Vitamin B6 (pyridoxine) causes neuropathy at intakes of 1000 mg per day or more, which is about 800 times the daily intake from foods. A report of neurotoxicity in 2 patients who had taken 24 mg and 40 mg of vitamin B6 per day respectively, may be coincidence rather than a true toxic effect of such relatively low doses.
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Uropathy at intakes of 1000 mg per day or more, which is about 800 times the daily intake from foods. There have also been occasional reports of toxicity at intakes of 100-300 mg per day. A report of neurotoxicity in 2 patients who had taken 24 mg and 40 mg of vitamin B6 per day respectively, may be coincidence rather than a true toxic effect of such relatively low doses.
However, physicians need to remain alert to high intakes of vitamin B6 as a cause of unexplained neuropath.
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N 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 intac.
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Background: B-Complex vitamins are essential for functioning of the nervous system, and supplementation is generally well tolerated. Herein, we report a case of reversible pyridoxine induced sensorimotor neuropathy and disequilibrium in an octogenarian.
She had absent deep tendon reflexes in both upper and lower extremities, and a steppage gait on the left. Additional work-up, including serum B12, hemoglobin A1c, thyroid panel, SPEP/UPEP were unremarkable. Conclusions: In conclusion, sensorimotor neuropathy secondary to pyridoxine toxicity can be debilitating, but is potentially reversible with timely cessation of vitamin B6 supplementation and intensive physiotherapy.
Disclosure: Dr. Moudgal has nothing to disclose.
Abstract
Vitamin B-6 in the form of pyridoxine (PN) is commonly used by the general population. Therefore, the present review is focused on investigating the mechanistic link between PN supplementation and sensory peripheral neuropathy.
Excessive PN intake induces neuropathy through the preferential injury of sensory neurons. The mechanism behind PDXK-induced neuropathy is unknown; however, there is reason to believe that it may be related to γ-aminobutyric acid (GABA) neurotransmission. For several reasons, we conclude that PDXK inhibition and consequently disrupted GABA neurotransmission is the most plausible mechanism of toxicity.