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Article: HDL dysfunction in obstructive sleep apnea

TitleHDL dysfunction in obstructive sleep apnea
Authors
KeywordsHDL dysfunction
Obstructive sleep apnea
Oxidative stress
Issue Date2006
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
Citation
Atherosclerosis, 2006, v. 184 n. 2, p. 377-382 How to Cite?
AbstractObjective: HDL is anti-atherogenic and has antioxidant property. HDL dysfunction has been reported in patients with coronary heart disease and we hypothesize that HDL may also be dysfunctional in obstructive sleep apnea (OSA), a condition associated with increased oxidative stress. Methods: 128 OSA patients and 82 controls were recruited. HDL dysfunction was determined by evaluating the ability of HDL to inhibit LDL oxidation ex vivo. Plasma HDL was incubated with native LDL in the presence of dichlorofluorescein which fluoresced upon interaction with lipid oxidation products. Plasma levels of oxidized LDL and 8-isoprostane were measured by ELISA and a specific enzyme immunoassay, respectively. Results: Plasma total 8-isoprostane levels were elevated in OSA subjects (p < 0.01). Despite having similar concentrations of plasma lipids and apolipoproteins as controls, OSA subjects had greater degree of HDL dysfunction (p < 0.01) and increased oxidized LDL levels (p < 0.05). The apnea-hypopnea index was the main determinant of HDL dysfunction in OSA, accounting for 30% of its variance, with oxidized LDL and apolipoprotein AI contributing to 8% and 5% of its variance respectively (p < 0.001). Conclusion: HDL is dysfunctional in preventing the formation and inactivation of oxidized lipids in OSA subjects and may partly contribute to their increased cardiovascular risk. © 2005 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/77081
ISSN
2023 Impact Factor: 4.9
2023 SCImago Journal Rankings: 1.461
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTan, KCBen_HK
dc.contributor.authorChow, WSen_HK
dc.contributor.authorLam, JCMen_HK
dc.contributor.authorLam, Ben_HK
dc.contributor.authorWong, WKen_HK
dc.contributor.authorTam, Sen_HK
dc.contributor.authorIp, MSMen_HK
dc.date.accessioned2010-09-06T07:28:03Z-
dc.date.available2010-09-06T07:28:03Z-
dc.date.issued2006en_HK
dc.identifier.citationAtherosclerosis, 2006, v. 184 n. 2, p. 377-382en_HK
dc.identifier.issn0021-9150en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77081-
dc.description.abstractObjective: HDL is anti-atherogenic and has antioxidant property. HDL dysfunction has been reported in patients with coronary heart disease and we hypothesize that HDL may also be dysfunctional in obstructive sleep apnea (OSA), a condition associated with increased oxidative stress. Methods: 128 OSA patients and 82 controls were recruited. HDL dysfunction was determined by evaluating the ability of HDL to inhibit LDL oxidation ex vivo. Plasma HDL was incubated with native LDL in the presence of dichlorofluorescein which fluoresced upon interaction with lipid oxidation products. Plasma levels of oxidized LDL and 8-isoprostane were measured by ELISA and a specific enzyme immunoassay, respectively. Results: Plasma total 8-isoprostane levels were elevated in OSA subjects (p < 0.01). Despite having similar concentrations of plasma lipids and apolipoproteins as controls, OSA subjects had greater degree of HDL dysfunction (p < 0.01) and increased oxidized LDL levels (p < 0.05). The apnea-hypopnea index was the main determinant of HDL dysfunction in OSA, accounting for 30% of its variance, with oxidized LDL and apolipoprotein AI contributing to 8% and 5% of its variance respectively (p < 0.001). Conclusion: HDL is dysfunctional in preventing the formation and inactivation of oxidized lipids in OSA subjects and may partly contribute to their increased cardiovascular risk. © 2005 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosisen_HK
dc.relation.ispartofAtherosclerosisen_HK
dc.rightsAtherosclerosis. Copyright © Elsevier Ireland Ltd.en_HK
dc.subjectHDL dysfunction-
dc.subjectObstructive sleep apnea-
dc.subjectOxidative stress-
dc.subject.meshAdulten_HK
dc.subject.meshAtherosclerosis - blood - etiologyen_HK
dc.subject.meshBiological Markers - blooden_HK
dc.subject.meshCholesterol, HDL - blooden_HK
dc.subject.meshDinoprost - analogs & derivatives - blooden_HK
dc.subject.meshDisease Progressionen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHypercholesterolemia - blood - complicationsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshOxidative Stressen_HK
dc.subject.meshPrognosisen_HK
dc.subject.meshRetrospective Studiesen_HK
dc.subject.meshRisk Factorsen_HK
dc.subject.meshSleep Apnea, Obstructive - blood - complicationsen_HK
dc.titleHDL dysfunction in obstructive sleep apneaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9150&volume=184&issue=2&spage=377&epage=82&date=2006&atitle=HDL+dysfunction+in+obstructive+sleep+apneaen_HK
dc.identifier.emailTan, KCB:kcbtan@hku.hken_HK
dc.identifier.emailIp, MSM:msmip@hku.hken_HK
dc.identifier.authorityTan, KCB=rp00402en_HK
dc.identifier.authorityIp, MSM=rp00347en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.atherosclerosis.2005.04.024en_HK
dc.identifier.pmid15975582-
dc.identifier.scopuseid_2-s2.0-30044437707en_HK
dc.identifier.hkuros113754en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-30044437707&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume184en_HK
dc.identifier.issue2en_HK
dc.identifier.spage377en_HK
dc.identifier.epage382en_HK
dc.identifier.isiWOS:000235317500018-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridTan, KCB=8082703100en_HK
dc.identifier.scopusauthoridChow, WS=7402281153en_HK
dc.identifier.scopusauthoridLam, JCM=25923453500en_HK
dc.identifier.scopusauthoridLam, B=9246012800en_HK
dc.identifier.scopusauthoridWong, WK=12753634200en_HK
dc.identifier.scopusauthoridTam, S=7202037323en_HK
dc.identifier.scopusauthoridIp, MSM=7102423259en_HK
dc.identifier.issnl0021-9150-

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