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dc.contributor.authorMiltiadous, G.en
dc.contributor.authorCariolou, M. A.en
dc.contributor.authorElisaf, M. S.en
dc.date.accessioned2015-11-24T19:14:24Z-
dc.date.available2015-11-24T19:14:24Z-
dc.identifier.issn0091-7370-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21301-
dc.rightsDefault Licence-
dc.subjectAdolescenten
dc.subjectAdulten
dc.subjectAgeden
dc.subjectApolipoproteins E/geneticsen
dc.subjectChilden
dc.subjectCholesterol, HDL/*blooden
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectHyperlipoproteinemia Type II/*blood/*geneticsen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subject*Mutation/geneticsen
dc.subjectPolymorphism, Genetic/physiologyen
dc.subjectReceptors, LDL/*geneticsen
dc.subjectReference Valuesen
dc.titleHDL cholesterol levels in patients with molecularly defined familial hypercholesterolemiaen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11848618-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2002-
heal.abstractFamilial hypercholesterolemia (FH) is the most common genetic disorder leading to premature atherosclerosis. Typically, it is due to mutations in the LDL receptor gene resulting in elevated total and LDL cholesterol levels. The type of the LDL receptor gene mutations may affect the severity of hypercholesterolemia and consequently the incidence of coronary atherosclerosis. Furthermore, high-density lipoprotein (HDL) cholesterol levels have been recently shown to be an independent risk factor for coronary heart disease in this population. We examined the effect of the type of the LDL receptor gene mutations and of common gene polymorphisms possibly affecting HDL metabolism [cholesterol ester transfer protein (CETP), apolipoprotein A-IV (ApoA-IV), angiotensin converting enzyme (ACE), and apolipoprotein E (ApoE)] on HDL cholesterol levels in patients with molecularly defined heterozygous FH who were attending our lipid clinic (n=84). The nature of the LDL receptor gene mutation (81T>G, n=12; 858C>A, n=13; 1285G>A, n=12; 1646G>A, n=22; and 1775G>A, n=25) did not significantly influence HDL cholesterol levels. Unlike other gene polymorphisms, the apolipoprotein (apo) E gene polymorphism did significantly affect these levels. In fact, the presence of the E4 allele was associated with lower HDL cholesterol levels compared to patients not carrying this allele. We conclude that HDL cholesterol levels in heterozygous FH patients may be affected by the apoE gene polymorphism.en
heal.journalNameAnn Clin Lab Scien
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

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