Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/8049
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dc.contributor.authorHahalis, G.en
dc.contributor.authorKremastinos, D. T.en
dc.contributor.authorTerzis, G.en
dc.contributor.authorKalogeropoulos, A. P.en
dc.contributor.authorChrysanthopoulou, A.en
dc.contributor.authorKarakantza, M.en
dc.contributor.authorKourakli, A.en
dc.contributor.authorAdamopoulos, S.en
dc.contributor.authorTselepis, A. D.en
dc.contributor.authorGrapsas, N.en
dc.contributor.authorSiablis, D.en
dc.contributor.authorZournbos, N. C.en
dc.contributor.authorAlexopoulos, D.en
dc.date.accessioned2015-11-24T16:38:28Z-
dc.date.available2015-11-24T16:38:28Z-
dc.identifier.issn0021-9150-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/8049-
dc.rightsDefault Licence-
dc.subjectthalassemiaen
dc.subjectcarotid atherosclerosisen
dc.subjectendotheliumen
dc.subjectiron-overloaden
dc.subjectinflammationen
dc.subjectnecrosis-factor-alphaen
dc.subjectintima-media thicknessen
dc.subjectcoronary-artery-diseaseen
dc.subjectblood mononuclear-cellsen
dc.subjectoxidative stressen
dc.subjectendothelial dysfunctionen
dc.subjectcarotid atherosclerosisen
dc.subjectimmune statusen
dc.subjectpseudoxanthoma elasticumen
dc.subjectperipheral-blooden
dc.titleGlobal vasomotor dysfunction and accelerated vascular aging in beta-thalassemia majoren
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primaryDOI 10.1016/j.atherosclerosis.2007.09.030-
heal.identifier.secondary<Go to ISI>://000257133600028-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0021915007005928/1-s2.0-S0021915007005928-main.pdf?_tid=e39b64b8233a2637e82eb062d64fee2c&acdnat=1333111284_a69e94e77c9bee320c75cf6f091f5c9a-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείαςel
heal.publicationDate2008-
heal.abstractBackground: Patients with beta-thalassemia major (beta-TM) demonstrate an increased incidence of vascular complications, which are thought to result from a procoagulant/proinflammatory environment. We investigated the arterial vasorelaxing capacity and sought for early carotid atherosclerosis and underlying pathophysiological correlates in these transfusion-dependent patients. Methods and results: The vasodilatory properties of the brachial artery and the carotid intima-media thickness (IMT) were examined with ultrasonography in 35 non-diabetic young adults with beta-TM (patient group) and 35 control subjects (control group). Among thalassemic patients, both endothelium-dependent (FMD) and -independent dilatation (FID) as well as their ratio was impaired, whereas IMT was increased (p<0.01). Patients on optimal, as compared with those on non-optimal chelation treatment had a non-significantly lower IMT. Vasodilatory capacity in the patient group was inversely correlated with IMT and independently associated either with the quality of chelation therapy (FMD) or serum ferritin levels (FID). Plasma concentrations of D-dimers, circulating markers of endothelial activation, inflammation and apoptosis were higher, while plasma cholesterol and fibrinogen levels were lower-than-normal in the patient group. Independent predictors of IMT among thalassemic patients were tumor necrosis factor-alpha levels and age. Conclusions: Young adults with beta-TM exhibit both a global impairment of arterial vasorelaxation and early carotid atherosclerosis. A procoagulant/proinflammatory state in these transfusion-dependent patients may overwhelm atheroprotective mechanisms, including an optimal chelation regimen, and promote vascular injury and atherogenesis. (C) 2007 Elsevier Ireland Ltd. All rights reserved.en
heal.journalNameAtherosclerosisen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά). ΧΗΜ

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