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 causes various symptoms, including seizures, intellectual disability, 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 undernutrition, malabsorption, alcoholism, use of pyridoxine-inactivating drugs (eg, anticonvulsants, isoniazid, cycloserine, hydralazine, corticosteroids, penicillamine), 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 peripheral neuropathy and 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

• Clinical evaluation

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 undernutrition.

Diagnosis is usually clinical. There is no single accepted laboratory test of vitamin B₆ status; measurement of serum pyridoxal phosphate is most common.

Pearls & Pitfalls If anticonvulsants do not stop seizures in infants, consider giving pyridoxine to treat possible vitamin B6 deficiency.

Treatment

• Pyridoxine
• Elimination of risk factors when possible

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 should also be given pyridoxine 30 to 50 mg po once/day. For deficiency due to increased metabolic demand, amounts larger than the daily recommended intake may be required. For most cases of inborn errors of metabolism, high doses of pyridoxine may be effective.

Key Points

• Vitamin B₆ deficiency is usually caused by pyridoxine-inactivating drugs (eg, isoniazid), protein-energy undernutrition, malabsorption, alcoholism, or excessive loss.
• Deficiency can cause peripheral neuropathy, seborrheic dermatitis, glossitis, and cheilosis, and, in adults, depression, confusion, and seizures.
• Suspect and diagnose based on clinical findings.
• Correct secondary causes, or give supplemental pyridoxine.

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 December 2012 by Larry E. Johnson, MD, PhD