The impact of CCR5-Δ32 deletion on C-reactive protein levels and cardiovascular disease: Results from the Danish Blood Donor Study

被引:9
作者
Dinh, Khoa M. [1 ]
Pedersen, Ole B. [2 ]
Petersen, Mikkel S. [1 ]
Sorensen, Erik [4 ]
Sorensen, Cecilie J. [1 ]
Kaspersen, Kathrine A. [1 ]
Larsen, Margit H. [4 ]
Moller, Bjarne [1 ]
Hjalgrim, Henrik [3 ]
Ullum, Henrik [4 ]
Erikstrup, Christian [1 ]
机构
[1] Aarhus Univ Hosp, Dept Clin Immunol, DK-8200 Aarhus N, Denmark
[2] Naestved Hosp, Dept Clin Immunol, DK-4700 Naestved, Denmark
[3] Statens Serums Inst, Dept Epidemiol Res, DK-2300 Copenhagen S, Denmark
[4] Rigshosp, Dept Clin Immunol, Copenhagen Univ Hosp, DK-2100 Copenhagen, Denmark
关键词
CCR5; receptor; Genetics; Atherosclerosis; Inflammation; Cardiovascular diseases; Epidemiology; CORONARY-ARTERY-DISEASE; MYOCARDIAL-INFARCTION; HEART-DISEASE; CCR5; RISK; POLYMORPHISMS; SUSCEPTIBILITY; RECEPTORS; DIAGNOSES; MUTATION;
D O I
10.1016/j.atherosclerosis.2015.07.031
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background and purpose: The C-C chemokine receptor 5-Delta 32 deletion (CCR5-Delta 32) has been associated with lower levels of C-reactive protein (CRP), but the effect on cardiovascular diseases is uncertain. This study addresses the impact of CCR5-Delta 32 on the risk of low-grade inflammation and hospitalization with cardiovascular diseases in a large cohort of blood donors. Methods: Genotyping of 15,206 healthy participants from The Danish Blood Donor Study for CCR5-Delta 32 was performed and combined with CRP measurements and questionnaire data. Cardiovascular disease diagnoses were identified by ICD-10 codes in the Danish National Patient Registry. Results: CCR5-Delta 32-carriers had a higher risk of hospitalization for cardiovascular diseases when compared with wild-type homozygotes (hazard ratio = 1.35, 95%-confidence interval: 1.00-1.87). CRP levels were unaffected by the CCR5-Delta 32 deletion. Conclusion: In this cohort, carriers of the CCR5-Delta 32 deletion had normal CRP levels but a borderline significant increased risk of cardiovascular diseases. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:222 / 225
页数:4
相关论文
共 16 条
[1]   Common CCR5-del32 frameshift mutation associated with serum levels of inflammatory markers and cardiovascular disease risk in the Bruneck population [J].
Afzal, Ali R. ;
Kiechl, Stefan ;
Daryani, Yousef P. ;
Weerasinghe, Arusha ;
Zhang, Yang ;
Reindl, Markus ;
Mayr, Agnes ;
Weger, Siegfried ;
Xu, Qingbo ;
Willeit, Johann .
STROKE, 2008, 39 (07) :1972-1978
[2]   Effects of polymorphisms in chemokine ligands and receptors on susceptibility to coronary artery disease [J].
Apostotakis, Stavros ;
Baritaki, Stavroula ;
Kochiadakis, Georgios E. ;
Igoumenidis, Nikolaos E. ;
Panutsopulos, Dimitrios ;
Spandidos, Demetrios A. .
THROMBOSIS RESEARCH, 2007, 119 (01) :63-71
[3]  
Charo I.F., 2004, CIRC RES, V95, P858
[4]   Genetic variation at the chemokine receptors CCR5/CCR2 in myocardial infarction [J].
González, P ;
Alvarez, R ;
Batalla, A ;
Reguero, JR ;
Alvarez, V ;
Astudillo, A ;
Cubero, GI ;
Cortina, A ;
Coto, E .
GENES AND IMMUNITY, 2001, 2 (04) :191-195
[5]   Genetic Association of the CCR5 Region With Lipid Levels in At-Risk Cardiovascular Patients [J].
Hyde, Craig L. ;
MacInnes, Alan ;
Sanders, Frances A. ;
Thompson, John F. ;
Mazzarella, Richard A. ;
Faergeman, Ole ;
van Wijk, Diederik F. ;
Wood, Linda ;
Lira, Maruja ;
Paciga, Sara A. .
CIRCULATION-CARDIOVASCULAR GENETICS, 2010, 3 (02) :162-168
[6]   Predictive values of acute coronary syndrome discharge diagnoses differed in the Danish National Patient Registry [J].
Joensen, Albert Marni ;
Jensen, Majken K. ;
Overvad, Kim ;
Dethlefsenc, Claus ;
Schmidt, Erik ;
Rasmussen, Lars ;
Tjonneland, Anne ;
Johnsen, Soren .
JOURNAL OF CLINICAL EPIDEMIOLOGY, 2009, 62 (02) :188-194
[7]   C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis [J].
Kaptoge, Stephen ;
Di Angelantonio, Emanuele ;
Lowe, Gordon ;
Pepys, Mark B. ;
Thompson, Simon G. ;
Collins, Rory ;
Danesh, John ;
Tipping, R. W. ;
Ford, C. E. ;
Pressel, S. L. ;
Walldius, G. ;
Jungner, I. ;
Folsom, A. R. ;
Chambless, L. ;
Ballantyne, C. M. ;
Panagiotakos, D. ;
Pitsavos, C. ;
Chrysohoou, C. ;
Stefanadis, C. ;
Knuiman, M. W. ;
Goldbourt, U. ;
Benderly, M. ;
Tanne, D. ;
Whincup, P. ;
Wannamethee, S. G. ;
Morris, R. W. ;
Kiechl, S. ;
Willeit, J. ;
Mayr, A. ;
Schett, G. ;
Wald, N. ;
Ebrahim, S. ;
Lawlor, D. ;
Yarnell, J. ;
Gallacher, J. ;
Casiglia, E. ;
Tikhonoff, V. ;
Nietert, P. J. ;
Sutherland, S. E. ;
Bachman, D. L. ;
Keil, J. E. ;
Cushman, M. ;
Psaty, B. M. ;
Tracy, R. ;
Tybjaerg-Hansen, A. ;
Nordestgaard, B. G. ;
Zacho, J. ;
Frikke-Schmidt, R. ;
Giampaoli, S. ;
Palmieri, L. .
LANCET, 2010, 375 (9709) :132-140
[8]   Validity of stroke diagnoses in a national register of patients [J].
Krarup, Lars-Henrik ;
Boysen, Gudrun ;
Janjua, Huma ;
Prescott, Eva ;
Truelsen, Thomas .
NEUROEPIDEMIOLOGY, 2007, 28 (03) :150-154
[9]   Distribution of the CCR5 gene 32-basepair deletion in West Europe. A hypothesis about the possible dispersion of the mutation by the Vikings in historical times [J].
Lucotte, G .
HUMAN IMMUNOLOGY, 2001, 62 (09) :933-936
[10]   Chemokine receptor CCR5: insights into structure, function, and regulation [J].
Oppermann, M .
CELLULAR SIGNALLING, 2004, 16 (11) :1201-1210