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== Treatment ==
Vitamins B6, B9, or B12 supplements, while they lower homocysteine level do not change the risk of heart disease, stroke, or death.<ref name=Art2015>{{cite journal|first1=Arturo J.|last1=Martí-Carvajal|first2=Ivan|last2=Solà|first3=Dimitrios|last3=Lathyris|title=Homocysteine-lowering interventions for preventing cardiovascular events|journal=The Cochrane Database of Systematic Reviews|date=15 January 2015|issn=1469-493X|pages=CD006612|volume=1|pmid=25590290|pmc=4164174|doi=10.1002/14651858.CD006612.pub4|editor1-last=Martí-Carvajal|editor1-first=Arturo J}}</ref>{{Update inline|reason=Updated version https://www.ncbi.nlm.nih.gov/pubmed/28816346|date = July 2018}} This also applies to people with [[kidney disease]] on [[dialysis]].<ref>{{cite journal|first1=Sagar U.|last1=Nigwekar|first2=Amy|last2=Kang|first3=Sophia|last3=Zoungas|first4=Alan|last4=Cass|title=Interventions for lowering plasma homocysteine levels in dialysis patients|journal=The Cochrane Database of Systematic Reviews|date=31 May 2016|issn=1469-493X|pages=CD004683|issue=5|pmid=27243372|doi=10.1002/14651858.CD004683.pub4|first5=Martin P.|last5=Gallagher|first6=Satyarth|last6=Kulshrestha|first7=Sankar D.|last7=Navaneethan|first8=Vlado|last8=Perkovic|first9=Giovanni F. M.|last9=Strippoli|first10=Meg J.|last10=Jardine}}</ref>
Hypotheses have been offered to address the failure of homocysteine-lowering therapies to reduce cardiovascular events. When [[folic acid]] is given as a supplement, it may increase the build-up of [[atherosclerosis|arterial plaque]]. A second hypothesis involves the [[methylation]] of genes in vascular cells by folic acid and vitamin B12, which may also accelerate plaque growth. Finally, altered methylation may catalyse l-arginine to asymmetric dimethylarginine, which is known to increase the risk of vascular disease.<ref>{{cite journal|last=Watson|first=KE|title=Lowering levels of lipids and homocysteine.|journal=Reviews in Cardiovascular Medicine|date=Fall 2006|volume=7|issue=4|pages=248–50|pmid=17224870}}</ref>
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