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Article: Hyperhomocysteinemia and impaired vasomotor function in type 2 diabetes mellitus

TitleHyperhomocysteinemia and impaired vasomotor function in type 2 diabetes mellitus
Authors
Issue Date2002
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/ECI
Citation
European Journal Of Clinical Investigation, 2002, v. 32 n. 5, p. 328-334 How to Cite?
AbstractBackground: Hyperhomocysteinemia has been shown to adversely affect vascular function. The aim of this study was to determine whether hyperhomocysteinemia was independently associated with changes in endothelium-dependent and -independent vasomotor functions in patients with type 2 diabetes mellitus. Materials and methods: Fasting homocysteine (tHcy) was measured in 123 patients with type 2 diabetes and in 61 nondiabetic controls. Endothelium-dependent and -independent vasodilation was measured using high-resolution vascular ultrasound. Results: Plasma tHcy concentration was increased in the diabetic patients (11.1 ± 3.7 μmol L-1 vs. 9.8 ± 2.9, P < 0.05). The prevalence of hyperhomocysteinemia (defined as tHcy > 15 μmol L-1) was higher in the diabetic patients (P < 0.05). Within group comparisons showed that both the abnormalities in endothelium-dependent and -independent vasodilation were significantly more severe in diabetic patients with tHcy 10-15 (P < 0.05) and tHcy > 15 μmol L-1 (P < 0.05) than in those patients with tHcy < 10 μmol L-1. When compared with nondiabetic controls matched for tHcy levels, impairment of endothelium-dependent and -independent vasodilation were already evident, even in patients with normal tHcy levels (P < 0.01). Despite significant univariate relationships between tHcy and endothelium-dependent (r = -0.24, P < 0.01) and -independent vasodilation (r = -0.33, P < 0.01) in patients with diabetes, only the relationship between tHcy and endothelium-independent vasodilation remained significant after adjusting for other cardiovascular risk factors in multiple regression analysis. Conclusions: Impairment of endothelium-dependent and -independent vasodilation was already present in diabetic patients with normal tHcy levels, and these abnormalities became more severe with increasing tHcy levels. Only the association between tHcy and endothelium-independent vasodilation was free of other cardiovascular risk factors.
Persistent Identifierhttp://hdl.handle.net/10722/162651
ISSN
2015 Impact Factor: 2.687
2015 SCImago Journal Rankings: 1.255
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTan, KCBen_US
dc.contributor.authorKarmin, Oen_US
dc.contributor.authorChow, WSen_US
dc.contributor.authorAi, VHGen_US
dc.contributor.authorSiow, YLen_US
dc.contributor.authorLam, KSLen_US
dc.date.accessioned2012-09-05T05:22:04Z-
dc.date.available2012-09-05T05:22:04Z-
dc.date.issued2002en_US
dc.identifier.citationEuropean Journal Of Clinical Investigation, 2002, v. 32 n. 5, p. 328-334en_US
dc.identifier.issn0014-2972en_US
dc.identifier.urihttp://hdl.handle.net/10722/162651-
dc.description.abstractBackground: Hyperhomocysteinemia has been shown to adversely affect vascular function. The aim of this study was to determine whether hyperhomocysteinemia was independently associated with changes in endothelium-dependent and -independent vasomotor functions in patients with type 2 diabetes mellitus. Materials and methods: Fasting homocysteine (tHcy) was measured in 123 patients with type 2 diabetes and in 61 nondiabetic controls. Endothelium-dependent and -independent vasodilation was measured using high-resolution vascular ultrasound. Results: Plasma tHcy concentration was increased in the diabetic patients (11.1 ± 3.7 μmol L-1 vs. 9.8 ± 2.9, P < 0.05). The prevalence of hyperhomocysteinemia (defined as tHcy > 15 μmol L-1) was higher in the diabetic patients (P < 0.05). Within group comparisons showed that both the abnormalities in endothelium-dependent and -independent vasodilation were significantly more severe in diabetic patients with tHcy 10-15 (P < 0.05) and tHcy > 15 μmol L-1 (P < 0.05) than in those patients with tHcy < 10 μmol L-1. When compared with nondiabetic controls matched for tHcy levels, impairment of endothelium-dependent and -independent vasodilation were already evident, even in patients with normal tHcy levels (P < 0.01). Despite significant univariate relationships between tHcy and endothelium-dependent (r = -0.24, P < 0.01) and -independent vasodilation (r = -0.33, P < 0.01) in patients with diabetes, only the relationship between tHcy and endothelium-independent vasodilation remained significant after adjusting for other cardiovascular risk factors in multiple regression analysis. Conclusions: Impairment of endothelium-dependent and -independent vasodilation was already present in diabetic patients with normal tHcy levels, and these abnormalities became more severe with increasing tHcy levels. Only the association between tHcy and endothelium-independent vasodilation was free of other cardiovascular risk factors.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/ECIen_US
dc.relation.ispartofEuropean Journal of Clinical Investigationen_US
dc.rightsEuropean Journal of Clinical Investigation. Copyright © Blackwell Publishing Ltd.-
dc.subject.meshAdulten_US
dc.subject.meshBrachial Artery - Ultrasonographyen_US
dc.subject.meshDiabetes Mellitus, Type 2 - Blood - Complications - Physiopathologyen_US
dc.subject.meshEndothelium, Vascular - Physiology - Ultrasonographyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHomocysteine - Blooden_US
dc.subject.meshHumansen_US
dc.subject.meshHyperhomocysteinemia - Blood - Complications - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshRisk Factorsen_US
dc.subject.meshVasodilation - Physiologyen_US
dc.titleHyperhomocysteinemia and impaired vasomotor function in type 2 diabetes mellitusen_US
dc.typeArticleen_US
dc.identifier.emailTan, KCB:kcbtan@hku.hken_US
dc.identifier.emailLam, KSL:ksllam@hku.hken_US
dc.identifier.authorityTan, KCB=rp00402en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1365-2362.2002.00990.xen_US
dc.identifier.pmid12027872-
dc.identifier.scopuseid_2-s2.0-0037003369en_US
dc.identifier.hkuros77596-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037003369&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume32en_US
dc.identifier.issue5en_US
dc.identifier.spage328en_US
dc.identifier.epage334en_US
dc.identifier.isiWOS:000175672200007-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridTan, KCB=8082703100en_US
dc.identifier.scopusauthoridKarmin, O=6604083266en_US
dc.identifier.scopusauthoridChow, WS=7402281153en_US
dc.identifier.scopusauthoridAi, VHG=6603342063en_US
dc.identifier.scopusauthoridSiow, YL=7003336463en_US
dc.identifier.scopusauthoridLam, KSL=8082870600en_US

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