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As a consequence of the biochemical reactions in which homocysteine is involved, deficiencies of
[[vitamin B6|vitamin B<sub>6</sub>]], [[folic acid]] (vitamin B<sub>9</sub>), and [[Cobalamin|vitamin B<sub>12</sub>]] can lead to high homocysteine levels.<ref name="Miller-p1033-9">{{cite journal |pmid=8172087 |year=1994 |last1=Miller |first1=J. W. |title=Vitamin B-6 deficiency vs folate deficiency: Comparison of responses to methionine loading in rats |journal=The American Journal of Clinical Nutrition |volume=59 |issue=5 |pages=1033–9 |last2=Nadeau |first2=M. R. |last3=Smith |first3=D |last4=Selhub |first4=J |doi=10.1093/ajcn/59.5.1033}}</ref> Other possible causes of hyperhomocysteinemia include genetics, excessive [[methionine]] intake, and other diseases.<ref
Hyperhomocysteinemia is typically managed with vitamin B<sub>6</sub>, vitamin B<sub>9</sub> and vitamin B<sub>12</sub> supplementation.<ref name="ExpertOpPharm2001-Coen">{{cite journal |doi=10.1517/14656566.2.9.1449 |pmid=11585023 |title=Homocysteine-lowering treatment: An overview |journal=Expert Opinion on Pharmacotherapy |volume=2 |issue=9 |pages=1449–60 |year=2005 |last1=Stehouwer |first1=Coen DA |last2=Guldener |first2=Coen van |s2cid=45945199 }}</ref> Hyperhomocysteinemia is a risk factor for cardiovascular disease; supplements of these vitamins may slightly reduce stroke outcome but not myocardial infarction, death from any cause or adverse events.<ref name=Cochrane2017>{{Cite journal |last=Martí-Carvajal |first=Arturo J |last2=Solà |first2=Ivan |last3=Lathyris |first3=Dimitrios |last4=Dayer |first4=Mark |date=2017-08-17 |editor-last=Cochrane Heart Group |title=Homocysteine-lowering interventions for preventing cardiovascular events |url=http://doi.wiley.com/10.1002/14651858.CD006612.pub5 |journal=Cochrane Database of Systematic Reviews |language=en |volume=2021 |issue=9 |doi=10.1002/14651858.CD006612.pub5 |pmc=6483699 |pmid=28816346}}</ref>
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