Pyridoxine deficiency overview
Overview
The classic clinical syndrome for Pyridoxine deficiency (or B6 deficiency) is a seborrheic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy.[1] Vitamin B6 is a co-factor for glutamic acid decarboxylase, an enzyme that converts Glutamate to GABA. Therefore, the concurrent increase in the excitatory neurotransmitter, Glutamate, and decrease in inhibitory neurotransmitter, GABA, resultant from B6 deficiency, may manifest itself in the form of seizures.
References
- ↑ Andrews' Diseases of the Skin, 10th Edition, Elsevier.