Vitamin B6 Toxicity

This blog post will walk you through: vitamin b6 toxicity. Don’t worry, we’ve got all the answers about this subject.

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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. The US authorities set the no-observed-adverse-effect-level at 200 mg per day and the safe upper limit at 100 mg per day.
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.

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To present the salient features, and reversibility of pyridoxine (vitamin B6) induced peripheral neuropathy, in conjunction with its electrodiagnostic correlate.
Herein, we report a case of reversible pyridoxine induced sensorimotor neuropathy and disequilibrium in an octogenarian. Sensory examination was notable for length dependent multimodal sensory loss in a stocking-glove pattern, and diminished joint position sense. Additional work-up, including serum B12, hemoglobin A1c, thyroid panel, SPEP/UPEP were unremarkable.
Mri of cervical-lumbar spine showed degenerative changes, and was otherwise unremarkable. Nerve conduction studies of the left lower extremity were notable for evidence of chronic, length-dependent, sensorimotor, axonal, peripheral polyneuropathy with extensive active denervation in distal muscles. Intervention: Pyridoxine supplementation was discontinued and the patient underwent intensive physiotherapy.
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. Dr. Awosika has nothing to disclos.


Vitamin B-6 in the form of pyridoxine (PN) is commonly used by the general population.
Recent reports on hereditary neuropathy due to pyridoxal kinase (PDXK) mutations may provide some insight into the mechanism, as genetic deficiencies in PDXK lead to the development of axonal sensory neuropathy. High circulating concentrations of PN may lead to a similar condition via the inhibition of PDXK. 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.
The absence of central nervous system-related symptoms in PDXK deficiency could be due to differences in the regulation of PDXK, where PDXK activity is preserved in the brain but not in peripheral tissues. As PN is relatively impermeable to the blood–brain barrier, PDXK inhibition would similarly be confined to the peripheries and, as a result, GABA signaling may be perturbed within peripheral tissues, such as sensory neurons.

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