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.

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.

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.

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.

[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.

Estimation of usual intake distributions of nutrients and foods.

The issue of estimating usual intake distributions using daily intake data as collected by nationwide food consumption surveys is discussed. Of interest are not only the usual nutrient intake distributions based on food intake alone, but also the total nutrient intake distributions that must be based on information on food and supplement consumption. The problems of estimating usual food intake distributions and distinguishing between frequently consumed and infrequently consumed food items are considered. Data needs as well as statistical methodologies available to carry out each of the tasks outlined above are discussed, with particular reference to the integrated National Health and Nutrition Examination Survey that is now in the field. The replicated 24-h recalls should be augmented with a propensity questionnaire to improve on the estimation of intake distributions for infrequently consumed nutrients, supplements and food items.

Homocysteine--a treatable risk factor for allograft vascular disease after heart transplantation?

Growing evidence suggests that elevated total plasma homocysteine (tHCY) levels are associated with cardiac allograft vasculopathy following heart transplantation. To assess the effect of folic acid supplementation on tHCY levels, we performed a prospective study in a cohort of 69 patients (7.0 +/- 3.2 years after heart transplantation; mean age, 55.0 +/- 9.6 years; 61 male) treated with 5 mg folic acid/day (n = 34) vs no medication (n = 35). Therapy with folic acid resulted in significantly decreased tHCY levels, from 22.6 +/- 9.6 micromol/liter to 17.3 +/- 5.5 micromol/liter (p = 0.001) within 3 months, whereas values in the control group remained unchanged. We conclude that folic acid supplementation (5 mg per day) provides a simple and effective measure to lower elevated tHCY levels in heart transplant recipients.

Vitamin B6 deficiency in elderly patients on chronic peritoneal dialysis.

Polyneuropathy is one of the most frequent manifestations in chronic uremia. Among the factors related to polyneuropathy, vitamin B6 deficiency is well known. The exact prevalence of vitamin B6 deficiency related to neurological manifestations has not been previously reported. We studied vitamin B6 status, collected self-reported symptoms, and carried out full neurological examinations in 66 patients on chronic peritoneal dialysis. Vitamin B6 status was estimated by direct measurement of pyridoxal phosphate. In general, symptoms related to vitamin B6 deficiency are peripheral neuropathies, such as paresthesia, burning and painful dysesthesias, and thermal sensations. These symptoms were reported and assigned one of five grade scores. Of our 66 patients, 12 patients complained at least one sensory abnormality. The levels of vitamin B6 in the patients varied between 1.0 ng/mL and 30 ng/mL. Patients who complained of neurological symptoms owing to vitamin B6 deficiency were significantly older than the other patients. In analyzing the symptomatic cases before and after vitamin B6 supplementation, a significant correlation was seen between the level of vitamin B6 and symptoms. Within one month after initiation of oral vitamin B6 supplementations (30 mg daily), levels of pyridoxal phosphate rose, and sensory abnormalities improved in 8 of 12 patients. When peripheral neuropathy is suspected in elderly patients on chronic peritoneal dialysis, vitamin B6 deficiency should be taken into consideration as the cause. If vitamin B6 deficiency is appropriately treated by oral supplementation, sensory abnormalities can be eliminated.

Risk of low vitamin B6 status in infants breast-fed exclusively beyond six months.

Our aim was to ascertain the adequacy of human milk as the sole source of vitamin B6 and the associations between maternal and infant status during extended exclusive breast-feeding. Vitamin B6 status was followed in lactating mothers and their exclusively breast-fed infants by determinations of erythrocyte pyridoxal 5'-phosphate concentration and the erythrocyte aspartate transaminase stimulation test at 2 months (n = 118), 4 months (n = 118), 6 months (n = 112), 7.5 months (n = 70), 9 months (n = 36), 10 months (n = 14), 11 months (n = 11), and 12 months (n = 7) postpartum. Of the mothers, 54% had used vitamin B6 supplement during pregnancy, and all received a pyridoxine hydrochloride supplement of 1 mg/day throughout lactation. The infants had a higher vitamin B6 status than their mothers. During the first 4 months, infant vitamin B6 status was generally adequate independently of the actual vitamin status of the nursing mother. Most of the infants with low status at 2 months were those born to mothers who were not supplemented during pregnancy. By 6 months of exclusive breast-feeding, 30% of cases of low vitamin B6 status in nursing mothers were reflected in their infants. Thereafter, the risk of low vitamin B6 status in exclusively breast-fed infants increased even if the mother's status was adequate. Our findings suggest that gestationally accumulated stores are important for the maintenance of adequate vitamin B6 status of infants during the early months and that for some infants, human milk alone, without supplementary foods, may be insufficient to meet vitamin B6 needs after 6 months of age.

Impaired brainstem auditory evoked potentials in patients with cystic fibrosis.

Brainstem auditory evoked potentials (BAEPs) were measured in 11 young patients with cystic fibrosis (CF). Though none had clinical evidence of neurological impairment, all had various abnormal components of brainstem auditory evoked potentials (BAEPs). Abnormal BAEPs may be attributed to nutritional deficiencies including deficiencies of vitamins E and B6. As patients with CF are often deficient in vitamin E despite daily supplementation and normal serum levels, the authors suggest that the abnormal BAEPs demonstrated in the present study may reflect prolonged intracellular vitamin E deficiency. This finding suggests that BAEP studies may be useful in the neurological evaluation of patients with CF.

The pathogenesis of decreased aspartate aminotransferase and alanine aminotransferase activity in the plasma of hemodialysis patients: the role of vitamin B6 deficiency.

The mechanisms responsible for the low plasma (p) AST and ALT activity in HD patients remain elusive. This prospective study was undertaken to clarify the relationship of AST, ALT and pyridoxal-5'-phosphate (PLP) levels (active form of vitamin B6) in these patients. A group of 52 HD patients were given oral pyridoxine HCl (30 mg daily), for 5 weeks. Prior to supplementation (Day 0), 17 (33%) patients had deficient pPLP levels (Group 1), the remainder (35 patients) had normal pPLP values (Group 2). A positive correlation was noted between pPLP and pAST (r = 0.57, p < 0.01) or pALT (r = 0.68, p < 0.01). The mean pAST (9.2 +/- 0.3 vs 13.4 +/- 0.7 U/l) and pALT (8.6 +/- 0.6 vs 11.4 +/- 0.9 U/l) were markedly lower in Group 1 than those in Group 2, respectively. These low AST and ALT levels increased to those seen in Group 2 where no change from basal values was seen despite vitamin B6 supplementation (Day 35). The administration of vitamin B6 resulted in a significant increase in pPLP in both groups (Day 35) but pPLP dropped to subnormal levels in 5 patients in Group 1 and 7 in Group 2 three months after supplementation was stopped (Day 125). The mean AST and ALT of these 12 pPLP deficient patients became lower than those of the remaining 40 patients with normal pPLP values (p < 0.05). In conclusion, low pAST and pALT levels in HD patients are in part due to a deficiency of pPLP which serves as a coenzyme for these transaminases.

Isoniazid-induced neurotoxicity in chronic dialysis patients: report of three cases and a review of the literature.

This report describes an increased incidence of neurotoxic side effects secondary to isoniazid therapy in patients with end-stage renal disease. Toxicity was observed only in those patients receiving pyridoxine supplements of less than 100 mg/day. The increased sensitivity of the dialysis population to isoniazid neurotoxicity is predominantly due to abnormal metabolism of pyridoxine resulting in low serum levels of the active metabolite, pyridoxal phosphate. In addition, there is rapid clearance of pyridoxal phosphate by hemodialysis, resulting in a severer deficiency of this active metabolite. In order to prevent the neurotoxicity associated with isoniazid therapy, we recommend that 100 mg/day of pyridoxine be given as a supplement to hemodialysis patients requiring isoniazid therapy.

Vitamin B6 requirements in chronic renal failure.

According to our results the long-term daily oral supplementation of 6 mg vitamin B6 was sufficient for prevention of vitamin B6 deficiency in chronic renal failure, regular dialysis treatment and CAPD groups of patients. Haemodialysis and charcoal haemoperfusion have led to non-significant decrease of erythrocyte vitamin B6. A favourable effect was found of daily oral administration of 50 mg pyridoxine on electrophoretic mobility of peripheral blood lymphocytes and cellular immunity.

Effect of pyridoxine supplementation on plasma oxalate concentrations in patients receiving dialysis.

Plasma oxalate and erythrocyte glutamic oxaloacetate transaminase activity (EGOT) (an indicator of nutritional status with respect to pyridoxine) were measured in 21 patients maintained on regular continuous ambulatory peritoneal dialysis or haemodialysis before and after a 4-month period of supplementation with pyridoxine, 100 mg day-1. Prior to supplementation 10/21 patients showed subnormal EGOT activity, although the increment in activity on addition of pyridoxal-5-phosphate in vitro was within the normal range in all cases. Mean plasma oxalate was 31.5 mumol l-1 (SEM 2.9) prior to supplementation and did not change significantly with supplementation, despite normalization of EGOT activity in all but 2/21 patients. We conclude that pyridoxine deficiency does not contribute significantly to hyperoxalaemia in patients receiving dialysis and that 100 mg of pyridoxine daily is insufficient to reduce oxalate generation by a pharmacological action on glycine transamination.

Daily requirement for pyridoxine supplements in chronic renal failure.

Vitamin B6 deficiency was evaluated in 37 patients with chronic renal failure and in 71 patients undergoing maintenance hemodialysis (HD) or intermittent peritoneal dialysis (PD). Vitamin B6 deficiency was assessed by the in vitro activity of erythrocyte glutamic pyruvic transaminase (EGPT), without (basal) and with (stimulated) the addition of pyridoxal-5-phosphate to the assay, and the EGPT index (stimulated activity ./. basal activity). Basal and stimulated EGPT activities were below normal in the HD patients, and the EGPT index was increased in each group of patients, indicating vitamin B6 deficiency. Supplemental pyridoxine hydrochloride was given to 30 HD patients who received 1.25 to 50 mg/day (37 studies), 6 PD patients who were given 1.25 or 2.5 mg/day (7 studies), and 8 nondialyzed patients with mild to severe renal failure who received 2.5 mg/ day. In all HD patients, 10 or 50 mg/day of pyridoxine hydrochloride rapidly corrected the abnormal EGPT index and maintained normal values; with supplements of 5.0 mg/day or less, the index was often abnormal, particularly in those who were septic or taking pyridoxine antagonists. In PD patients and nondialyzed patients with renal failure, 2.5 mg/day of pyridoxine hydrochloride was inadequate to correct rapidly the abnormal index in all patients. These findings suggest that HD patients should receive 10 mg/day of supplemental pyridoxine hydrochloride (8.2 mg/day pyridoxine). PD patients and patients with chronic renal failure should receive about 5.0 mg/day of supplemental pyridoxine hydrochloride (4.1 mg/day pyridoxine). When sepsis intervenes or vitamin B6 antagonists are taken, 10 mg/day of pyridoxine hydrochloride may be a safer supplement for all patients.