Vitamin B 6
(See also Overview of Vitamins.)
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 (see Table: Sources, Functions, and Effects of Vitamins).
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 vitamin B6deficiency, though rare, can develop because extensive processing can deplete foods of vitamin B6.
Secondary vitamin B6deficiency most often results from
Use of pyridoxine-inactivating drugs (eg, anticonvulsants, isoniazid, cycloserine, hydralazine, corticosteroids, penicillamine)
Excessive loss during hemodialysis
Rarely, secondary deficiency results from increased metabolic demand (eg, in hyperthyroidism).
Rare inborn errors of metabolism can affect pyridoxine metabolism.
Vitamin B6 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.
Vitamin B6 deficiency should be considered in
Diagnosis of vitamin B6 deficiency is usually clinical. There is no single accepted laboratory test of vitamin B6 status; measurement of serum pyridoxal phosphate is most common.
For secondary vitamin B6 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.
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.
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 of vitamin B6 toxicity is clinical.
Treatment of vitamin B6 toxicity is to stop taking vitamin B6. Recovery is slow and, for some patients, incomplete.