Title of article :
Influence of the CD14 C260T Promoter Polymorphism on C-Reactive Protein Levels in Patients With Coronary Artery Disease
Author/Authors :
Bernardo، نويسنده , , Esther and Angiolillo، نويسنده , , Dominick J. and Ramيrez، نويسنده , , Celia and Cavallari، نويسنده , , Ugo and Trabetti، نويسنده , , Elisabetta and Sabaté، نويسنده , , Manel and Hernلndez، نويسنده , , Rosana and Moreno، نويسنده , , Raul and Escaned، نويسنده , , Javier and Alfonso، نويسنده , , Fernando and Baٌuelos، نويسنده , , Camino and Costa، نويسنده , , Marco A. and Bas، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2006
Pages :
3
From page :
1182
To page :
1184
Abstract :
The CD14 receptor is an important mediator of inflammatory reactions, and its expression is under genetic control. The allelic variant of the C260T polymorphism located in the promoter region of the CD14 gene is associated with receptor expression and ischemic risk. To date, most studies assessing the functional implications of the C260T polymorphism have been performed under proinflammatory conditions (e.g., acute coronary syndromes), and whether gene sequence variations of the CD14 receptor have any functional effect on systemic inflammation in patients in a stable phase of their atherosclerotic disease process is unknown. Eighty-two patients with stable coronary artery disease were studied. High-sensitivity C-reactive protein (hs-CRP) was used as a measurement of systemic inflammation. The genotype distribution of the C260T polymorphism of the CD14 gene was as follows: CC in 18 of 82 patients (22%), TC in 48 of 82 patients (58.5%), and TT in 16 of 82 patients (19.5%). TT subjects had increased hs-CRP levels compared with carriers of the C allele (p = 0.04). A higher percentage of T allele homozygotes had hs-CRP levels >0.3 mg/dl (p = 0.01). Homozygosis status of the T allele was independently associated with hs-CRP levels >0.3 mg/dl (p = 0.004). In conclusion, these observations may support the findings in large-scale studies that T homozygotes of this functional polymorphism are at increased ischemic risk.
Journal title :
American Journal of Cardiology
Serial Year :
2006
Journal title :
American Journal of Cardiology
Record number :
1901587
Link To Document :
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