Vitamin B6 toxicity may be caused by ingestion of megadoses (> 500 mg/day) of pyridoxine. Toxicity may cause peripheral neuropathy. Diagnosis is clinical. Recovery is slow and sometimes incomplete.
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, central nervous system, 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).
Dietary sources of vitamin B6 include organ meats (eg, liver), whole-grain cereals, fish, and legumes. (See also Overview of Vitamins.)
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
Clinical evaluation
Diagnosis of vitamin B6 toxicity is clinical.
Treatment of Vitamin B6 Toxicity
Treatment of vitamin B6 toxicity is to stop taking vitamin B6.
Recovery is slow and, for some patients, incomplete.
