Pyridoxine

Regressive pyridoxine-induced sensory neuronopathy in a patient with homocystinuria.[Pubmed:29954767]

BMJ Case Rep. 2018 Jun 28;2018. pii: bcr-2018-225059.

Pyridoxine (vitamin B6) is an essential vitamin playing a crucial role in amino acid metabolism. Pyridoxine is used for isoniazid side-effects prevention, Pyridoxine-dependent epilepsy treatment and cystathionine beta-synthase deficiency (homocystinuria) treatment. However, vitamin B6 hypervitaminosis is neurotoxic and may provoke a progressive sensory neuronopathy (sensory ganglionopathy), usually when daily uptake is above 50 mg. We describe the case of a 30-year-old patient with homocystinuria who was treated with Pyridoxine 1250-1750 mg/day for 20 years and developed progressive sensory neuropathy with ataxia and impaired sensation in the extremities. Electrodiagnostic testing demonstrated non-length-dependent abnormalities of sensory nerve potentials, and sensory ganglionopathy was diagnosed. Pyridoxine dosage was reduced to 500 mg/day, resulting in the disappearance of sensory symptoms and ataxia, and the normalisation of sensory nerve potentials. Our case indicates that Pyridoxine-induced sensory ganglionopathy may be reversible, even after prolonged ingestion of high doses of vitamin B6 for more than 20 years.

A randomized phase II study evaluating pyridoxine for the prevention of hand-foot syndrome associated with capecitabine therapy for advanced or metastatic breast cancer.[Pubmed:29948956]

Breast Cancer. 2018 Nov;25(6):729-735.

BACKGROUND: Pyridoxine, an activated form of vitamin B6 used to treat allergic dermatitis, may prevent capecitabine-associated hand-foot syndrome (HFS), although evidence of the benefit of prophylactic Pyridoxine is lacking. The aim of this open-label, multicenter, randomized phase II study was to determine whether prophylactic Pyridoxine could delay the onset of capecitabine-induced HFS in patients with advanced or metastatic breast cancer. METHODS: Patients received either concomitant Pyridoxine (60 mg per day; Pyridoxine group), or no Pyridoxine but treatment with capecitabine-containing regimens (no Pyridoxine group). Study treatment was administered until the development of grade 2 or worse HFS or disease progression. The primary endpoint was the time to onset of grade 2 or worse HFS from the start of protocol treatment. RESULTS: A total of 135 patients were randomized to the Pyridoxine (n = 67) or no Pyridoxine (n = 68) groups. Grade 2 or worse HFS developed in 19 of 66 patients (28.8%) versus 21 of 67 patients (31.3%) in the Pyridoxine and no Pyridoxine groups, respectively. The median time to onset of grade 2 or worse HFS was 13.6 and 10.6 months in the Pyridoxine and no Pyridoxine groups, respectively [hazard ratio = 0.75 (80% confidence interval 0.50-1.13), one-sided P = 0.18]. CONCLUSIONS: Prophylactic Pyridoxine was not shown to have an effect on the onset of capecitabine-associated HFS in this study.

Efficacy of Hydroxy-L-proline (HYP) analogs in the treatment of primary hyperoxaluria in Drosophila Melanogaster.[Pubmed:29980178]

BMC Nephrol. 2018 Jul 6;19(1):167.

BACKGROUND: Substrate reduction therapy with analogs reduces the accumulation of substrates by inhibiting the metabolic pathways involved in their biosynthesis, providing new treatment options for patients with primary hyperoxalurias (PHs) that often progress to end-stage renal disease (ESRD). This research aims to evaluate the inhibition efficacy of Hydroxy-L-proline (HYP) analogs against calcium oxalate (CaOx) crystal formation in the Drosophila Melanogaster (D. Melanogaster) by comparing them with Pyridoxine (Vitamin B6). METHODS: Three stocks of Drosophila Melanogaster (W(118), CG3926 RNAi, and Act5C-GAL4/CyO) were utilized. Two stocks (CG3926 RNAi and Act5C-GAL4 /CyO) were crossed to generate the Act5C > dAGXT RNAi recombinant line (F1 generation) of D. Melanogaster which was used to compare the efficacy of Hydroxy-L-proline (HYP) analogs inhibiting CaOx crystal formation with Vitamin B6 as the traditional therapy for primary hyperoxaluria. RESULTS: Nephrolithiasis model was successfully constructed by downregulating the function of the dAGXT gene in D. Melanogaster (P-Value = 0.0045). Furthermore, the efficacy of Hydroxy-L-proline (HYP) analogs against CaOx crystal formation was demonstrated in vivo using D. Melanogaster model; the results showed that these L-Proline analogs were better in inhibiting stone formation at very low concentrations than Vitamin B6 (IC50 = 0.6 and 1.8% for standard and dietary salt growth medium respectively) compared to N-acetyl-L-Hydroxyproline (IC50 = 0.1% for both standard and dietary salt growth medium) and Baclofen (IC50 = 0.06 and 0.1% for standard and dietary salt growth medium respectively). Analysis of variance (ANOVA) also showed that Hydroxy-L-proline (HYP) analogs were better alternatives for CaOx inhibition at very low concentration especially when both genetics and environmental factors are intertwined (p < 0.0008) for the dietary salt growth medium and (P < 0.063) for standard growth medium. CONCLUSION: Addition of Hydroxy-L-Proline analogs to growth medium resulted in the reduction of CaOx crystals formation. These analogs show promise as potential inhibitors for oxalate reduction in Primary Hyperoxaluria.

Pyridoxine (Pyridoxol) is a pyridine derivative. Pyridoxine exerts antioxidant effects in cell model of Alzheimer's disease via the Nrf-2/HO-1 pathway.

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