Helicobacter pylori is associated with modified lipid profile:: impact on Lipoprotein(a)

被引:47
作者
Chimienti, G
Russo, F
Lamanuzzi, BL
Nardulli, M
Messa, C
Di Leo, A
Correale, M
Giannuzzi, V
Pepe, G [1 ]
机构
[1] Univ Bari, Dept Biochem & Mol Biol, Bari, Italy
[2] CNR, IBBE, I-70126 Bari, GP, Italy
[3] IRCCS S Bellis, Lab Expt Biochem, Bari, Italy
[4] IRCCS S Bellis, Clin Pathol Lab, Bari, Italy
关键词
Helicobacter pylori; Cag(A) antigen; lipid profile; Lp(a); atherogenic risk;
D O I
10.1016/S0009-9120(03)00063-8
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Objectives: Helicobacter pylori is a controversial risk factor for atherosclerosis. We investigated whether the bacterium persistent inflammation or the expression of the cytotoxin-associated gene A (CagA) may affect serum lipids as well as Lipoprotein(a). Design and methods: Two hundred-eleven healthy volunteers were evaluated for lipids and Lipoprotein(a). Helicobacter pylori was characterized by Urea Breath Test and IgG-anti-CagA. apo(a) Kringle-IV polymorphism was genotyped. Results: Prevalence of the infection was 72%; 43% of subjects expressed CagA reactivity. Infected subjects showed increased levels of cholesterol, LDL-cholesterol, and cholesterol/HDL-cholesterol atherogenic index. Association with the Helicobacter pylori CagA(-) strains persisted after the adjustment for covariates. Significant difference between infected and uninfected subjects was found in Lipoprotein(a) levels. This difference did not arise from the Kringle-IV genotype. Conclusions: The infection per se significantly modified serum lipid and Lipoprotein(a) concentrations. CagA does not seem to be a reliable marker of pathogenicity for the atherogenic complications of H. pylori infection. (C) 2003 The Canadian Society of Clinical Chemists. All rights reserved.
引用
收藏
页码:359 / 365
页数:7
相关论文
共 33 条
[1]  
BLASER MJ, 1995, CANCER RES, V55, P2111
[2]   Sequence polymorphisms in the apolipoprotein(a) gene and their association with lipoprotein(a) levels and myocardial infarction. The ECTIM Study [J].
Brazier, L ;
Tiret, L ;
Luc, G ;
Arveiler, D ;
Ruidavets, JB ;
Evans, A ;
Chapman, J ;
Cambien, F ;
Thillet, J .
ATHEROSCLEROSIS, 1999, 144 (02) :323-333
[3]   Effect of Helicobacter pylori infection on gastric emptying and gastrointestinal hormones in dyspeptic and healthy subjects [J].
Chiloiro, M ;
Russo, F ;
Riezzo, G ;
Leoci, C ;
Clemente, C ;
Messa, C ;
Di Leo, A .
DIGESTIVE DISEASES AND SCIENCES, 2001, 46 (01) :46-53
[4]   APO(a) variants and lipoprotein(a) in men with or without myocardial infarction [J].
Chimienti, G ;
Lamanuzzi, BL ;
Nardulli, M ;
Colacicco, AM ;
Capurso, A ;
La Gioia, R ;
Scrutino, D ;
Pepe, G .
EXPERIMENTAL AND MOLECULAR PATHOLOGY, 2002, 73 (01) :28-34
[5]   High risk strategies for atherosclerosis [J].
Cullen, P ;
Assmann, G .
CLINICA CHIMICA ACTA, 1999, 286 (1-2) :31-45
[6]   Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses [J].
Danesh, J ;
Whincup, P ;
Walker, M ;
Lennon, L ;
Thomson, A ;
Appleby, P ;
Gallimore, JR ;
Pepys, MB .
BMJ-BRITISH MEDICAL JOURNAL, 2000, 321 (7255) :199-204
[7]   HDL-cholesterol as a marker of coronary heart disease risk:: the Quebec cardiovascular study [J].
Després, JP ;
Lemieux, I ;
Dagenais, GR ;
Cantin, B ;
Lamarche, B .
ATHEROSCLEROSIS, 2000, 153 (02) :263-272
[8]  
Di Leo A, 1999, IMMUNOPHARM IMMUNOT, V21, P803, DOI 10.3109/08923979909007143
[9]   Current infection with Helicobacter pylori, but not seropositivity to Chlamydia pneumoniae or cytomegalovirus, is associated with an atherogenic, modified lipid profile [J].
Hoffmeister, A ;
Rothenbacher, D ;
Bode, G ;
Persson, K ;
März, W ;
Nauck, MA ;
Brenner, H ;
Hombach, V ;
Koenig, W .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (03) :427-432
[10]   Lipoproteins and their subfractions in psoriatic arthritis: identification of an atherogenic profile with active joint disease [J].
Jones, SM ;
Harris, CPD ;
Lloyd, J ;
Stirling, CA ;
Reckless, JPD ;
McHugh, NJ .
ANNALS OF THE RHEUMATIC DISEASES, 2000, 59 (11) :904-909