Pyridoxine deficiency
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Pyridoxine_deficiency".

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]

Pyridoxine (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.

Causes

• Lack of pyridoxine in the diet
• Another cause of vitamin B6 deficiency is the use of the tuberculostatic medication isoniazid, and for this reason, it is recommended to supplement with vitamin B6 when using this drug.
• Grumpiness and irritability are also often symptomatic of a deficiency according to "Body, Mind, and the B Vitamins" by Ruth Adams and Frank Murray.
• A meta-analysis of three databases (MEDLINE, EMBASE, and Cochrane Library), including only double-blind, randomized controlled trials, found that vitamin B6 has a significant effect compared to placebos in treating morning sickness, similar to that of ginger.^[2]
• Supporters of a debated medical condition known as Pyroluria believe it may be one potential cause of vitamin B6 deficiency.

Diagnostic testing for pyridoxine deficiency

A positive diagnosis test for pyridoxine deficiency can be assertained by measuring erythrocyte levels of aspartate aminotransferase and transketolase in serum.

References

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