Influence of the CD14 C260T promoter polymorphism on C-reactive protein levels in patients with coronary artery disease

被引:11
作者
Bernardo, Esther
Angiolillo, Dominick J. [1 ]
Ramirez, Celia
Cavallari, Ugo
Trabetti, Elisabetta
Sabate, Manel
Hernandez, Rosana
Moreno, Raul
Escaned, Javier
Alfonso, Fernando
Banuelos, Camino
Costa, Marco A.
Bass, Theodore A.
Pignatti, Pier Franco
Macaya, Carlos
Fernandez-Ortiz, Antonio
机构
[1] Univ Florida Shands Jacksonville, Div Cardiol, Jacksonville, FL USA
[2] San Carlos Univ Hosp, Cardiovasc Inst, Madrid, Spain
[3] Univ Verona, Dept Mother & Child & Biol Genet, I-37100 Verona, Italy
关键词
D O I
10.1016/j.amjcard.2006.06.013
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 > 03 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. (c) 2006 Elsevier Inc. All rights reserved.
引用
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页码:1182 / 1184
页数:3
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