Editing Vitamin B6 (section)

===Signs and symptoms===
The classic clinical syndrome for vitamin B<sub>6</sub> deficiency is a [[seborrheic dermatitis]]-like eruption, [[atrophic glossitis]] with [[mouth ulcer|ulceration]], [[angular cheilitis]], [[conjunctivitis]], [[intertrigo]], abnormal [[electroencephalograms]], [[microcytic anemia]] (due to impaired [[heme]] synthesis), and neurological symptoms of [[somnolence]], confusion, depression, and [[neuropathy]] (due to impaired [[sphingosine]] synthesis).<ref name=ODS/>

In infants, a deficiency in vitamin B<sub>6</sub> can lead to irritability, abnormally acute hearing, and convulsive seizures.<ref name=ODS/>

Less severe cases present with metabolic disease associated with insufficient activity of the [[coenzyme]] [[Pyridoxal phosphate|pyridoxal 5' phosphate]] (PLP).<ref name=ODS/> The most prominent of the lesions is due to impaired [[tryptophan]]–[[Niacin (substance)|niacin]] conversion. This can be detected based on urinary excretion of [[xanthurenic acid]] after an oral tryptophan load. Vitamin B<sub>6</sub> deficiency can also result in impaired [[transsulfuration]] of [[methionine]] to [[cysteine]]. The PLP-dependent transaminases and glycogen phosphorylase provide the vitamin with its role in [[gluconeogenesis]], so deprivation of vitamin B<sub>6</sub> results in impaired [[glucose tolerance]].<ref name=ODS/><ref name="Combs"/>