Vitamin B6

VITAMIN B 6 refers to several PICOLINES (especially PYRIDOXINE; PYRIDOXAL; and PYRIDOXAMINE) that are efficiently converted by the body to PYRIDOXAL PHOSPHATE which is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, and aminolevulinic acid. During transamination of amino acids, pyridoxal phosphate is transiently converted into PYRIDOXAMINE phosphate. Although pyridoxine and Vitamin B 6 are still frequently used as synonyms, especially by medical researchers, this practice is erroneous and sometimes misleading (EE Snell; Ann NY Acad Sci, vol 585 pg 1, 1990). Most of vitamin B6 is eventually degraded to PYRIDOXIC ACID and excreted in the urine.

Prospective cohort studies of dietary vitamin B6 intake and risk of cause-specific mortality.[Pubmed:29764693]

Clin Nutr. 2018 May 4. pii: S0261-5614(18)30167-5.

BACKGROUND & AIMS: Vitamin B6 has been postulated to play an important role in determining chronic diseases. However, few studies have evaluated associations between dietary Vitamin B6 and cause-specific mortality comprehensively. METHODS: We investigated the associations between Vitamin B6 from diet and risk of all-cause, and cause-specific mortality in 134,480 participants from the Shanghai Men's Health Study (2002-2014) and Shanghai Women's Health Study (1997-2014). The median follow-up periods for men and women were 10.3 and 16.2 years, respectively. We estimated hazard ratio (HR) and 95% confidence interval (CI) using Cox proportional hazards models. RESULTS: After adjustment for suspected confounders, the multivariable-adjusted HRs for the highest versus lowest quintiles for total, CVD, stroke and CHD mortality among men were 0.83 (95%CI = 0.76, 0.90), 0.73 (95%CI = 0.63, 0.85), 0.71 (95%CI = 0.58, 0.88), 0.66 (95%CI = 0.47, 0.91), accordingly. Women with the highest intake had significantly 17% (HR = 0.83; 95% CI = 0.77, 0.90), 20% (HR = 0.80; 95% CI = 0.70, 0.92), and 28% (HR = 0.72; 95% CI = 0.59, 0.86) lower risks of total, CVD and stroke mortality compared with those of women with lowest Vitamin B6 intake. No significant association was observed between dietary Vitamin B6 and cancer mortality both among men and women. CONCLUSIONS: In the current study with two prospective Chinese cohorts, high dietary Vitamin B6 consumption was inversely associated with risk of all-cause and CVD mortality.

Multimodal characterization of a novel mutation causing vitamin B6-responsive gyrate atrophy.[Pubmed:29757052]

Ophthalmic Genet. 2018 Aug;39(4):512-516.

PURPOSE: Gyrate atrophy (GA) is a rare chorioretinal degeneration that results in the deterioration of night and peripheral vision, eventually leading to blindness. The disorder is caused by mutations in the gene encoding ornithine aminotransferase (OAT), causing increased levels of plasma ornithine. Treatment revolves around lowering plasma ornithine levels, with Vitamin B6 supplementation being the preferred treatment. Nevertheless, most patients do not respond to this therapy. Here, we report a rare case of Vitamin B6-responsive GA caused by a novel mutation in OAT and characterize the presentation with multimodal imaging. METHODS: This is a single-patient case report with a clinical diagnosis based on history, multimodal retinal imaging, laboratory findings, and DNA sequencing analysis. We include a 3D structure prediction of the novel mutant protein. RESULTS: DNA sequencing analysis demonstrated that there is a homozygous, novel variant c.473A>C: p.Y158S in OAT. Upon undergoing two weeks of Vitamin B6 supplementation, the patient exhibited a 28.5% reduction in plasma ornithine levels. In a follow-up visit two years later, plasma ornithine levels were reduced by 24.1% from the levels at initial presentation and disease progression was retarded based on clinical findings. CONCLUSION: One novel homozygous missense mutation in OAT was identified and considered to be pathogenic in a patient with GA. The response for the Vitamin B6 supplementation was positive, which is rare in all the GA cases reported in the literature. Our data suggests that further studies regarding the relationship between genotype and responsiveness to Vitamin B6 should be conducted.

Vitamin B6 in Health Supplements and Neuropathy: Case Series Assessment of Spontaneously Reported Cases.[Pubmed:29737502]

Drug Saf. 2018 Sep;41(9):859-869.

INTRODUCTION: In the literature, Vitamin B6 has been linked to the development of polyneuropathy. Most often, these complaints were seen when taking high doses of Vitamin B6 for a long time. Evidence as to whether a lower dosage range of Vitamin B6 (< 50 mg/day) can also induce neuropathy is scarce. OBJECTIVE: We aim to comprehensively describe the cases of neuropathy associated with Vitamin B6 received by the Netherlands Pharmacovigilance Centre Lareb and to assess the case series concerning the use of Vitamin B6 and neuropathic complaints. METHODS: We describe the number and nature of the reported cases, including suspect product, dosage, duration of use, and Vitamin B6 serum levels. In addition, we describe the causality for the individual cases (Naranjo Probability Scale) and for the entire case series (Bradford Hill criteria). RESULTS: In total, 90 reports on products containing Vitamin B6 included at least one adverse drug reaction in the standardized Medical Dictionary for Regulatory Activities (MedDRA((R))) query (SMQ; broad) 'peripheral neuropathy'. The amount of Vitamin B6 in the products varied between 1.4 and 100 mg per tablet. The serum Vitamin B6 level was known in 36 cases (88-4338 nmol/l), and the mean serum Vitamin B6 level was 907 nmol/l. However, no statistical correlation between dosage and Vitamin B6 blood levels was found. DISCUSSION AND CONCLUSION: Causality assessment of the case series of 90 reports to Lareb shows it is plausible for the Vitamin B6 supplements to have caused complaints such as neuropathies. This is especially the case with higher dosages and prolonged use, but dosages < 50 mg/day also cannot be excluded.

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