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Peripheral Neuropathy
Published in Charles Theisler, Adjuvant Medical Care, 2023
Vitamin B6: Peripheral neuropathy from pyridoxine deficiency is treated with supplementation 10-30 mg/day.17,19 Pyridoxine hydrochloride is also given to patients at risk (e.g., alcoholics) or during long-term therapy with isoniazid to prevent peripheral neuropathy.20
Nutritional Diseases
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Chelsea Kesty, Madeline Hooper, Erin McClure, Emily Chea, Cynthia Bartus
Overview: Pyridoxine deficiency and toxicity can occur. Primary deficiency is rare, but secondary causes include heavy alcohol consumption, isoniazid use, oral contraceptive use, chronic hepatitis, chronic renal failure, and malnutrition. Toxicity occurs secondary to over-supplementation (>500 mg/day).
Vitamins
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
Dietary pyridoxine deficiency can also produce seizures. An example of this was an infant formula accidentally deficient in vitamin B6. Infants given a pyridoxine deficient diet for 1 to 6 months exhibit irritability and generalized seizures including infantile spasms (7). Certain drugs are pyridoxine antagonists. Isonicotinic acid hydrazide (INH), used to treat tuberculosis, and progesterone-estrogen contraceptives increase the requirements for pyridoxine. Seizures have been reported in association with INH administration (5).
Mechanisms of action of vitamin B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin) in pain: a narrative review
Published in Nutritional Neuroscience, 2023
A. M. Paez-Hurtado, C. A. Calderon-Ospina, M. O. Nava-Mesa
Inhibitory control in central circuits under basal conditions is necessary for modulate pain transmission and control excitability. Correspondingly, in an in vivo study, the effect of intracortical microinjection of vitamin B12 was investigated on penicillin-induced epileptiform activity in rats. Combined treatments with vitamin B12 and diazepam resulted in better antiepileptiform effects. The antiepileptic effects of vitamin B12 and diazepam were prevented by flumazenil (GABA-A receptor blocker). Therefore, this result suggests that antiepileptiform effects of vitamin B12 is mediated by GABA-benzodiazepine receptor complex [96]. Moreover, epilepsy secondary to pyridoxine deficiency also indicate that B vitamins are involved in control of glutamate effects in the CNS [141]. Indeed, in vitro studies have shown that combination of B vitamins has protective effects from glutamate induced NMDA-excitotoxicity in neuronal cultures [142,143].
Chapter 9: Pediatric tuberculosis
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2022
Rachel Dwilow, Charles Hui, Fatima Kakkar, Ian Kitai
In children under the age of 10 years, or weighing less than 30 kg, the recommended dose of INH is 10-15 mg/kg/day (maximum 300 mg).23 Administration is affected by food and INH is better absorbed on an empty stomach. Fat and sugars reduce its absorption.61 A sorbitol-based suspension avoids this problem but may cause diarrhea, especially in children weighing more than 5 kg.62 Crushed pills are ideally mixed with water but few children will accept this and administration with small amounts of food/liquid is often suggested.63 Doses of INH above 10 mg/kg/day are sometimes associated with pyridoxine deficiency. Pyridoxine supplementation should be given to children on meat and milk-deficient diets, breastfed infants, those with nutritional deficiencies, children with symptomatic HIV infection and adolescents who are pregnant or breastfeeding.23 Breastfed infants of mothers who are taking INH with supplementary pyridoxine but who themselves are not receiving INH do not need supplementary pyridoxine.
Neonatal pyridoxine administration long lastingly accelerates cortical spreading depression in male rats, without affecting anxiety-like behavior
Published in Nutritional Neuroscience, 2021
Kelly Rayanne Gondim-Silva, Joselma M. da-Silva, Laís A. V. de Souza, Rubem C. A. Guedes
However, little is known about the brain effects of excessive pyridoxine; in animals, behavioral alterations, denoted by expressive vocalization, aggressiveness against another rat of the same cage and behavior of postural instability have been reported under conditions of excessive pyridoxine administration [9]. The amount of the pyridoxine present in the body is essential for the balance between the states of excitation and neuronal inhibition. Pyridoxine deficiency causes significant effects on different electrophysiological variables [4]. In brain excitability-related diseases, pyridoxine supplementation has been used in the treatment of infant seizures, to reduce seizures in neonatal epileptic encephalopathy, in isoniazid-induced epilepsy and ALDH7A1 mutation or pyridoxine-dependent epilepsy. These conditions do not respond to conventional anticonvulsant therapy, and the treatment consists of pyridoxine monotherapy, the main cofactor for the enzymatic conversion of the neurotransmitter glutamate to GABA [11,12]. Therefore, the development of experimental models to study the pyridoxine/brain excitability relationship is highly desirable.