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BMJ Clinical Evidence Mar 2014More than half of pregnant women suffer from nausea and vomiting, which typically begins by the fourth week and disappears by the 16th week of pregnancy. The cause of... (Review)
Review
INTRODUCTION
More than half of pregnant women suffer from nausea and vomiting, which typically begins by the fourth week and disappears by the 16th week of pregnancy. The cause of nausea and vomiting in pregnancy is unknown, but may be due to the rise in human chorionic gonadotrophin concentration. In 1 in 200 women, the condition progresses to hyperemesis gravidarum, which is characterised by prolonged and severe nausea and vomiting, dehydration, and weight loss.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of treatment for nausea and vomiting in early pregnancy? What are the effects of treatments for hyperemesis gravidarum? We searched: Medline, Embase, The Cochrane Library, and other important databases up to September 2013 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found 32 studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review we present information relating to the effectiveness and safety of the following interventions: acupressure; acupuncture; corticosteroids; ginger; metoclopramide; ondansetron; prochlorperazine; promethazine; and pyridoxine (vitamin B6).
Topics: Acupressure; Acupuncture Therapy; Adrenal Cortex Hormones; Antiemetics; Female; Zingiber officinale; Humans; Nausea; Pregnancy; Pyridoxine; Vomiting
PubMed: 24646807
DOI: No ID Found -
CNS Neuroscience & Therapeutics Jan 2020Neurotropic B vitamins play crucial roles as coenzymes and beyond in the nervous system. Particularly vitamin B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin)... (Review)
Review
BACKGROUND
Neurotropic B vitamins play crucial roles as coenzymes and beyond in the nervous system. Particularly vitamin B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin) contribute essentially to the maintenance of a healthy nervous system. Their importance is highlighted by many neurological diseases related to deficiencies in one or more of these vitamins, but they can improve certain neurological conditions even without a (proven) deficiency.
AIM
This review focuses on the most important biochemical mechanisms, how they are linked with neurological functions and what deficits arise from malfunctioning of these pathways.
DISCUSSION
We discussed the main role of B Vitamins on several functions in the peripheral and central nervous system (PNS and CNS) including cellular energetic processes, antioxidative and neuroprotective effects, and both myelin and neurotransmitter synthesis. We also provide an overview of possible biochemical synergies between thiamine, pyridoxine, and cobalamin and discuss by which major roles each of them may contribute to the synergy and how these functions are inter-related and complement each other.
CONCLUSION
Taking into account the current knowledge on the neurotropic vitamins B1, B6, and B12, we conclude that a biochemical synergy becomes apparent in many different pathways in the nervous system, particularly in the PNS as exemplified by their combined use in the treatment of peripheral neuropathy.
Topics: Animals; Central Nervous System; Humans; Nervous System Diseases; Nervous System Physiological Phenomena; Peripheral Nervous System; Pyridoxine; Thiamine; Vitamin B 12; Vitamin B Complex
PubMed: 31490017
DOI: 10.1111/cns.13207 -
Nutrients Jun 2023Vitamin B6 is a water-soluble vitamin that is naturally present in many foods and is accessible in many dietary supplements. The three natural forms are pyridoxine,... (Review)
Review
INTRODUCTION
Vitamin B6 is a water-soluble vitamin that is naturally present in many foods and is accessible in many dietary supplements. The three natural forms are pyridoxine, pyridoxal, and pyridoxamine. Both vitamin B6 deficiency and high B6 intake have been described as risk factors for developing peripheral neuropathy (PN). The aim of this systematic review is to characterize and comprehensively describe B6-related PN.
METHOD
A systematic, computer-based search was conducted using the PubMed database. Twenty articles were included in this review.
RESULTS
Higher vitamin B6 levels, which usually occur following the taking of nutritional supplements, may lead to the development of a predominantly, if not exclusively, sensory neuropathy of the axonal type. After pyridoxine discontinuation, such patients subjectively report improved symptoms. However, although low vitamin B6 levels can be seen in patients suffering from peripheral neuropathy of various etiologies, there is no firm evidence that low B6 levels have a direct causal relationship with PN. Many studies suggest subjective improvement of neuropathy symptoms in patients suffering from PN of various etiologies after receiving B6 supplementation; however, no data about B6 administration as a monotherapy exist, only as part of a combination treatment, usually with other vitamins. Therefore, the potential therapeutic role of B6 cannot be confirmed to date. Supplementation with vitamin B6, even as part of a nutritional multivitamin supplement, has not been proven harmful at permitted daily doses in patients who already suffer from PN.
CONCLUSION
Current scientific evidence supports a neurotoxic role of B6 at high levels. Although some studies suggest that low B6 is also a potential risk factor, further studies in this area are needed.
Topics: Humans; Pyridoxine; Vitamin B 6; Pyridoxal; Pyridoxamine; Vitamins; Peripheral Nervous System Diseases
PubMed: 37447150
DOI: 10.3390/nu15132823 -
Advances in Nutrition (Bethesda, Md.) Oct 2021Vitamin B-6 in the form of pyridoxine (PN) is commonly used by the general population. The use of PN-containing supplements has gained lots of attention over the past... (Review)
Review
Vitamin B-6 in the form of pyridoxine (PN) is commonly used by the general population. The use of PN-containing supplements has gained lots of attention over the past years as they have been related to the development of peripheral neuropathy. In light of this, the number of reported cases of adverse health effects due to the use of vitamin B-6 have increased. Despite a long history of study, the pathogenic mechanisms associated with PN toxicity remain elusive. Therefore, the present review is focused on investigating the mechanistic link between PN supplementation and sensory peripheral neuropathy. Excessive PN intake induces neuropathy through the preferential injury of sensory neurons. Recent reports on hereditary neuropathy due to pyridoxal kinase (PDXK) mutations may provide some insight into the mechanism, as genetic deficiencies in PDXK lead to the development of axonal sensory neuropathy. High circulating concentrations of PN may lead to a similar condition via the inhibition of PDXK. The mechanism behind PDXK-induced neuropathy is unknown; however, there is reason to believe that it may be related to γ-aminobutyric acid (GABA) neurotransmission. Compounds that inhibit PDXK lead to convulsions and reductions in GABA biosynthesis. The absence of central nervous system-related symptoms in PDXK deficiency could be due to differences in the regulation of PDXK, where PDXK activity is preserved in the brain but not in peripheral tissues. As PN is relatively impermeable to the blood-brain barrier, PDXK inhibition would similarly be confined to the peripheries and, as a result, GABA signaling may be perturbed within peripheral tissues, such as sensory neurons. Perturbed GABA signaling within sensory neurons may lead to excitotoxicity, neurodegeneration, and ultimately, the development of peripheral neuropathy. For several reasons, we conclude that PDXK inhibition and consequently disrupted GABA neurotransmission is the most plausible mechanism of toxicity.
Topics: Humans; Peripheral Nervous System Diseases; Pyridoxal Kinase; Pyridoxine; Vitamin B 6; Vitamins
PubMed: 33912895
DOI: 10.1093/advances/nmab033 -
Journal of Medicine and Life Jun 2023The prevalence of nephrolithiasis is increasing across all demographic groups. Apart from the morbidity associated with an acute occurrence, preventative treatment is... (Review)
Review
The prevalence of nephrolithiasis is increasing across all demographic groups. Apart from the morbidity associated with an acute occurrence, preventative treatment is essential for stone disease, which can become a long-term problem. Simple interventions like fluid intake optimization and dietary modification are effective for most stone types. However, patients with specific metabolic abnormalities may require pharmaceutical therapy if lifestyle changes are insufficient to reduce the risk of stone recurrence. The treatment of citrates and/or pyridoxines may help eliminate or prevent recurrences of kidney stones, especially when they are composed of uric acid, calcium oxalate, calcium phosphate, or the latter two together. In cases of struvite stones, which often necessitate a surgical approach, acetohydroxamic acid emerges as a valuable second-line treatment option. Thiol-binding agents may be needed for cystinuria, as well as lifestyle modifications. Successful treatment reduces stone recurrence and the need to remove stones surgically.
Topics: Humans; Pyridoxine; Citrates; Kidney Calculi; Calcium Oxalate; Life Style
PubMed: 37675156
DOI: 10.25122/jml-2023-0234 -
Neurology Dec 2022Pyridoxine-dependent epilepsy (PDE-ALDH7A1) is a developmental epileptic encephalopathy characterized by seizure improvement after pyridoxine supplementation. Adjunct...
BACKGROUND AND OBJECTIVES
Pyridoxine-dependent epilepsy (PDE-ALDH7A1) is a developmental epileptic encephalopathy characterized by seizure improvement after pyridoxine supplementation. Adjunct lysine reduction therapies (LRTs) reduce the accumulation of putative neurotoxic metabolites with the goal to improve developmental outcomes. Our objective was to examine the association between treatment with LRTs and cognitive outcomes.
METHODS
Participants were recruited from within the International Registry for Patients with Pyridoxine-Dependent Epilepsy from August 2014 through March 2021. The primary outcome was standardized developmental test scores associated with overall cognitive ability. The relationship between test scores and treatment was analyzed with multivariable linear regression using a mixed-effects model. A priori, we hypothesized that treatment in early infancy with pyridoxine and LRTs would result in a normal developmental outcome. A subanalysis was performed to evaluate the association between cognitive outcome and LRTs initiated in the first 6 months of life.
RESULTS
A total of 112 test scores from 60 participants were available. On average, treatment with pyridoxine and LRTs was associated with a nonsignificant increase of 6.9 points (95% CI -2.7 to 16.5) on developmental testing compared with treatment with pyridoxine alone. For the subanalysis, a total of 14 developmental testing scores were available from 8 participants. On average, treatment with pyridoxine and LRTs in the first 6 months of life was associated with a significant increase of 21.9 points (95% CI 1.7-42.0) on developmental testing.
DISCUSSION
Pyridoxine and LRTs at any age was associated with mild improvement in developmental testing, and treatment in early infancy was associated with a clinically significant increase in developmental test scores. These results provide insight into the mechanism of intellectual and developmental disability in PDE-ALDH7A1 and emphasize the importance of treatment in early infancy with both pyridoxine and LRTs.
CLASSIFICATION OF EVIDENCE
This study provides Class IV evidence that in PDE-ALDH7A1, pyridoxine and LRTs compared with pyridoxine alone is not significantly associated with overall higher developmental testing scores, but treatment in the first 6 months of life is associated with significantly higher developmental testing scores.
Topics: Humans; Lysine; Pyridoxine; Epilepsy; Cognition; Aldehyde Dehydrogenase
PubMed: 36008148
DOI: 10.1212/WNL.0000000000201222 -
Developmental Medicine and Child... Jun 2001
Review
Topics: Humans; Infant, Newborn; Magnetic Resonance Imaging; Metabolism, Inborn Errors; Molecular Biology; Pyridoxine; Recurrence; Seizures; Tomography, X-Ray Computed; Treatment Outcome
PubMed: 11409832
DOI: 10.1017/s0012162201000779 -
Nephrologie & Therapeutique Jul 2011Primary hyperoxalurias are rare recessive inherited inborn errors of glyoxylate metabolism. They are responsible for progressive renal involvement, which further lead to...
Primary hyperoxalurias are rare recessive inherited inborn errors of glyoxylate metabolism. They are responsible for progressive renal involvement, which further lead to systemic oxalate deposition, which can even occur in infants. Primary hyperoxaluria type 1 is the most common form in Europe and is due to alanine-glyoxylate aminostransferase deficiency, a hepatic peroxisomal pyridoxin-dependent enzyme. Therefore primary hyperoxaluria type 1 is responsible for hyperoxaluria leading to aggressive stone formation and nephrocalcinosis. As glomerular filtration rate decreases, systemic oxalate storage occurs throughout all the body, and mainly in the skeleton. The diagnosis is first based on urine oxalate measurement, then on genotyping, which may also allow prenatal diagnosis to be proposed. Conservative measures - including hydration, crystallization inhibitors and pyridoxine - are safe and may allow long lasting renal survival, provided it is given as soon as the diagnosis has been even suspected. No dialysis procedure can remove enough oxalate to compensate oxalate overproduction from the sick liver, therefore a combined liver and kidney transplantation should be planned before advanced renal disease has occurred, in order to limit/avoid systemic oxalate deposition. In the future, primary hyperoxaluria type 1 may benefit from hepatocyte transplantation, chaperone molecules, etc.
Topics: Alanine Transaminase; Disease Progression; Genotype; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Transplantation; Liver Transplantation; Mutation; Peritoneal Dialysis; Pyridoxine; Treatment Outcome; Vitamin B Complex
PubMed: 21636340
DOI: 10.1016/j.nephro.2011.03.004 -
Molecular Genetics & Genomic Medicine Oct 2022Typical patients with KCNQ2 (OMIM# 602235) epileptic encephalopathy present early neonatal-onset intractable seizures with a burst suppression EEG pattern and severe... (Review)
Review
BACKGROUND
Typical patients with KCNQ2 (OMIM# 602235) epileptic encephalopathy present early neonatal-onset intractable seizures with a burst suppression EEG pattern and severe developmental delay or regression, and those patients always fail first-line treatment with sodium channel blockers. Vitamin B6, either pyridoxine or pyridoxal 50-phosphate, has been demonstrated to improve seizure control in intractable epilepsy.
METHODS
Here, we collected and summarized the clinical data for four independent cases diagnosed with pyridoxine-responsive epileptic encephalopathy, and their exome sequencing data. Moreover, we reviewed all published cases and summarized the clinical features, genetic variants, and treatment of pyridoxine-responsive KCNQ2 epileptic encephalopathy.
RESULTS
All four cases showed refractory seizures during the neonatal period or infancy, accompanied by global development delay. Four pathogenetic variants of KCNQ2 were uncovered and confirmed by Sanger sequencing: KCNQ2 [NM_172107.4: c.2312C > T (p.Thr771Ile), c.873G > C (p.Arg291Ser), c.652 T > A (p.Trp218Arg) and c.913-915del (p. Phe305del)]. Sodium channel blockers and other anti-seizure medications failed to control their seizures. The frequency of seizures gradually decreased after treatment with high-dose pyridoxine. In case 1, case 2, and case 4, clinical seizures relapsed when pyridoxine was withdrawn, and seizures were controlled again when pyridoxine treatment was resumed.
CONCLUSION
Our study suggests that pyridoxine may be a promising adjunctive treatment option for patients with KCNQ2 epileptic encephalopathy.
Topics: Electroencephalography; Epilepsy, Generalized; Humans; Infant, Newborn; KCNQ2 Potassium Channel; Phosphates; Pyridoxal; Pyridoxine; Sodium Channel Blockers
PubMed: 35906921
DOI: 10.1002/mgg3.2024 -
American Journal of Physiology. Cell... Dec 2019Pyridoxine (vitamin B), an essential micronutrient for normal cell physiology, plays an important role in the function of the exocrine pancreas. Pancreatic acinar cells...
Pyridoxine (vitamin B), an essential micronutrient for normal cell physiology, plays an important role in the function of the exocrine pancreas. Pancreatic acinar cells (PACs) obtain vitamin B from circulation, but little is known about the mechanism involved in the uptake process; limited information also exists on the effect of pyridoxine availability on the gene expression profile in these cells. We addressed both these issues in the current investigation using mouse-derived pancreatic acinar 266-6 cells (PAC 266-6) and human primary PACs (hPACs; obtained from organ donors), together with appropriate physiological and molecular (RNA-Seq) approaches. The results showed [H]pyridoxine uptake to be ) pH and temperature (but not Na) dependent, ) saturable as a function of concentration, ) -inhibited by unlabeled pyridoxine and its close structural analogs, ) -stimulated by unlabeled pyridoxine, ) regulated by an intracellular Ca/calmodulin-mediated pathway, ) adaptively-regulated by extracellular substrate (pyridoxine) availability, and ) negatively impacted by exposure to cigarette smoke extract. Vitamin B availability was found (by means of RNA-Seq) to significantly (FDR < 0.05) modulate the expression profile of many genes in PAC 266-6 cells (including those that are relevant to pancreatic health and development). These studies demonstrate, for the first time, the involvement of a regulatable and specific carrier-mediated mechanism for pyridoxine uptake by PACs; the results also show that pyridoxine availability exerts profound effects on the gene expression profile in mammalian PACs.
Topics: Acinar Cells; Animals; Biological Transport; Calcium; Calmodulin; Cell Line; Cigarette Smoking; Complex Mixtures; Gene Expression Profiling; Gene Expression Regulation; Humans; Hydrogen-Ion Concentration; Mice; Pancreas, Exocrine; Primary Cell Culture; Pyridoxine; Temperature; Transcriptome
PubMed: 31483702
DOI: 10.1152/ajpcell.00225.2019