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Vitamin B6 Deficiency (Pyridoxine)

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Last Update: October 27, 2018.


Water-soluble vitamin B6 is widely present in many foods, including meat, fish, nuts, beans, grains, fruits and vegetables. Additionally, B6 is present in many multivitamin preparations for adults and children and added to foods as a supplement to breakfast foods, power bars, and powders.

There are several active compounds or vitamers which fall under the generic B6. These include (1) pyridoxine an alcohol, (2) pyridoxal an aldehyde, (3) pyridoxamine which differs from the first two with an amine group, and (4) a 2,5' phosphate esters. The major esters are the active coenzyme form and are pyridoxal 5'phosphate(PLP) and pyridoxamine 5'phosphate(PMP). The major form of B6 in meats are the esters, and the major plant source is pyridoxine, which is less bioavailable. Pyridoxine is the most common form found in multivitamins. 

As a coenzyme, B6 is involved as a cofactor in over 100 enzyme reactions including amino acid metabolism, particularly homocysteine; carbohydrate metabolism, including gluconeogenesis and glycogenolysis; and lipid metabolism. B6 has a role in cognitive development thru neurotransmitter synthesis, immune function with interleukin-2 production, and hemoglobin formation.

Fetal brain development requires adequate B6, and this continues throughout infancy. Vitamin B6 recommendations are made in accordance with age and life stage with pregnancy and breastfeeding involving the highest recommended daily allowance.


In the United States and other western cultures, deficiency is rare with adequate diets, including B6 sources from poultry, fish, organ meats, potatoes, grains, legumes and noncitrus fruits.

Vitamin B6 deficiency is rare in isolation and usually found in association with other B vitamin deficiencies such as folic acid and B12. 

Low plasma levels of active B6 are found in chronic alcohol dependence, with obese states, pregnancy, preeclampsia and eclampsia, and malabsorptive states such as celiac, inflammatory bowel disease, and bariatric surgery.

Additional at-risk groups with inadequate intake or increased metabolic requirements may become functionally deficient in B6.  Included in this group are those with renal impairment, autoimmune disorders, and chronic alcohol use. Patients with chronic renal failure, especially those receiving hemodialysis or peritoneal dialysis, have low plasma levels of B6. Autoimmune disorders, such as rheumatoid arthritis, have increased catabolism of B6, resulting in higher demand for dietary supplementation of B6.

Of great clinical importance in toxicology is that drug antagonists to vitamin B6 occurs with the tuberculosis medicine isoniazid. Also, penicillamine and levodopa, as well as some anticonvulsant medications, may interfere with B6 metabolism.


Risk factors for altered B6 may include excessive or inadequate ingestion. Specifics causes of B6 deficiency have been attributed to inadequate gastrointestinal (GI) absorption, hepatic dysfunction, and drug interaction or antagonism.

The human body cannot store B6, and thus a daily source is required. There appears to be a bioavailability preference for meat over plant source B6. This may be important to those who favor a plant-based diet exclusively. These individuals may need added supplementation. The major supplement in multivitamins is a pyridoxine hydrochloride. Dietary intake and the bioavailability of ingested B6 may vary, as well as the urinary excretion.

RDA or recommended dietary allowance for  B6 in adults is 1 to 1.7mg per day. Children ages 1 to 3 are recommended to have 0.5 mg per day, and those 3 to 13 are recommended to have 1 mg per day. During pregnancy and lactation, the recommendations are 1.9 mg and 2 mg per day.

The average diet for adults is estimated to include 6 to 10 mg of Pyridoxine vitamers. Excessive amounts exceed 250 mg per day and, on a chronic basis, may result in toxicity leading to untoward effects on skin, GI, and the neurologic system.


Vitamin B6 is predominantly absorbed in the small intestine jejunum and is metabolized at the cellular level in the mitochondria and cytosol to active forms in the liver. Excretion of excess B6 occurs in the kidney and is albumin-bound in plasma.  The half-life elimination exceeds 15 to 20 days.

Vitamin B6 deficiency may present with seizures in the young.  Severely deficient adults commonly present with rashes and mental status changes. Additional clinical findings of deficiency may include a normocytic anemia, a nonspecific pruritic rash, cheilitis with scaly lip skin and cracks in the corner of the mouth and glossitis (swelling of the tongue). Depression is associated with a severe B6 deficiency as well.

Current studies are evaluating the role of B6 deficiency in heart disease, cancer, and cognitive decline as medical conditions that may respond to supplementation. To date, there is no clear evidence to support supplement use beyond the normal dietary intake.  However, some studies indicate a reduction of symptoms in the premenstrual syndrome with supplementation of B6, particularly a decrease in moodiness, irritability, and forgetfulness. The American College of Obstetrics and Gynecology recommend vitamin B6 supplementation (1.9 mg per day) for hyperemesis gravidarum.


Vitamin B6 is water soluble. B6 is one of three water-soluble vitamins that can have toxicity at excessive doses; the others being Niacin (Vitamin B2) and Ascorbic acid (Vitamin C).

It is rare to develop B6 toxicity for an individual on ordinary food diets without supplementation. Excessive supplementation for chronic periods (months to greater than a year) has resulted in sensory neuropathies and movement disorders. The severity of symptoms is dose-dependent. Additional clinical findings of toxicity may include photosensitivity, GI symptoms such as nausea and heartburn, as well as painful dermatological eruptions. These symptoms resolve for the most part over time with the elimination of the B6 supplement. The B6 toxicity-induced sensory polyneuropathy causes decreased touch, temperature, and vibration sensation and results in poor coordination.  

In toxicology, Vitamin B6 is clinically important in the treatment of Isoniazid (INH), ethylene glycol, and Gyromitrin (toxic mushroom) poisoning.  Additionally, it is used preventatively during isoniazid (INH) therapy of tuberculosis to prevent INH-induced polyneuropathy.

History and Physical

History should be targeted, and age focused. In the neonate with seizures, mothers with poor nutritional status may be suggestive of a vitamin B6 deficiency.  Also, consideration should be given to inborn error of metabolism that is Vitamin B6-dependent.

The older patient should be questioned on nutritional intake, supplement use, and medication history. Also critically important is eliciting a history of potential malabsorption syndromes which have been strongly associated with Vitamin B6 deficiency such as inflammatory bowel disease, celiac, or surgery of the small intestines including bariatric surgery. On a review of systems, the finding of weakness, mental status change, paresthesias, or other sensory or dermatological symptoms may suggest the diagnosis.

Physical exam findings may include confusion and skin lesions, particularly facial lesions such as stomatitis, glossitis, seborrheic dermatitis, and angular cheilitis. Objective physical findings may include peripheral neuropathies, skin photosensitivity, and movement disorders.


Early or subclinical vitamin B6 deficiency may have vague or fleeting symptoms; however, new onset sensory polyneuropathy, altered mental status, dermatitis in adults, or seizures in infancy should raise clinical suspicion of a clinically significant B6 deficiency. Testing for vitamin B6 can be difficult in real time in many clinical scenarios. Direct serum measurement of the active vitamin Pyridoxal 5′-phosphate (PLP) form is available in some clinical settings, however, the assay is not widely available or timely.  A clinical alternative is an indirect measurement technique of vitamin B6, which includes measuring urinary excretion of xanthurenic acid (an amino acid catabolite of tryptophan) following a measured bolus of tryptophan. Increased levels of xanthurenic acid may indicate inadequate active B6 for the formation of the amino acid tryptophan.

Treatment / Management

In vitamin B6-deficient states and illnesses, treatment dosage is variable and depends on the severity of symptoms. The vitamin is available therapeutically in both oral and parenteral formulations. Neonates with B6 deficiency seizures may require 10 to 100 mg intravenous (IV) for effective treatment of active seizures. Less serious or less acute presentations can be supplemented with doses ranging from 25 mg to 600 mg per day orally depending on symptom complex.

Importantly, Vitamin B6 therapy can be life-saving in refractory INH overdose-induced seizures. The dose is equal to the known amount of INH ingested or a maximum of 5 gms and is dosed 1 to 4 grams IV as the first dose, then 1 g IM or IV every 30 minutes. In ethylene glycol overdose, vitamin B6 is recommended at 50 to 100 mg IV every 6 hours to facilitate shunting the metabolism of ethylene glycol to nontoxic pathways leading to glycine (nontoxic) instead of toxic pathways leading to toxic metabolites such as formate.

Additional, less common uses are in hydralazine overdose where the recommended dose of vitamin B6 is 25 mg/kg, the first third administered intramuscularly and the remainder as a 3-hour IV infusion. Gyromitra (mushroom) toxicity treatment is at 25 mg/kg infused IV over 30 min.

Hyperemesis gravidarum may respond to vitamin B6 at a dosage of 25 mg orally every 8 hours.

Differential Diagnosis

The differential is wide due to the multitude of symptoms and clinical findings associated with B6 deficiency. Some specific disease states with similar symptoms include porphyria, beriberi (thiamine deficiency), normocytic anemias, depression, and the various disorders associated with cognitive decline, folic acid deficiency, INH toxicity, and neonatal seizures.


If diagnosed appropriately, the deficiency is effectively treated with adequate oral or parenteral supplementation.

Pearls and Other Issues

Pyridoxine is the emergency antidote for isoniazid (INH) overdose, ethylene glycol, hydralazine, and gyromitrin mushroom poisoning.  The two most common uses of vitamin B6 are in the treatment of the toxicological emergencies: INH and ethylene glycol overdoses. In INH overdose-related seizure, the dose is 5 grams in adults and 1 gram in children unless the amount of INH is specifically known. Pyridoxine can be given at a rate of 0.5 to 1 gram/minute until seizures stop or maximum dose given. Patients who are asymptomatic and have not had seizures after a potentially toxic ingestion of isoniazid within 2 hours, should receive the recommended dose of pyridoxine. In ethylene glycol overdose, vitamin B6 is recommended at 50 to 100 mg IV every 6 hours to facilitate shunting the metabolism of ethylene glycol to nontoxic pathways leading to glycine (nontoxic) instead of toxic pathways leading to toxic metabolites such as formate.


To access free multiple choice questions on this topic, click here.


Ramos RJ, Pras-Raves ML, Gerrits J, van der Ham M, Willemsen M, Prinsen H, Burgering B, Jans JJ, Verhoeven-Duif NM. Vitamin B6 is essential for serine de novo biosynthesis. J. Inherit. Metab. Dis. 2017 Nov;40(6):883-891. [PubMed: 28801717]
Vrolijk MF, Opperhuizen A, Jansen EHJM, Hageman GJ, Bast A, Haenen GRMM. The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function. Toxicol In Vitro. 2017 Oct;44:206-212. [PubMed: 28716455]
Pellitero S, Martínez E, Puig R, Leis A, Zavala R, Granada ML, Pastor C, Moreno P, Tarascó J, Balibrea J, Puig-Domingo M. Evaluation of Vitamin and Trace Element Requirements after Sleeve Gastrectomy at Long Term. Obes Surg. 2017 Jul;27(7):1674-1682. [PubMed: 28161887]
Dave HN, Eugene Ramsay R, Khan F, Sabharwal V, Irland M. Pyridoxine deficiency in adult patients with status epilepticus. Epilepsy Behav. 2015 Nov;52(Pt A):154-8. [PubMed: 26418265]
Riikonen R, Mankinen K, Gaily E. Long-term outcome in pyridoxine-responsive infantile epilepsy. Eur. J. Paediatr. Neurol. 2015 Nov;19(6):647-51. [PubMed: 26310861]
Lee DG, Lee Y, Shin H, Kang K, Park JM, Kim BK, Kwon O, Lee JJ. Seizures Related to Vitamin B6 Deficiency in Adults. J Epilepsy Res. 2015 Jun;5(1):23-4. [PMC free article: PMC4494992] [PubMed: 26157671]
Lakdawala N, Grant-Kels JM. Acrodermatitis enteropathica and other nutritional diseases of the folds (intertriginous areas). Clin. Dermatol. 2015 Jul-Aug;33(4):414-9. [PubMed: 26051055]
Cupa N, Schulte DM, Ahrens M, Schreiber S, Laudes M. Vitamin B6 intoxication after inappropriate supplementation with micronutrients following bariatric surgery. Eur J Clin Nutr. 2015 Jul;69(7):862-3. [PubMed: 26039319]
Chawla J, Kvarnberg D. Hydrosoluble vitamins. Handb Clin Neurol. 2014;120:891-914. [PubMed: 24365359]
Cellini B, Montioli R, Oppici E, Astegno A, Voltattorni CB. The chaperone role of the pyridoxal 5'-phosphate and its implications for rare diseases involving B6-dependent enzymes. Clin. Biochem. 2014 Feb;47(3):158-65. [PubMed: 24355692]
Baumgart A, Spiczak Sv, Verhoeven-Duif NM, Møller RS, Boor R, Muhle H, Jähn JA, Klitten LL, Hjalgrim H, Lindhout D, Stephani U, van Kempen MJ, Helbig I. Atypical vitamin B6 deficiency: a rare cause of unexplained neonatal and infantile epilepsies. J. Child Neurol. 2014 May;29(5):704-7. [PubMed: 24114605]
Ahmad I, Mirza T, Qadeer K, Nazim U, Vaid FH. Vitamin B6: deficiency diseases and methods of analysis. Pak J Pharm Sci. 2013 Sep;26(5):1057-69. [PubMed: 24035968]
Mintzer S, Skidmore CT, Sperling MR. B-vitamin deficiency in patients treated with antiepileptic drugs. Epilepsy Behav. 2012 Jul;24(3):341-4. [PubMed: 22658435]
Valle-Morales L, Cortés-Cros E, Santana A, Barber M, Figueras T, García-Hernández JA. Epileptic status refractory to conventional treatment caused by vitamin B6 deficiency. J Perinatol. 2009 Mar;29(3):252-3. [PubMed: 19240731]
Waldmann A, Dörr B, Koschizke JW, Leitzmann C, Hahn A. Dietary intake of vitamin B6 and concentration of vitamin B6 in blood samples of German vegans. Public Health Nutr. 2006 Sep;9(6):779-84. [PubMed: 16925884]
Depeint F, Bruce WR, Shangari N, Mehta R, O'Brien PJ. Mitochondrial function and toxicity: role of B vitamins on the one-carbon transfer pathways. Chem. Biol. Interact. 2006 Oct 27;163(1-2):113-32. [PubMed: 16814759]
Clayton PT. B6-responsive disorders: a model of vitamin dependency. J. Inherit. Metab. Dis. 2006 Apr-Jun;29(2-3):317-26. [PubMed: 16763894]
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