2.50
Hdl Handle:
http://hdl.handle.net/2336/54813
Title:
Hómósystein, áhættuþáttur æðasjúkdóma
Other Titles:
Hyperhomocysteinemia, a cardiovascular risk factor
Authors:
Margrét Árnadóttir
Citation:
Læknablaðið 1997, 83(11):731-4, 736-8, 740-2
Issue Date:
1-Nov-1997
Abstract:
The rare syndrome of homocystinuria is characterized by very high plasma concentration of the amino acid homocysteine. Homocystinuric patients are at greatly increased risk of atherosclerotic complications independent of the underlying cause of the syndrome. Based on these observations, the homocysteine theory of atherosclerosis was formulated 20 years ago proposing that homocysteine as such was responsible for the vascular damage. It was also proposed that the mild hyperhomocysteinemia, commonly found in the general population, constituted a cardiovascular risk factor. The homocysteine theory of atherosclerosis is supported by the results of a few large prospective investigations and many small retrospective studies which showed significantly higher plasma homocysteine concentrations in patients suffering from atherosclerotic complications than in controls. Moreover, according to multiple regression analyses of these study results, the risk associated with hyperhomocysteinemia is independent of other cardiovascular risk factors. The mechanism is unclear but clinical studies and animal experiments indicate that homocysteine induces endothelial damage and influences blood coagulation. Treatment with folic acid effectively lowers plasma homocysteine concentration. To date, it is not known whether such treatment lowers the incidence of atherosclerotic complications.; Heilkennið hómósystínmiga einkennist af feykihárri þéttni amínósýrunnar hómósysteins í blóðvökva og mjög aukinni hættu á fylgikvillum æðakölkunar. Fyrir 20 árum var sett fram sú tilgáta að hómósystein sem slíkt væri skaðlegt æðum, jafnvel þegar um vægt aukna þéttni hómósysteins er að ræða. Niðurstöður fjölda rannsókna styðja þessa tilgátu. Nokkrar stórar framskyggnar rannsóknir ásamt fleiri tugum afturskyggnra athugana hafa sýnt hærri hómósysteinþéttni hjá sjúklingum með æðasjúkdóma en hjá viðmiðunarhópum og tölfræðileg úrvinnsla hefur jafnan sýnt hómósystein sem sjálfstæðan áhættuþátt æðakölkunar. Klínískar rannsóknir og dýratilraunir benda til að hómósystein skaði æðaþel og stuðli að blóðstorknun. Hómósysteinþéttni í blóðvökva má lækka á einfaldan og ódýran hátt með fólínsýru. Pó hefur enn ekki verið rannsakað hvort fólínsýrumeðferð dregur úr þróun æðabreytinga.
Description:
Neðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/Open
Additional Links:
http://www.laeknabladid.is

Full metadata record

DC FieldValue Language
dc.contributor.authorMargrét Árnadóttir-
dc.date.accessioned2009-03-12T13:10:44Z-
dc.date.available2009-03-12T13:10:44Z-
dc.date.issued1997-11-01-
dc.date.submitted2009-03-12-
dc.identifier.citationLæknablaðið 1997, 83(11):731-4, 736-8, 740-2en
dc.identifier.issn0023-7213-
dc.identifier.urihttp://hdl.handle.net/2336/54813-
dc.descriptionNeðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/Openen
dc.description.abstractThe rare syndrome of homocystinuria is characterized by very high plasma concentration of the amino acid homocysteine. Homocystinuric patients are at greatly increased risk of atherosclerotic complications independent of the underlying cause of the syndrome. Based on these observations, the homocysteine theory of atherosclerosis was formulated 20 years ago proposing that homocysteine as such was responsible for the vascular damage. It was also proposed that the mild hyperhomocysteinemia, commonly found in the general population, constituted a cardiovascular risk factor. The homocysteine theory of atherosclerosis is supported by the results of a few large prospective investigations and many small retrospective studies which showed significantly higher plasma homocysteine concentrations in patients suffering from atherosclerotic complications than in controls. Moreover, according to multiple regression analyses of these study results, the risk associated with hyperhomocysteinemia is independent of other cardiovascular risk factors. The mechanism is unclear but clinical studies and animal experiments indicate that homocysteine induces endothelial damage and influences blood coagulation. Treatment with folic acid effectively lowers plasma homocysteine concentration. To date, it is not known whether such treatment lowers the incidence of atherosclerotic complications.en
dc.description.abstractHeilkennið hómósystínmiga einkennist af feykihárri þéttni amínósýrunnar hómósysteins í blóðvökva og mjög aukinni hættu á fylgikvillum æðakölkunar. Fyrir 20 árum var sett fram sú tilgáta að hómósystein sem slíkt væri skaðlegt æðum, jafnvel þegar um vægt aukna þéttni hómósysteins er að ræða. Niðurstöður fjölda rannsókna styðja þessa tilgátu. Nokkrar stórar framskyggnar rannsóknir ásamt fleiri tugum afturskyggnra athugana hafa sýnt hærri hómósysteinþéttni hjá sjúklingum með æðasjúkdóma en hjá viðmiðunarhópum og tölfræðileg úrvinnsla hefur jafnan sýnt hómósystein sem sjálfstæðan áhættuþátt æðakölkunar. Klínískar rannsóknir og dýratilraunir benda til að hómósystein skaði æðaþel og stuðli að blóðstorknun. Hómósysteinþéttni í blóðvökva má lækka á einfaldan og ódýran hátt með fólínsýru. Pó hefur enn ekki verið rannsakað hvort fólínsýrumeðferð dregur úr þróun æðabreytinga.is
dc.language.isoisen
dc.publisherLæknafélag Íslands, Læknafélag Reykjavíkuren
dc.relation.urlhttp://www.laeknabladid.isen
dc.subjectÆðakölkunen
dc.subject.meshHomocysteineen
dc.subject.meshThrombosisen
dc.subject.meshAtherosclerosisen
dc.titleHómósystein, áhættuþáttur æðasjúkdómais
dc.title.alternativeHyperhomocysteinemia, a cardiovascular risk factoren
dc.typeArticleen
dc.identifier.journalLæknablaðiðen
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