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Lingenhel, A.* ; Kollerits, B.* ; Schwaiger, J.P.* ; Hunt, S.C.* ; Gress, R.* ; Hopkins, P.N.* ; Schoenborn, V.* ; Heid, I.M. ; Kronenberg, F.*

Serum bilirubin levels, UGT1A1 polymorphisms and risk for coronary artery disease.

Exp. Gerontol. 43, 1102-1107 (2008)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Low levels of the antioxidative serum bilirubin are associated with vascular aging and an increased risk for coronary artery disease (CAD). UGT1A1 is the major gene influencing bilirubin concentrations. Therefore, we investigated an association of bilirubin levels and two polymorphisms in the promoter of UGT1A1 I (-53(TA-repeat) polymorphism and T-3279C) in 477 patients with premature, familial CAD and 619 age-and sex-matched controls. Bilirubin concentrations were significantly lower in cases than in controls (0.62 +/- 0.36 vs. 0.76 +/- 0.41 mg/dl for men, p = 1.2 x 10(-10) and 0.42 +/- 0.29 vs. 0.55 +/- 0.23 mg/dl, p = 1.9 x 10(-9) for women). Both polymorphisms showed a strong association with bilirubin levels with higher levels for homozygote carriers of the minor allele. These associations were most pronounced in male controls and patients (p = 5.9 x 10(-26) and p = 3.4 x 10(-16), respectively, for the -53(TA-repeat) polymorphism). Logistic regression analysis revealed low bilirubin levels but not the UGT1A1 polymorphisms to be significantly associated with CAD: OR (95% CI) 0.90 (0.86-0.94), p = 2.6 x 10(-6) for men and 0.77 (0.68-0.87), p = 3.2 x 10(-5) for women, respectively for each 0.1 mg/dl increase of bilirubin. These results indicate that it is rather decreased bilirubin levels in general than the changes in the genetic variation of this gene that increase the risk for CAD.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Bilirubin; Coronary artery disease; UGT1A1; Association study; Polymorphism
ISSN (print) / ISBN 0531-5565
e-ISSN 0531-5565
Zeitschrift Experimental Gerontology
Quellenangaben Band: 43, Heft: 12, Seiten: 1102-1107 Artikelnummer: , Supplement: ,
Verlag Elsevier
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology (EPI)