Vitamin B6 deficiency most commonly occurs as a result of alcoholism or interactions with medications, especially isoniazid, cycloserine, penicillamine, and oral contraceptives. A number of inborn errors of metabolism and other pyridoxine-responsive syndromes, particularly pyridoxine-responsive anemia, are not clearly due to vitamin deficiency but commonly respond to high doses of the vitamin. Patients with common variable immunodeficiency may have concomitant vitamin B6 deficiency.
Vitamin B6 deficiency results in clinical symptoms similar to those of other B vitamin deficiencies, including mouth soreness, glossitis, cheilosis, weakness, and irritability. Severe deficiency can result in peripheral neuropathy, anemia, and seizures. Studies have suggested a potential relationship of low vitamin B6 levels and a variety of clinical conditions including inflammatory diseases and certain cancers.
The diagnosis of vitamin B6 deficiency can be confirmed by measurement of pyridoxal phosphate in blood. Normal levels vary per laboratory but are typically greater than 5.0 ng/mL.
Vitamin B6 deficiency can be effectively treated with vitamin B6 supplements (10–20 mg/day orally). Some patients taking medications that interfere with pyridoxine metabolism (such as isoniazid) may need doses as high as 50–100 mg/day orally to prevent vitamin B6 deficiency. This is particularly true for patients who are more likely to have diets marginally adequate in vitamin B6, such as older patients, patients with alcoholism, or patients of lower socioeconomic status. Inborn errors of metabolism and pyridoxine-responsive syndromes often require doses up to 600 mg/day orally.
Clinical trials have shown that vitamin B6 supplementation, combined with other B vitamins, has no benefit on cardiovascular disease outcomes.