MyD88 proinflammatory pathway in alcohol consumption–related WE.

Association of Serum Pyridoxal Phosphate Levels with Established Status Epilepticus.

The objective of this study was to determine the prevalence of pyridoxine deficiency, measured by pyridoxal phosphate (PLP) levels, in patients admitted to the hospital with established (benzodiazepine-resistant) status epilepticus (SE) (eSE) and to compare to three control groups: intensive care unit (ICU) patients without SE (ICU-noSE), non-ICU inpatients without SE (non-ICU), and outpatients with or without a history of epilepsy (outpatient). This retrospective cohort study was conducted at the University of North Carolina Hospitals and Yale New Haven Hospital. Participants included inpatients and outpatients who had serum PLP levels measured during clinical care between January 2018 and March 2021. The first PLP level obtained was categorized as normal (> 30nmol/L), marginal (≤ 30nmol/L), deficient (≤ 20nmol/L), and severely deficient (≤ 5nmol/L). A total of 293 patients were included (52 eSE, 40 ICU-noSE, 44 non-ICU, and 157 outpatient). The median age was 55 (range 19-99) years. The median PLP level of the eSE group (12nmol/L) was lower than that of the ICU-noSE (22nmol/L, p = 0.003), non-ICU (16nmol/L, p = 0.05), and outpatient groups (36nmol/L, p < 0.001). Patients with eSE had a significantly higher prevalence of marginal and deficient PLP levels (90 and 80%, respectively) than patients in each of the other three groups (ICU-noSE: 70, 50%; non-ICU: 63, 54%; outpatient: 38, 21%). This significantly higher prevalence persisted after correcting for critical illness severity and timing of PLP level collection. Our study confirms previous findings indicating a high prevalence of pyridoxine deficiency (as measured by serum PLP levels) in patients with eSE, including when using a more restricted definition of pyridoxine deficiency. Prevalence is higher in patients with eSE than in patients in all three control groups (ICU-noSE, non-ICU, and outpatient). Considering the role of pyridoxine, thus PLP, in the synthesis of γ-aminobutyric acid and its easy and safe administration, prospective studies on pyridoxine supplementation in patients with eSE are needed.

Acquired Sideroblastic Anemia: An Exploratory Comparative Statistical Analysis Between Clonal and Non-clonal Cases.

Sideroblastic anemia (SA) is a rare heterogenous group of inherited and acquired bone marrow disorders. We retrospectively studied the clinicopathologic characteristics, cytogenetic findings, and disease outcome of patients with acquired sideroblastic anemia (ASA) and performed a comparative analysis between clonal and non-clonal cases. 15 patients of ASA were detected: clonal SA (10 cases, 66.7%) including MDS, MDS/MPN, AML and t-MNs with ring sideroblasts) and SA secondary to non-clonal causes (5 cases; 33.3%), including copper deficiency (2 sideroblastic anemia, copper deficiency, non-clonal sideroblastic anemia cases), pyridoxine deficiency diagnosed during pregnancy, and 2 patients with idiopathic SA.Key Keywords: sideroblastic anemia, copper deficiency, non-clonal sideroblastic anemia

Micronutrient deficiencies in critically ill patients receiving continuous renal replacement therapy.

Continuous renal replacement therapy (CRRT) is essential to the management of acute kidney injury (AKI) in critical illness. Unfortunately, large quantities of micronutrients are shown to be lost in CRRT effluent. Current literature describes serum micronutrient values in CRRT patients to be below-reference range, yet seldom compares such values to other critically ill populations unexposed to CRRT. The aim of this study was to describe and compare the prevalence of micronutrient and carnitine deficiencies in critically ill patients at high malnutrition risk exposed to CRRT to a group of patient unexposed to CRRT. A retrospective chart review was conducted at Duke University Hospital using the electronic medical record. The study group consisted of patients at high malnutrition risk requiring intensive care unit (ICU) admission from 01/01/2017-12/31/2018 with one or more of the following serum micronutrient levels checked: carnitine, copper, zinc, selenium, and vitamins B1, B6, B9, and C. Micronutrient deficiencies were defined as below the reference range and carnitine deficiencies were interpreted as an acyl to free carnitine ratio (ACFR) of >0.4. 106 ICU patients met inclusion criteria and 46% were exposed to CRRT. At least one micronutrient deficiency was reported in 90% of CRRT patients compared to 61% patients unexposed to CRRT (p=0.002). A greater percentage of copper (p<0.001) and carnitine (p<0.001) deficiencies were found among patients exposed to CRRT, while more zinc deficiencies were noted among non-CRRT patients (p=0.001). The vast majority of CRRT patients presented with micronutrient deficiencies. Clinicians should have a heightened awareness of the risk for serum copper, carnitine, and vitamin B6 deficiencies among CRRT patients. Further prospective and randomized-controlled trials are needed to better define this new category of malnutrition and test supplementation strategies to address and prevent these clinically-relevant deficiencies.

ACUTE IZONIAZID POISONING WITH PRESENTATION OF A CLINICAL CASE

Rimicid or isonide a group of medications which belong to anti-tuberculosis medicaments. The active substance isoniazid is used to treat pulmonary and extrapulmonary forms of tuberculosis, as well as prophylaxis in case of contact with infected individuals. Isoniazid is rapidly absorbed, reaching a maximum serum concentration in 2 hours, and penetrates all body fluids. The volume of distribution is approximately 0.6 l/kg. Isoniazid causes pyridoxine deficiency in two ways: - by hydrazones, isoniazid metabolites inhibit the pyridoxal kinase, which converts pyridoxine to the active form, pyridoxal-5-phosphate, and - pyridoxine deficiency disrupts the synthesis and metabolism of GABA, the main inhibitory mediator of the central nervous system. Isonicotinic acid poisoning metabolism is subject to individualized factors, and in some people, this metabolism can be in a significantly slower. A clinical case of poisoning with 30 tablets of Rimicid by a 16-year-old girl suicidal attempt was presented. The results of the TC analysis confirm intoxication with the drug, and the retrospective assessment of the concentration over a past period of time using the elimination half-life has revealed an extremely high dose of ingested isoniazid.

Functional Vitamin B12 Deficiency in Sleep Disorders in Children

It has been known for some time that an absolute deficiency in vitamin B12 is often associated with sleep disorders in children. The mechanism for the sleep disorders, though, is not generally stated. We have identified a cohort of children, who suffered from long term sleep disorders, who were characterized by elevated serum vitamin B12 levels. Retrospective Organic Acid Analysis of the urine of the children identified many markers of functional vitamin B12 deficiency, despite the elevated serum B12. As such the children may have paradoxical B12 in which serum levels of vitamin B12 were normal or elevated, however they had elevated markers of functional vitamin B12 deficiency. This functional vitamin B12 deficiency appeared to be the result of functional vitamin B2 deficiency. The mechanism is discussed. Effective treatment required resolution of the functional vitamin B2 deficiency as well as high dose vitamin B12 administration.

Functional Vitamin B12 deficiency in Chronic Fatigue Syndrome

Chronic Fatigue Syndrome/Myalgic encephalomyelitis (CFS/ME) is a complex chronic condition, characterized by periods of extreme fatigue, for which an underlying medical condition has previously not been identified. Many of the symptoms of CFS/ME, are, though, similar to those with vitamin B12 deficiency. In contrast to nutritional vitamin B12 deficiency, the majority of individuals with CFS have been shown to have functional vitamin B12 deficiency as well as functional vitamin B2 deficiency. This functional B12 deficiency occurred despite elevated serum B12 being found, and hence presents as Paradoxical vitamin B12 deficiency. As such, CFS due to functional B2 deficiency presents as Paradoxical B12 deficiency. Maintenance of vitamin B12 functional activity is critically dependent upon functional B2 sufficiency, and hence resolution of CFS there must first be resolution of functional B2 deficiency before treatment with vitamin B12 can be effective.

Clinical analysis of Wernicke encephalopathy after liver transplantation

BackgroundWernicke encephalopathy (WE) is an acute neurological disease resulting from vitamin B1 deficiency, and there are only very few case reports of WE after liver transplantation. The present study aimed to investigate the clinical characteristics, etiology, magnetic resonance imaging (MRI) features, treatment and prognosis of patients with WE after liver transplantation. MethodsTwenty-three patients with WE after liver transplantation from the First Affiliated Hospital, Zhejiang University School of Medicine and Jiangxi Provincial People's Hospital between January 2011 and December 2021 were retrospectively analyzed. ResultsAmong the 23 patients diagnosed with WE after liver transplantation, 6 (26%) had a classic triad of impaired consciousness, oculomotor palsy and ataxia, and 17 (74%) had two features. The misdiagnosis rate was 65%. After treatment with high-dose vitamin B1, 19 (83%) patients showed improvement, whereas 4 (17%) showed no improvement, including 3 with residual short-term memory impairments and 1 with residual spatial and temporal disorientation and ataxia. ConclusionsThe misdiagnosis rate is high in the early stage of WE, and the prognosis is closely associated with whether WE is diagnosed early and treated timely. High-dose glucose or glucocorticoids can trigger WE and cannot be administered before vitamin B1 treatment. Vitamin B1 is suggested to be used as a prophylactic treatment for patients with WE after liver transplantation.

Pitfalls of iron supplementation in parenteral nutrition admixtures for children with intestinal failure.

Pediatric patients with intestinal failure are at increased risk for iron deficiency. Supplementation is not routinely included in parenteral nutrition solutions. There is currently limited research related to the safety of iron supplementation in parenteral nutrition and for intravenous forms used in patients with intestinal failure. Current American Society for Parenteral and Enteral Nutrition and ESPGHAN guidelines promote the use of enteral iron, acknowledging the risks of using iron supplementation within parenteral nutrition admixtures. We review a patient case and the current available literature related to iron in parenteral nutrition. Five major concerns are identified: peroxidation reactions, incompatibility, hypersensitivity, infection risk, and iron overload. We propose an argument against the preferential use of iron supplementation within parenteral nutrition in children with intestinal failure when enteral supplementation or intermittent parenteral infusion may be sufficient.

Alcoholic Cardiomyopathy: A Literature Review

Background: Cardiomyopathy is a heart muscle disorder so which the heart cannot contract optimally. Alcoholic cardiomyopathy is a type of cardiomyopathy that dilates due to long-term alcohol consumption. The prevalence of alcoholic cardiomyopathy is higher in men than women. The age group with the most alcoholic cardiomyopathy was 45 to 74 year. Death from alcoholic cardiomyopathy had an autopsy result marked muscle dilatation. A toxicological examination can show the level of alcohol consumed. The cause of death in alcoholic cardiomyopathy is muscle dilatation due to chronic ethanol abuse (Dolinak, 2005). Islam expressly forbids something that makes losing mind, like alcohol. Alcohol has many disadvantages for the consumer in the form of loss of mind and turning away from Allah. Objective: This report aims to learn more about the definition, pathophysiology, clinical manifestation, and treatment of Alcoholic Cardiomyopathy. Also, Knowing and explaining Alcoholic Cardiomyopathy in terms of death and Islamic views. Methods: The design of this research is a literature review or library review, which is a systematic, direct, and reproducible research method by identifying, evaluating, and synthesizing published research. Result: Alcoholic cardiomyopathy is a clinical diagnosis made in a patient with a set of findings that include a history of excessive alcohol consumption, possible physical signs of alcohol abuse (e.g., parotid disease, telangiectasia or spider angiomata, altered mental status, cirrhosis), heart failure, and other evidence consistent with dilated cardiomyopathy. People who frequently consume alcohol can cause nutritional disorders, especially vitamin B1 deficiency can cause cardiomyopathy. Alcohol will also cause abnormalities in the structure and function of mitochondria in heart cells. These abnormalities include enlarged mitochondrial structure, decreased metabolism, lack of several enzymes decreased ion transport, increased calcium flow, glycogen accumulation, and decreased ATP production. Conclusion: Cardiomyopathy is a heart muscle function disorder characterized by the loss of the ability of the heart muscle to pump blood so that the blood supply is not optimal and results in death. The most common cause is chronic alcohol consumption, which causes dilatation of the heart muscle. At the same time, alcohol is an ingredient that is forbidden to be consumed by Muslims because of its more significant impact.

Dry beriberi after sleeve gastrectomy: An undiagnosed case report.

Introduction and importanceSleeve gastrectomy (SG) is a popular surgery for morbid obesity because of minimal complications, while somewhere uncommon micronutrient deficiencies occur that make problems. One of these rare complications is dry beriberi (BB).Case presentationA 20-year-old girl with obesity that a few months after SG had non-specific symptoms like nausea, vomiting, debilitating weakness, burning, and tingling in her feet, which led to more tests and imaging and confused the physicians. During the next two months, she had a 40 kg weight loss. The critical test that helped diagnosis was Electromyography and Nerve Conduction Velocity (EMG/NCV), which showed subacute axonal sensory-motor polyneuropathy and decreased level of vitamin B1, proved the patient's diagnosis was dray BB.Clinical discussionSG may contribute to vitamin and trace elements deficiency development. One of the micronutrients that deficiencies can disturb the patient is vitamin B1 deficiency. Vitamin B1 deficiencies could be demonstrated with peripheral polyneuropathy, beriberi, or Wernicke-Korsakoff syndrome. Based on decreased vitamin B1 and EMG/NCV results, the diagnosis had been dry beriberi corrected with supplement therapy.ConclusionThiamine deficiency should be suspected in all patients with vomiting, neurological symptoms, and rapid weight loss post-bariatric surgery (BS), even after restrictive surgery. Especially when a patient reports substantial weight loss and vomiting in short order. Hopefully, this case report will make any patient hospitalized with similar conditions evaluated for beriberi and again multivitamin supplementation therapy after SG is emphasized.

Diagnosis and Management of Refeeding Syndrome

Refeeding syndrome (RFS) is described as a syndrome of electrolyte abnormalities and changes in body fluids with metabolic abnormalities in malnourished patients who receive refeeding either orally, enteral, or parenterally. Patients at risk for RFS are patients who have lost 10% of their previous body weight in the last 3-6 months, cancer patients who are on chemotherapy, geriatric patients with malnutrition, and patients with anorexia. Clinical manifestations are caused by electrolyte changes that affect neurons, heart and muscle disorders with various symptoms, and even death. The specific characteristics of RFS are the presence of hypophosphatemia and accompanied by other symptoms of electrolyte imbalance such as changes in sodium levels, changes in glucose, protein, fat metabolism, vitamin B1 deficiency, hypokalemia, and hypomagnesemia. The principle of management of RFS is to correct biochemical abnormalities and electrolyte and fluid imbalances. Preventive steps that can be taken are identifying individuals at risk for RFS, monitoring refeeding and administering an appropriate diet regimen.

Prevalence of Postoperative Micronutrient Deficiencies in Bariatric Surgery Patients Who Use Transdermal Patches for Supplementation: A Pilot Study.

BackgroundPatients require vitamin and mineral supplementation after bariatric surgery to prevent the development of micronutrient deficiencies. Consuming oral supplements is challenging due to gastric volume restriction. A transdermal patch dosage form may provide adequate micronutrient supplementation without pill burden. The study aims to determine the percentage of patients who have two or more nutritional deficiencies one year after surgery and to determine serum nutrient concentrations and gastrointestinal symptoms over time.MethodsPatients who planned to undergo bariatric surgery and preferred transdermal patches versus oral supplements were recruited during preoperative office visits. Enrolled patients were instructed to use a transdermal multivitamin patch as per the manufacturer’s instructions. Serum nutrient concentrations and Gastrointestinal Symptom Response Scale scores were determined at baseline and three months, six months, and one year after surgery.ResultsNinety-two participants completed the study protocol. Twenty-five participants had a full panel of study labs one year after surgery. Among these patients, 19% had two or more micronutrient deficiencies. Vitamin D was the most common deficiency followed by vitamin B6; however, median serum concentrations of both nutrients increased over time. Vitamin B1, folate, and zinc deficiencies were also observed. There were no changes in gastrointestinal symptoms.ConclusionsAdditional studies, including randomized controlled trials, are required to determine if the PatchMD Multivitamin Plus patch (Pilot Rd. STE. B, Las Vegas) can provide adequate supplementation of vitamins and minerals. The patch was not associated with changes in gastrointestinal symptoms.

Correlation between nutritional status parameters and hemoglobin level of teenage girls and hemoglobin level

Malnutrition is caused by the absence of any essential nutritional factor in the diet, including defects in the formation of hemoglobin or low absorption of essential nutrients. Some malnutrition due to lack of iron in the diet or high quality protein, vitamin B6 deficiency which affects the heme protein in the synthesis of hemoglobin, vitamin E deficiency which affects the stability of the membranes of red blood cells it happens. Copper is not part of the hemoglobin molecule but it affects the absorption of iron in the liver. Iron deficiency is the most common nutritional disorder in the world. Worldwide, anemia is estimated to affect 2 billion people, or 30 per cent of the world’s population and is more severe in developing countries due to frequent malaria and insect infestation. It particularly affects women in the reproductive age group and young children in tropical and sub-tropical regions. The World Bank estimates that malnutrition is a direct contributor to global diseases. Malnutrition occurs at all stages of life, but is most common in pregnant women, young children and teenage girls. Iron deficiency and malnutrition are a major public health problem among teenagers. Studies indicate that anemia in teenagers increases with age and the rate of growth is highest during teenage.

Low Serum Pyridoxine Levels Worsen Seizure Control in Adult Epilepsy Patients.

Background: Vitamin B6 (pyridoxine) is an important cofactor in the process by which glutamic acid decarboxylase (GAD) converts the excitatory, pro-epileptogenic neurotransmitter, glutamate, into the inhibitory, anti-epileptogenic neurotransmitter, gamma-aminobutyric acid (GABA). This concept has been established in infants with pyridoxine-dependent epilepsy as well as adult patients with other epilepsy subtypes who presented with medication-resistant status epilepticus, with both patient groups experiencing cessation of seizure activity following pyridoxine administration. Given our knowledge of the role of vitamin B6 in the conversion of glutamate to GABA, its effect on seizure control in infants with specific epilepsy subtypes, reports of adult-onset seizures associated with vitamin B6 deficiency, and vitamin B6’s role in terminating status epilepticus in adult patients with other types of epilepsy, we suspect that low vitamin B6 levels in adult epilepsy patients may correlate with poor seizure control across all epilepsy subtypes. This study seeks to determine whether there is a relationship between pyridoxine levels and the level of seizure control in adults with epilepsy, regardless of their seizure type.Methods: After obtaining institutional review board approval, we prospectively enrolled 32 patients (age range: 25-57 years) with epilepsy who presented to our clinic. Patients who did not meet the study criteria or who were diagnosed with psychogenic non-epileptic seizures (PNES) were excluded from the study (n = 2). Patients were classified as well-controlled (WC) or poorly controlled (PC) based on the absence or presence of a seizure within the last three months, respectively. After classification as WC or PC, pyridoxine serum levels and anti-seizure medication (ASM) levels were drawn in that clinic visit, following patient consent. All patients were contacted regarding pyridoxine and serum ASM levels, and patients that were found to be deficient in pyridoxine were treated with appropriate supplementation. At the end of the recruitment period, we performed analyses to determine if there was a statistically significant relationship between PC status and serum pyridoxine levels.Results: Of 32 patients, two patients were diagnosed with psychogenic non-epileptic events and were subsequently excluded. Of 30 patients, 10 had PC epilepsy. Median (interquartile range) serum B6 levels were 35.8 (26.8-54.2) in patients with WC epilepsy and 17.5 (10.1-41.3) in patients with PC epilepsy (P = 0.11). In the PC group, 6/10 (60%) of the patients demonstrated low serum pyridoxine compared to 3/20 (15%) in the WC group (P = 0.03).Conclusion: There was a statistically significant relationship between serum pyridoxine levels and seizure control. If appropriate, pyridoxine supplementation should be considered, especially in critically ill adult patients with refractory or PC seizures despite good adherence to ASMs.

Enhanced expression of PDX1 accumulates vitamin B6 in transgenic wheat seeds

Humans fulfill their daily requirement of vitamin B6, a vital micronutrient for strong metabolism and immunity, from various food components. Bio-fortified wheat, a staple crop, holds the potential to overcome vitamin B6 deficiency. Thus, in the present work, endogenous PDX1 gene was expressed in wheat under endosperm promoter. Calli from immature embryos of two wheat varieties, FSD-08 and Galaxy were transformed via Agrobacterium with transformation efficiency of 1.82% and 1.09%, respectively. After BASTA and PCR confirmation, T1 generation of twenty transgenic lines was analyzed for mRNA expression via quantitative real-time PCR and vitamin B6 levels via HPLC along with various biochemical and morphological traits. The transgenic lines exhibited 1.04–19.46 fold increase in PDX1 gene expression and upto 34.96 fold increase in vitamin B6 content of seeds as compared to control. Enhanced carbohydrate content was observed in half of the transgenics while majority of the lines had insignificant variation in their chlorophyll, protein and starch content. Among the morphological traits studied, only seed yield increased in majority of transgenic lines. In conclusion, over-expression of PDX1 in wheat endosperm successfully augmented vitamin B6 content of seeds without posing adverse effects on biochemical or morphological traits in either varieties.

Associations of Vitamin B6 Intake and Plasma Pyridoxal 5'-Phosphate with Plasma Polyunsaturated Fatty Acids in US Older Adults: Findings from NHANES 2003-2004.

Previous evidence suggests a potential dual impact of aging and vitamin B6 (B6) deficiency on polyunsaturated fatty acid (PUFA) metabolism; gender may influence PUFA biosynthesis. Perturbation of PUFA compositions during B6 deficiency could be linked to age-related health outcomes. However, little is known about the interrelationships between vitamin B6, PUFA, and gender in the older population. Therefore, we investigated whether gender-specific associations of B6 intake and plasma pyridoxal 5’-phosphate (PLP) concentration, respectively, with plasma PUFA concentrations and ratios (eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA), EPA + DHA, EPA/AA, and (EPA + DHA)/AA) existed in older adults. We further examined the relationships of adequate B6 status (PLP ≥ 20 nmol/L) with high (above median) plasma PUFA relative to deficient B6 status. This cross-sectional study analyzed 461 participants aged ≥60 years from NHANES 2003–2004. Nutrient intakes were assessed using two 24-h recalls and supplement questionnaires. PLP and PUFA concentrations were measured. Multivariate linear regression assessed the association of B6 intake and PLP with PUFA; multivariate logistic regression evaluated the relationship of adequate B6 status with high plasma PUFA, adjusting for demographic, socioeconomic, and dietary factors; physical activity; smoking; alcohol; medication; and BMI. There were interactions between gender and B6 intake on EPA (P-interaction = 0.008) and AA (P-interaction = 0.004) only, whereas no interaction existed between gender and PLP on PUFA. PLP was directly associated with EPA (β = 0.181, P = 0.002), DHA (β = 0.109, P = 0.005), EPA + DHA (β = 0.14, P = 0.002), EPA/AA (β = 0.186, P = 0.004), and (EPA + DHA)/AA (β = 0.13, P = 0.026). The odds of having high plasma EPA (adjusted (a) OR: 2.03, P = 0.049) and EPA/AA (aOR: 3.83, P < 0.0001) were greater in those with adequate B6 status compared to those with deficient B6 status. In conclusion, in US older adults, a higher PLP level was associated with a greater level of EPA, DHA, EPA + DHA, EPA/AA, and (EPA + DHA)/AA. Adequate B6 status was associated with high EPA and EPA/AA status. These findings suggest that sufficient vitamin B6 status may positively influence PUFA metabolism in older adults.

Vitamin B6 Deficiency Promotes Loss of Heterozygosity (LOH) at the Drosophila warts (wts) Locus

The active form of vitamin B6, pyridoxal 5′-phosphate (PLP), is a cofactor for more than 200 enzymes involved in many metabolic pathways. Moreover, PLP has antioxidant properties and quenches the reactive oxygen species (ROS). Accordingly, PLP deficiency causes chromosome aberrations in Drosophila, yeast, and human cells. In this work, we investigated whether PLP depletion can also cause loss of heterozygosity (LOH) of the tumor suppressor warts (wts) in Drosophila. LOH is usually initiated by DNA breakage in heterozygous cells for a tumor suppressor mutation and can contribute to oncogenesis inducing the loss of the wild-type allele. LOH at the wts locus results in epithelial wts homozygous tumors easily detectable on adult fly cuticle. Here, we found that PLP depletion, induced by two PLP inhibitors, promotes LOH of wts locus producing significant frequencies of wts tumors (~7% vs. 2.3%). In addition, we identified the mitotic recombination as a possible mechanism through which PLP deficiency induces LOH. Moreover, LOH of wts locus, induced by PLP inhibitors, was rescued by PLP supplementation. These data further confirm the role of PLP in genome integrity maintenance and indicate that vitamin B6 deficiency may impact on cancer also by promoting LOH.

Korsakoff Syndrome: A Chronic Nutritional Deficiency Neuropsychiatric condition

In this review we have focused on Korsakoff syndrome, which is an aftermath of Wernicke encephalopathy (WE). Wernicke-Encephalopathy is neuropathologically marked by thiamine or vitamin B1 deficiency, typically induced by excessive alcohol use over an extended period of time in alcoholic patients, while in Nonalcoholic patients, it may be due to impaired utilization or accelerated usage of thiamine. Wernicke-Korsakoff syndrome (WKS) affects the brain region such as the mammillary bodies, periaqueductal and periventricular grey matter, colliculi bodies, and thalamus. The classic triads of WE are ophthalmoplegia, Nystagmus, and ataxia. The brain is examined using MRI and shows damage to the nuclei or memory transit- papez circuit that connects mamillary bodies to the anterior thalamus using the mammillothalamic tract responsible for the recollective memory in the diencephalon. Patients can be treated by parenteral thiamine administration and by abstinence of alcohol within their lifestyle. Keywords: Korsakoff Syndrome, alcoholic, non-alcoholic, Alzheimer's, memory-loss Wernicke encephalopathy, Wernicke-Korsakoff syndrome