Document Detail

CagA-positive Helicobacter pylori strains enhanced coronary atherosclerosis by increasing serum OxLDL and HsCRP in patients with coronary heart disease.
MedLine Citation:
PMID:  20503072     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: The role of infection in the pathogenesis of atherosclerosis is still a matter of debate.
AIMS: This study aimed to investigate the effect of CagA-positive Helicobacter pylori (H. pylori) strains infection on coronary atherosclerosis in patients with coronary heart disease and to elucidate how cytotoxin-associated gene A (CagA)-positive H. pylori strains infections were involved in coronary heart disease by examining the levels of serum lipid, high-sensitivity C-reactive protein (hsCRP) and oxidized low-density protein (oxLDL).
METHODS: Recruited for this study were 159 patients with coronary heart disease. The severity of coronary heart disease was estimated by calculating the Gensini score. Serum oxLDL and hsCRP were examined in all subjects. Current H. pylori infection was determined in all participants by means of a modified (13C) urea breath test (>200 dpm classified as positive). IgG antibodies against CagA protein were analyzed by enzyme immunoassays. Antibody titers against CagA (≥8 U/ml) were classified as positive. All subjects were divided into three groups, including an uninfected group (n=30), an H. pylori +CagA- group (n=69), and an H. pylori +CagA+ group (n=60).
RESULTS: Significant differences were found among the three groups in levels of total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, serum hsCRP, oxLDL, and severity of coronary atherosclerosis (p<0.05). The levels of total cholesterol, LDL, apolipoprotein B, serum hsCRP, oxLDL were significantly elevated and the severity of coronary atherosclerosis was significantly increased in H. pylori +CagA+ group (p<0.05).
CONCLUSIONS: More serious coronary atherosclerosis was observed in CHD patients with H. pylori +CagA+ infection. H. pylori +CagA+ infection might be involved in coronary atherosclerosis by modifying serum lipids, enhancing LDL oxidation, and activating the inflammatory responses.
Bingsheng Huang; Ying Chen; Qiang Xie; Guixiong Lin; Yuyan Wu; Yanlin Feng; Jingcao Li; Yufeng Zhuo; Peng Zhang
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-05-26
Journal Detail:
Title:  Digestive diseases and sciences     Volume:  56     ISSN:  1573-2568     ISO Abbreviation:  Dig. Dis. Sci.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-24     Completed Date:  2011-01-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7902782     Medline TA:  Dig Dis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  109-14     Citation Subset:  AIM; IM    
Department of Cardiology, The He Xian Memorial Hospital of Panyu District, Guangzhou, People's Republic of China.
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MeSH Terms
Aged, 80 and over
Antigens, Bacterial / metabolism*
Bacterial Proteins / metabolism*
C-Reactive Protein / metabolism*
Coronary Artery Disease / blood,  microbiology*,  physiopathology
Coronary Disease / blood*,  physiopathology
Helicobacter Infections / complications
Helicobacter pylori / classification*,  metabolism*
Lipids / blood
Lipoproteins, LDL / blood*
Middle Aged
Retrospective Studies
Reg. No./Substance:
0/Antigens, Bacterial; 0/Bacterial Proteins; 0/Lipids; 0/Lipoproteins, LDL; 0/cagA protein, Helicobacter pylori; 0/oxidized low density lipoprotein; 9007-41-4/C-Reactive Protein

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