Vitamin B6 Status among Vegetarians: Findings from a Population-Based Survey.

Vitamin B6 from plant foods may have lower bioavailability than vitamin B6 from animal foods, but studies on objectively measured vitamin B6 status among vegetarians compared to non-vegetarians are lacking. Thus, the vitamin B6 status among vegetarians, but also pescatarians, and flexitarians, compared to meat-eaters was assessed in the population-based NHANES study (cycles 2007-2008 and 2009-2010). Data on serum pyridoxal-5'-phosphate (PLP) and 4-pyridoxic acid (4-PA) measured by high-performance liquid chromatography (HPLC) as well as dietary intakes from 24-h recalls were available for 8968 adults aged 20-80 years. Geometric mean (±standard error) PLP concentrations were 58.2 ± 6.0, 52.1 ± 3.7, 49.2 ± 4.6 and 51.0 ± 1.1 nmol/L among vegetarians, pescatarians, flexitarians, and meat-eaters. The 4-PA concentrations were 32.7 ± 4.0, 29.0 ± 2.5, 34.8 ± 5.6 and 33.0 ± 0.7, respectively. There were no statistically significant differences in PLP, 4-PA, and their ratio across the groups in multivariable linear regression models. Overall, the use of vitamin B6 supplements was the strongest predictor of the vitamin B6 status, followed by the dietary vitamin B6 intake. Interestingly, several other covariates were significantly associated with vitamin B6 biomarker levels, particularly serum albumin, creatinine and alkaline phosphatase, and should be considered when assessing the vitamin B6 status. In summary, our findings suggest that a vegetarian diet does not pose a risk for vitamin B6 deficiency.

[Food Poisoning by Ginkgo Seeds through Vitamin B6 Depletion].

Overconsumption of Ginkgo biloba seeds induces food poisoning characterized by tonic-clonic convulsions and vomiting. The primary toxic component, 4'-O-methylpyridoxine (MPN), was purified from the seeds in 1985. This review includes the following aspects of ginkgo seed poisoning: 1) toxicity related to the content of MPN and MPN glucoside in G. biloba seeds; 2) the effect of MPN on vitamin B6 analogs, including an increase in pyridoxal and pyridoxic acid and decrease in pyridoxal-5'-phosphate plasma concentrations; 3) case reports of ginkgo seed poisoning in Asia, North America, and Europe, and their effective treatment via vitamin B6 administration. Considering the increase in the use of G. biloba seeds, it is essential to raise global awareness of their potential toxicity.

Vitamin B6 blood concentrations in paediatric dialysis patients.

OBJECTIVES: We investigated vitamin B6 blood concentrations in children on long-term dialysis at our centre. METHODS: Retrospective cross-sectional review of vitamin B6 blood concentrations in children on maintenance dialysis [peritoneal dialysis (PD), intermittent haemodialysis (IHD)]. RESULTS: We reviewed 28 children (16 boys), 15 IHD and 13 PD with median (interquartile range, IQR) age of 9.4 (2.4, 14.3) years. The median (IQR) vitamin B6 concentration was 223.4 (74.2, 392.8) nmol/L measured a median (IQR) of 9 (4, 16.5) months following commencement of dialysis. None of the children had vitamin B6 deficiency. Vitamin B6 concentrations were raised in 17 (61%), eight of these received a supplement. Nineteen (68%) received vitamin B6 and/or a supplement containing vitamin B6 whilst 11 (39%) received an enteral feed and a supplement. In those with normal vitamin B6 concentrations who were not receiving an enteral feed or an oral nutritional supplement (n = 6), all achieved normal concentrations without need for vitamin B6 supplementation. There were no differences between those on PD versus IHD (269.2 nmol/L vs. 130 nmol/L, P = 0.65). CONCLUSIONS: We report no children with vitamin B6 deficiency although > 50% had elevated vitamin B6 concentrations. We suggest if dietary assessment of vitamin B6 intake indicates insufficient intake, measurement of blood concentrations will help confirm if supplementation is required. Routine vitamin B6 supplementation and monitoring is currently not indicated in children on chronic dialysis.

Pyridoxal-5'-phosphate deficiency is associated with hyperhomocysteinemia regardless of antioxidant, thiamine, riboflavin, cobalamine, and folate status in critically ill patients.

BACKGROUND & AIMS: Critically ill patients develop severe stress, inflammation and a clinical state that may raise the utilization and metabolic replacement of pyridoxal-5'-phosphate decreasing their body reserves. This study was designed to assess the nutritional pyridoxal-5'-phosphate status in critical care patients with systemic inflammatory response syndrome, comparing them with a group of healthy people, and studying it's association with factors involved in the pyridoxine and other B vitamins metabolism, as the total antioxidant capacity and Hcy as cardiovascular risk biomarker. METHODS: Prospective, multicentre, comparative, observational and analytic study. One hundred and three critically ill patients from different hospitals, and eighty four healthy subjects from Granada, Spain, all with informed consent. Data from daily nutritional assessment, ICU severity scores, clinical and nutritional parameters, antioxidant status and homocysteine levels was taken at admission and at the seventh day of the ICU stay. RESULTS: Thiamine, riboflavin, pyridoxine and folate status proved deficient in a large number of patients, being significantly lower in comparison with control group, and significantly decreased at 7th day of ICU stay. Higher homocysteine was observed in patients compared with control group (p < 0.05) where 31.5 and 26.8 percent of subjects presented hyperhomocysteinemia at initial and final of study, respectively. Antioxidant status was lower than control group in two periods analysed, and decreased at 7th day of ICU stay (p < 0.05) being associated with PLP deficiency. PLP deficiency was also correlated with hyperhomocysteinemia at two times measured (r. -0.73, p < 0.001; r. -0.69, p < 0.001, respectively), showing at day 7 an odds ratio of 6.62 in our multivariate model. CONCLUSION: Critically ill patients with SIRS show deficient B vitamin and low antioxidant statuses. Despite association found between PLP deficiency and low antioxidant status in critically ill patients, PLP deficiency was only associated with hyperhomocysteinemia regardless of antioxidant, riboflavin, cobalamine, and folate statuses in critically ill patients with SIRS at seventh day of ICU stay. PLP deficient patients presented about six times more risk of cardiovascular disease than non deficients.

Pyridoxine deficiency in adult patients with status epilepticus.

An 8-year-old girl treated at our facility for superrefractory status epilepticus was found to have a low pyridoxine level at 5 µg/L. After starting pyridoxine supplementation, improvement in the EEG for a 24-hour period was seen. We decided to look at the pyridoxine levels in adult patients admitted with status epilepticus. We reviewed the records on patients admitted to the neurological ICU for status epilepticus (SE). Eighty-one adult patients were identified with documented pyridoxine levels. For comparison purposes, we looked at pyridoxine levels in outpatients with epilepsy (n=132). Reported normal pyridoxine range is >10 ng/mL. All but six patients admitted for SE had low normal or undetectable pyridoxine levels. A selective pyridoxine deficiency was seen in 94% of patients with status epilepticus (compared to 39.4% in the outpatients) which leads us to believe that there is a relationship between status epilepticus and pyridoxine levels.

Pyridoxine supplementation does not alter in vivo kinetics of one-carbon metabolism but modifies patterns of one-carbon and tryptophan metabolites in vitamin B-6-insufficient oral contraceptive users.

BACKGROUND: Low chronic vitamin B-6 status can occur in a subset of women who use oral contraceptives (OCs) with uncertain metabolic consequences. An insufficiency of cellular pyridoxal 5'-phosphate (PLP), which is the coenzyme form of vitamin B-6, may impair many metabolic processes including one-carbon and tryptophan metabolism. OBJECTIVE: We investigated the effects of vitamin B-6 supplementation on the in vivo kinetics of one-carbon metabolism and the concentration of one-carbon and tryptophan metabolites in vitamin B-6-deficient OC users. DESIGN: A primed, constant infusion of [(13)C5]methionine, [3-(13)C]serine, and [(2)H3]leucine was performed on 10 OC users (20-40 y old; plasma PLP concentrations <30 nmol/L) before and after 28 d of supplementation with 10 mg pyridoxine hydrochloric acid/d. In vivo fluxes of total homocysteine remethylation, the remethylation of homocysteine from serine, and rates of homocysteine and cystathionine production were assessed. Targeted metabolite profiling was performed, and data were analyzed by using orthogonal partial least-squares-discriminant analysis and paired t tests adjusted for multiple testing. RESULTS: Pyridoxine supplementation increased the mean ± SD plasma PLP concentration from 25.8 ± 3.6 to 143 ± 58 nmol/L (P < 0.001) and decreased the leucine concentration from 103 ± 17 to 90 ± 20 nmol/L (P = 0.007) and glycine concentration from 317 ± 63 to 267 ± 58 nmol/L (P = 0.03). Supplementation did not affect in vivo rates of homocysteine remethylation or the appearance of homocysteine and cystathionine. A multivariate analysis showed a clear overall effect on metabolite profiles resulting from supplementation. Leucine, glycine, choline, cysteine, glutathione, trimethylamine N-oxide, and the ratios glycine:serine, 3-hydroxykynurenine:kynurenine, 3-hydroxykynurenine:3-hydroxyanthranilic acid, and 3-hydroxykynurenine:anthranilic acid were significant discriminating variables. CONCLUSIONS: Consistent with previous vitamin B-6-restriction studies, fluxes of one-carbon metabolic processes exhibited little or no change after supplementation in low-vitamin B-6 subjects. In contrast, changes in the metabolic profiles after supplementation indicated perturbations in metabolism, suggesting functional vitamin B-6 deficiency. This study was registered at clinicaltrials.gov as NCT01128244.

Anemia attributed to vitamin B6 deficiency in post-pancreaticoduodenectomy patients.

Micronutrient deficiencies such as vitamin A, iron, zinc, and selenium have been known to occur as a consequence of pancreaticoduodenectomy (PD), but vitamin B6 deficiency has not been previously reported. We report two post-PD patients who developed anemias attributed to vitamin B6 deficiency. Oral supplementations of vitamin B6 significantly improved anemias in both cases. Micronutrients including vitamin B6 should be monitored in post-PD patients, and supplementations should be carried out when necessary.

Micronutrient status in phenylketonuria.

Patients with phenylketonuria (PKU) encompass an 'at risk' group for micronutrient imbalances. Optimal nutrient status is challenging particularly when a substantial proportion of nutrient intake is from non-natural sources. In PKU patients following dietary treatment, supplementation with micronutrients is a necessity and vitamins and minerals should either be added to supplement phenylalanine-free l-amino acids or given separately. In this literature review of papers published since 1990, the prevalence of vitamin and mineral deficiency is described, with reference to age of treatment commencement, type of treatment, dietary compliance, and dietary practices. Biological micronutrient inadequacies have been mainly reported for zinc, selenium, iron, vitamin B12 and folate. The aetiology of these results and possible clinical and biological implications are discussed. In PKU there is not a simple relationship between the dietary intake and nutritional status, and there are many independent and interrelated complex factors that should be considered other than quantitative nutritional intake.

Very low adequacy of micronutrient intakes by young children and women in rural Bangladesh is primarily explained by low food intake and limited diversity.

Documentation of micronutrient intake inadequacies among developing country populations is important for planning interventions to control micronutrient deficiencies. The objective of this study was to quantify micronutrient intakes by young children and their primary female caregivers in rural Bangladesh. We measured 24-h dietary intakes on 2 nonconsecutive days in a representative sample of 480 children (ages 24-48 mo) and women in 2 subdistricts of northern Bangladesh by using 12-h weighed food records and subsequent 12-h recall in homes. We calculated the probability of adequacy (PA) of usual intakes of 11 micronutrients and an overall mean PA, and evaluated dietary diversity by counting the total number of 9 food groups consumed. The overall adequacy of micronutrient intakes was compared to dietary diversity scores using correlation and multivariate regression analyses. The overall mean prevalence of adequacy of micronutrient intakes for children was 43% and for women was 26%. For children, the prevalence of adequate intakes for each of the 11 micronutrients ranged from a mean of 0 for calcium to 95% for vitamin B-6 and was <50% for iron, calcium, riboflavin, folate, and vitamin B-12. For women, mean or median adequacy was <50% for all nutrients except vitamin B-6 and niacin and was <1% for calcium, vitamin A, riboflavin, folate, and vitamin B-12. The mean PA (MPA) was correlated with energy intake and dietary diversity, and multivariate models including these variables explained 71-76% of the variance in MPA. The degree of micronutrient inadequacy among young children and women in rural Bangladesh is alarming and is primarily explained by diets low in energy and little diversity of foods.

Folic acid fortification ameliorates hyperhomocysteinemia caused by a vitamin B6-deficient diet supplemented with L-methionine.

Vitamin B6 (B6) deficiency affects homocysteine metabolism, and this leads to hyperhomocysteinemia. In this study, we examined i) the effects of B6-deficiency and graduated levels of dietary methionine on homocysteine metabolism, and ii) the effects of fortified folate on homocysteine metabolism. In experiment 1, Wistar male rats were fed a control or a B6-deficient diet supplemented with L-methionine at a level of 3, 6, or 9 g/kg of diet for 5 weeks. The resulting plasma homocysteine levels in the B6-deficient groups increased in relation to the increase in dietary methionine level. Next, in experiment 2, rats were fed a control, B6-deficient, or folate enriched (10 mg pteroylmonoglutamic acid/kg) B6-deficient diet containing L-methionine at 9 g/kg for 5 weeks. Although the B6-deficient diet induced hyperhomocysteinemia, folate fortification ameliorated the plasma homocysteine concentration. Overall, our results indicate that folate fortification ameliorates the hyperhomocysteinemia induced by B6 deficiency and supplemental methionine intake.

Type 1 diabetes impairs vitamin B(6) metabolism at an early stage of women's adulthood.

Vitamin B(6) (pyridoxine) metabolism in diabetes has never been investigated except for a few reports on plasma pyridoxal 5'-phosphate (PLP). These studies indicated that this most active (coenzyme) vitamer can be reduced. The present clinical investigation aimed to measure all vitamers in blood and urine by high performance liquid chromatography as well as important related factors, in women during active reproductive years. Thirty-two insulin-treated type 1 diabetic (T1D) patients, without renal complication, and 27 well-matched healthy controls, aged 30 to 40 years old, were recruited using rigorous criteria. Both groups had normal hemoglobin and serum albumin levels. Plasma PLP and pyridoxal (PL) did not differ significantly in the T1D group but alkaline phosphatase (ALP) activity was greater (p < 0.01). This produced a shift in plasma PLP-PL profile, as evidenced by a lower plasma PLP/PL ratio (p < 0.05). Enhanced ALP activity meant more PLP being dephosphorylated to PL (the membrane transfer form), with more ending up in erythrocytes to be rephosphorylated in its active form, as suggested by the significant positive correlation (p < 0.001) between plasma PL and erythrocyte PLP. More PL into blood circulation also means more oxidation of this vitamer to 4'-pyridoxic acid in kidneys, as confirmed by the positive correlation between plasma PL and urinary 4'-pyridoxic acid (p < 0.001). The positive correlation (p < 0.001) between ALP activity and glycosylated hemoglobin indicated a direct effect of the disease. The T1D-induced alteration in vitamin B(6) metabolism, consecutive to enhanced ALP activity, may put patients at greater risk of vitamin B(6) deficiency and diabetic complications.

Oral contraceptive use: impact on folate, vitamin B6, and vitamin B12 status.

Since many unplanned pregnancies occur while women are using oral contraceptives (OCs), it is important to understand the potential impact of these drugs on folate, vitamin B6 , and vitamin B12 status. Although a number of early studies concluded that OCs negatively impact folate status, the majority of these studies were conducted when the estrogen content of OCs was much higher. In addition, the interpretation of findings from many of these studies is problematic since no controls were included for potentially confounding factors. The presently available data do not support a conclusion that currently used OCs negatively impact folate status. In regard to vitamin B6 , however, existing population-based data do provide evidence that current low-dose OCs may negatively impact vitamin B6 status. The observed depression in plasma pyridoxal 5'-phosphate concentrations in OC users may reflect decreased body reserves of the vitamin, which could put women who discontinue OCs and become pregnant at risk for vitamin B6 inadequacy during pregnancy. Functional indicators of vitamin B12 status are not significantly impacted by OC use. Definitive conclusions, however, await further investigations.

Kidney damage in acute intermittent porphyria.

BACKGROUND: Acute intermittent and variegate porphyria are an autosomal dominant hereditary diseases caused by the deficient activity of porphobilinogen deaminase in the haem biosynthesis. Acute intermittent porphyria (AIP) in 11 patients (8 women and 3 men) and variegate porphyria (VP) in one patient were diagnosed and long-term treated during 15-22 years. Eleven patients had in acute attack abdominal pain, they were agitated and restless and suffered from insomnia. Besides they had various neurological signs. Examination of kidney function during remission showed hypertension and tubulointerstitial impairment of the kidneys in 10 patients (hyposthenuria and impairment of tubular excretory phase in isotopic renography). Deficiency of serum erythropoietin in 4 patients, significant deficiency of plasma and erythrocyte vitamin B6, significant hyperoxalaemia and hyperoxaluria in all patients were found. Direct relationship between plasma oxalic acid and effect of pyridoxal-5-phosphate (PLP), (effect of PLP was in indirect relationship with the concentration of erythrocyte vitamin B6), in AIP patients was found. Deficiency of vitamin B6 was probably a cause of hyperoxalaemia and hyperoxaluria in those patients. The effective therapy was repeated i.v. administration of haem-arginate during acute attacks (4-5 days). Besides during remission the patients were treated by pyridoxine (40-60 mg/day), by glucose, sodium chloride and phenothiazines. All patients showed significant improvement and had regular ambulatory check-up every three months. Currently, they are in clinical and laboratory remission.

[Vitamin B-6 in chronic renal insufficiency]. / Witamina B-6 w przewleklej niewydolnosci nerek.

Chronic diseases, including chronic renal insufficiency, predispose to deficiency of vitamin B-6. Prevalence of that phenomenon, the need and appropriate level of supplementation remain controversial. The paper is a review of literature concerning those topics. Causes of deficiency, as well as advantages and dangers of supplementation were referred.

Incidence of vitamin deficiency after laparoscopic Roux-en-Y gastric bypass in a university hospital setting.

Vitamin deficiency after gastric bypass surgery is a known complication. The purpose of this study was to measure the incidence of vitamin deficiency after laparoscopic Roux-en-Y gastric bypass in a university hospital setting. All patients who underwent laparoscopic Roux-en-Y gastric bypass from January 2002 to December 2004 and completed a 1- and 2-year follow-up after surgery were selected. Of the total 493 patients, 318 (65%) had vitamin results at 1-year follow-up. Of the 366 eligible for the 2-year follow-up, 141 (39%) had vitamin results. Patients were further grouped based on gender, race, and Roux limb length, and incidence of vitamin deficiencies were studied. The incidence of vitamin A (retinol) deficiency was 11 per cent, vitamin C was 34.6 per cent, vitamin D25OH was 7 per cent, vitamin B1 was 18.3 per cent, vitamin B2 was 13.6 per cent, vitamin B6 was 17.6 per cent, and vitamin B12 was 3.6 per cent 12 months after surgery. There was no statistical difference in the incidence of vitamin deficiencies between 1 and 2 years. In univariate and multivariate logistic regression of 1- and 2-year follow up, black patients (vitamins A, D, and B1 for 1 year and B1 and B6 for 2 years) and women (vitamin C at 1 year) were more likely to have vitamin deficiencies. Vitamin deficiencies after laparoscopic Roux-en-Y gastric bypass are more common and involve more vitamins, even those that are water soluble, than previously appreciated. Black patients tend to have more deficiencies than other groups. The bariatric surgeon should be committed to the long-term follow-up and care of these patients. Further prospective and randomized studies are necessary to provide appropriate guidelines for supplementation.

[Therapy-resistant microcytic hypochromic anemia from malabsorption-related vitamin B6 deficiency after a gastrointestinal operation].

We present a case of a 33-year-old man, who had a past history of a total pancreatectomy for duodenal malignant lymphoma complicated by life-threatening bleeding during chemotherapy at 23 years of age. He achieved complete remission and received no more chemotherapy. Around August 1999 he developed anemia, which failed to improve following intravenous administration of iron, and he was hospitalized. The cause of the anemia remained unclear and he received a blood transfusion. Because of the increasing frequency of transfusions, he was admitted to our hospital to evaluate his anemia in September 2000. On examinations, laboratory findings revealed a low level of serum vitamin B6 (B6) with iron deficiency. Intravenous administration of B6 was performed in addition to iron, with the result that the patient's hemoglobin level was kept at 10 g/dl without blood transfusion. An oral B6 administration test resulted in a low level of B6. These results suggest that B6 deficiency due to malabsorption may cause therapy-resistant anemia. Some reports say that B6 deficiency causes microcytic hypochromic anemia, since B6 is necessary for erythrocytic hemopoiesis as a coenzyme for heme biosynthesis. In the case of microcytic hypochromic anemia, if the cause is unclear, evaluation should be performed, taking the possibility of a hidden cause of B6 deficiency into consideration.