Vitamin B6 Toxicity
Pyridoxine, pyridoxamine, pyridoxal, and the phosphorylated derivative of each of these compounds
Symptoms
Vitamin B6 toxicity manifests with peripheral neuropathy, dermatoses, photosensitivity, dizziness, and nausea
Patients will typically present with bilateral sensory or motor changes, although a unilateral presentation is possible if there has been previous trauma or neurologic injury to an extremity.
Sources
Pyroxidine and pyridoxamine are found in plant foods
Pyroxidal in animal products
Cooking, processing and storing reduces availability 10 to 50%
Metabolism
Converted in the liver to the active form
Catabolised and excreted in urine
Actions
Needed in gluconeogenesis
Decarboxylates AAs
Tryptophan to Niacin
Heme synthesis
Immune function
Neurotransmitter synthesis
Steroid and hormone modulation
Deficiency
Rare
Marginal deficiencies may be more common, manifested as nonspecific stomatitis, glossitis, cheilosis, irritability, confusion, and depression, and possibly peripheral neuropathy
Toxicity
Cases of peripheral neuropathy, dermatoses, photosensitivity, dizziness, and nausea have been reported with long-term megadoses of pyridoxine over 250 mg/day; a few cases of neuropathy appear to have been caused by chronic intake of 100 to 200 mg/day
Cases of acute intoxication typically present with paresthesias, generalized sensory loss, and autonomic dysfunction, without weakness
The clinical picture is similar to that of animal models of pyridoxine toxicity and may be caused by a sensory ganglion neuronopathy
Treatment
There is no specific treatment or antidote for pyridoxine toxicity. Treatment involves cessation of supplemental pyridoxine promptly following diagnosis, symptomatic management, and supportive care for any continued or irreversible symptoms
Prognosis
Prognosis is usually favorable, with symptoms resolving or decreasing when supratherapeutic pyridoxine has been discovered and stopped.
References
Vitamin B6 Update - TGA
Vitamin B6 Toxicity - Stat Pearls