Editing Vitamin B6 (section)

==Deficiency==
===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"/>

===Diagnosis===
The assessment of vitamin B<sub>6</sub> status is essential, as the clinical signs and symptoms in less severe cases are not specific.<ref>{{cite book|chapter-url=https://books.google.com/books?id=lBlu7UKI3aQC|title=Principles of Nutritional Assessment|vauthors=Gibson RS|publisher=Oxford University Press|year=2005|isbn=978-0-19-517169-3|edition=2nd|location=New York|pages=575–594|chapter=Assessment of vitamin B<sub>6</sub> status|lccn=2004054778|oclc=884490740|access-date=April 20, 2018|archive-date=December 31, 2023|archive-url=https://web.archive.org/web/20231231072056/https://books.google.com/books?id=lBlu7UKI3aQC|url-status=live}}</ref> The three biochemical tests most widely used are plasma PLP concentrations, the activation coefficient for the erythrocyte enzyme aspartate aminotransferase, and the urinary excretion of vitamin B<sub>6</sub> degradation products, specifically urinary PA. Of these, plasma PLP is probably the best single measure, because it reflects tissue stores. Plasma PLP of less than 10&nbsp;nmol/L is indicative of vitamin B<sub>6</sub> deficiency.<ref name=Ueland2015>{{cite journal |vauthors=Ueland PM, Ulvik A, Rios-Avila L, Midttun Ø, Gregory JF |title=Direct and Functional Biomarkers of Vitamin B6 Status |journal=Annu Rev Nutr |volume=35 |issue= |pages=33–70 |date=2015 |pmid=25974692 |pmc=5988249 |doi=10.1146/annurev-nutr-071714-034330 |url=}}</ref> A PLP concentration greater than 20&nbsp;nmol/L has been chosen as a level of adequacy for establishing Estimated Average Requirements and Recommended Daily Allowances in the USA.<ref name="DRItext" /> Urinary PA is also an indicator of vitamin B<sub>6</sub> deficiency; levels of less than 3.0&nbsp;mmol/day is suggestive of vitamin B<sub>6</sub> deficiency.<ref name=Ueland2015 /> Other methods of measurement, including [[Ultraviolet–visible spectroscopy|UV spectrometric]], [[Fluorescence spectroscopy|spectrofluorimetric]], [[Mass spectrometry|mass spectrometric]], [[thin-layer chromatography|thin-layer]] and [[High-performance liquid chromatography|high-performance liquid chromatographic]], [[Electrophoresis|electrophoretic]], [[electrochemistry|electrochemical]], and enzymatic, have been developed.<ref name=Ueland2015 /><ref>{{cite journal |vauthors=Ahmad I, Mirza T, Qadeer K, Nazim U, Vaid FH |title=Vitamin B6: deficiency diseases and methods of analysis |journal=Pak J Pharm Sci |volume=26 |issue=5 |pages=1057–69 |date=September 2013 |pmid=24035968 |doi= |url=}}</ref>

The classic clinical symptoms for vitamin B<sub>6</sub> deficiency are rare, even in developing countries. A handful of cases were seen between 1952 and 1953, particularly in the United States, having occurred in a small percentage of infants who were fed a formula lacking in pyridoxine.<ref name="TCN">{{cite book |url=https://books.google.com/books?id=og-0AAAAIAAJ |title=Textbook of Child Neurology |last=Menkes |first=John H. |publisher=Henry Kimpton Publishers |year=1980 |isbn=978-0-8121-0661-9 |edition=2nd |location=Philadelphia |page=486 |lccn=79010975 |oclc=925196268 |access-date=April 20, 2018 |archive-date=December 31, 2023 |archive-url=https://web.archive.org/web/20231231072058/https://books.google.com/books?id=og-0AAAAIAAJ |url-status=live }}</ref>

===Causes===
A deficiency of vitamin B<sub>6</sub> alone is relatively uncommon and often occurs in association with other vitamins of the B complex. Evidence exists for decreased levels of vitamin B<sub>6</sub> in women with [[type 1 diabetes]] and in patients with [[systemic inflammation]], liver disease, [[rheumatoid arthritis]], and those infected with [[HIV]].<ref>{{cite journal | vauthors = Massé PG, Boudreau J, Tranchant CC, Ouellette R, Ericson KL | title = Type 1 diabetes impairs vitamin B(6) metabolism at an early stage of women's adulthood | journal = Applied Physiology, Nutrition, and Metabolism| volume = 37 | issue = 1 | pages = 167–75 | date = February 2012 | pmid = 22288928 | doi = 10.1139/h11-146 }}</ref><ref>{{cite journal | vauthors = Ulvik A, Midttun Ø, Pedersen ER, Eussen SJ, Nygård O, Ueland PM | title = Evidence for increased catabolism of vitamin B-6 during systemic inflammation | journal = The American Journal of Clinical Nutrition | volume = 100 | issue = 1 | pages = 250–5 | date = July 2014 | pmid = 24808485 | doi = 10.3945/ajcn.114.083196 | doi-access = free }}</ref> Use of [[oral contraceptive]]s and treatment with certain [[anticonvulsant]]s, [[isoniazid]], [[cycloserine]], [[penicillamine]], and [[hydrocortisone]] negatively impact vitamin B<sub>6</sub> status.<ref name=ODS/><ref>{{cite journal | vauthors = Wilson SM, Bivins BN, Russell KA, Bailey LB | title = Oral contraceptive use: impact on folate, vitamin B<sub>6</sub>, and vitamin B<sub>12</sub> status | journal = Nutrition Reviews | volume = 69 | issue = 10 | pages = 572–83 | date = October 2011 | pmid = 21967158 | doi = 10.1111/j.1753-4887.2011.00419.x | doi-access = free }}</ref><ref>{{cite journal | vauthors = Schwaninger M, Ringleb P, Winter R, Kohl B, Fiehn W, Rieser PA, Walter-Sack I | title = Elevated plasma concentrations of homocysteine in antiepileptic drug treatment | journal = Epilepsia | volume = 40 | issue = 3 | pages = 345–50 | date = March 1999 | pmid = 10080517 | doi = 10.1111/j.1528-1157.1999.tb00716.x | doi-access = free }}</ref> [[Hemodialysis]] reduces vitamin B<sub>6</sub> plasma levels.<ref>{{cite journal | vauthors = Corken M, Porter J | title = Is vitamin B(6) deficiency an under-recognized risk in patients receiving haemodialysis? A systematic review: 2000-2010 | journal = Nephrology | volume = 16 | issue = 7 | pages = 619–25 | date = September 2011 | pmid = 21609363 | doi = 10.1111/j.1440-1797.2011.01479.x | s2cid = 22894817 | doi-access = free }}</ref> Overconsumption of ''[[Ginkgo biloba]]'' seeds can also deplete vitamin B<sub>6</sub>.<ref name="Kobayashi2019">{{cite journal |last1=Kobayashi |first1=Daisuke |title=Food poisoning by Ginkgo seeds through vitamin B<sub>6</sub> depletion (article in Japanese) |journal=Yakugaku Zasshi |volume=139 |issue=1 |year=2019 |pages=1–6 |issn=0031-6903 |doi=10.1248/yakushi.18-00136 |pmid=30606915 |doi-access=free}}</ref><ref name="WadaIshigaki1985">{{cite journal |last1=Wada |first1=Keiji |last2=Ishigaki |first2=Seikou |last3=Ueda |first3=Kaori |last4=Sakata |first4=Masakatsu |last5=Haga |first5=Masanobu |title=An antivitamin B6, 4'-methoxypyridoxine, from the seed of Ginkgo biloba L. |journal=Chemical & Pharmaceutical Bulletin |volume=33 |issue=8 |year=1985 |pages=3555–3557 |issn=0009-2363 |doi=10.1248/cpb.33.3555 |pmid=4085085 |doi-access=free}}</ref>

====Genetic defects====
Genetically confirmed diagnoses of diseases affecting vitamin B<sub>6</sub> metabolism ([[ALDH7A1]] deficiency, [[PNPO|pyridoxine-5'-phosphate oxidase deficiency]], [[Pyridoxal phosphate|PLP binding protein deficiency]], [[hyperprolinaemia type II]] and [[hypophosphatasia]]) can trigger vitamin B<sub>6</sub> deficiency-dependent [[epilepsy|epileptic seizures]] in infants. These are responsive to pyridoxal 5'-phosphate therapy.<ref name="Ghatge2021">{{cite journal |vauthors=Ghatge MS, Al Mughram M, Omar AM, Safo MK |title=Inborn errors in the vitamin B6 salvage enzymes associated with neonatal epileptic encephalopathy and other pathologies |journal=Biochimie |volume=183 |issue= |pages=18–29 |date=April 2021 |pmid=33421502 |doi=10.1016/j.biochi.2020.12.025 |s2cid=231437416 |url=|pmc=11273822 }}</ref><ref name="Mastrangelo2019">{{cite journal |vauthors=Mastrangelo M, Cesario S |title=Update on the treatment of vitamin B6 dependent epilepsies |journal=Expert Rev Neurother |volume=19 |issue=11 |pages=1135–47 |date=November 2019 |pmid=31340680 |doi=10.1080/14737175.2019.1648212 |s2cid=198496085 |url=}}</ref>