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Vitamin B₆ includes a group of closely related compounds: pyridoxine, pyridoxal, and pyridoxamine. They are metabolized in the body to pyridoxal phosphate, which acts as a coenzyme in many important reactions in blood, CNS, and skin metabolism. Vitamin B₆ is important in heme and nucleic acid biosynthesis and in lipid, carbohydrate, and amino acid metabolism.

Vitamin B₆ Deficiency and Dependency

Because vitamin B₆ is present in most foods, dietary deficiency is rare. Secondary deficiency may result from various conditions. Symptoms can include peripheral neuropathy, a pellagra-like syndrome, anemia, and seizures, which, particularly in infants, may not resolve when treated with anticonvulsants. Impaired metabolism (dependency) is rare; it produces various symptoms, including seizures, mental retardation, and anemia. Diagnosis is usually clinical; no laboratory test readily assesses vitamin B₆ status. Treatment consists of giving oral vitamin B₆ and, when possible, treating the cause.

Dietary deficiency, though rare, can develop because extensive processing can deplete foods of vitamin B₆. Secondary deficiency most often results from protein-energy malnutrition, malabsorption, alcoholism, use of pyridoxine-inactivating drugs (eg, anticonvulsants, isoniazid Some Trade Names
INH
NYDRAZID
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, cycloserine Some Trade Names
SEROMYCIN
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, hydralazine Some Trade Names
APRESOLINE
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, corticosteroids, penicillamine Some Trade Names
CUPRIMINE
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), or excessive loss. Rarely, it results from increased metabolic demand (eg, in hyperthyroidism).

Rare inborn errors of metabolism can affect pyridoxine metabolism.

The role of vitamin B₆ deficiency in increasing plasma homocysteine levels and in contributing to vascular disorders is under study.

Symptoms and Signs

Deficiency causes a pellagra-like syndrome, with seborrheic dermatitis, glossitis, and cheilosis, and, in adults, can cause depression, confusion, EEG abnormalities, and seizures. Rarely, deficiency or dependency causes seizures in infants. Seizures, particularly in infants, may be refractory to treatment with anticonvulsants. Normocytic, microcytic, or sideroblastic anemia can also develop.

Diagnosis

Vitamin B₆ deficiency should be considered in any infant who has seizures, any patient who has seizures refractory to treatment with anticonvulsants, and any patient with deficiencies of other B vitamins, particularly in patients with alcoholism or protein-energy malnutrition. Diagnosis is usually clinical. There is no single accepted laboratory test of vitamin B₆ status; measurement of plasma pyridoxal phosphate is most common.

Prevention and Treatment

For secondary deficiency, causes (eg, use of pyridoxine-inactivating drugs, malabsorption) should be corrected if possible. Usually, pyridoxine 50 to 100 mg po once/day corrects the deficiency in adults. Most people taking isoniazid Some Trade Names
INH
NYDRAZID
Click for Drug Monograph
should also be given pyridoxine 30 to 50 mg/day. For deficiency due to increased metabolic demand, amounts larger than the daily recommended intake (DRI) may be required. For most cases of inborn errors of metabolism, high doses of pyridoxine may be effective.

Vitamin B₆ Toxicity

The ingestion of megadoses (> 500 mg/day) of pyridoxine (eg, taken to treat carpal tunnel syndrome or premenstrual syndrome although efficacy is unproved) may cause peripheral neuropathy with deficits in a stocking-glove distribution, including progressive sensory ataxia and severe impairment of position and vibration senses. Senses of touch, temperature, and pain are less affected. Motor and central nervous systems are usually intact.

Diagnosis is clinical. Treatment is to stop taking vitamin B₆. Recovery is slow and, for some patients, incomplete.

Last full review/revision April 2007 by Larry E. Johnson, MD, PhD

Content last modified April 2007