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Shiqiao, China

Huang B.,He Xian Memorial Hospital | Chen Y.,He Xian Memorial Hospital | Xie Q.,He Xian Memorial Hospital | Lin G.,He Xian Memorial Hospital | And 5 more authors.
Digestive Diseases and Sciences | Year: 2011

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. © 2010 Springer Science+Business Media, LLC.

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