Cardiovascular Risk Factors in Subjects with Helicobacter pylori Infection

Takashima, Toshiharu; Adachi, Kyoichi; Kawamura, Akira; Yuki, Mika; Fujishiro, Hirofumi; Rumi, M.A. Karim; Ishihara, Shunji; Watanabe, Makoto; Kinoshita, Yoshikazu

doi:10.1046/j.1083-4389.2002.00064.x

Cited by 48 publications

(42 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These results were consistent with previous reports 26,27) . It has been shown that HDL-cholesterol was significantly decreased in HP-positive elderly subjects 28,29) . HDL-cholesterol has been shown to increase after successful eradication of HP 26,27) .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Possible Association of Atrophic Gastritis and Arterial Stiffness in Healthy Middle-Aged Japanese

Torisu

Takata

Ansai

et al. 2009

JAT

View full text Add to dashboard Cite

Aim: Helicobacter pylori (HP) has been implicated as a risk factor for cardiovascular and atherosclerotic diseases. Arterial stiffness determined by pulse wave velocity (PWV) or the cardio-ankle vascular index (CAVI) has been shown to be higher in HP-positive subjects than in HP-negative subjects; however, this result has been observed only in young subjects. The aim of the study was to investigate the possible correlation between HP infection and PWV or CAVI in middle-aged subjects.

show abstract

Section: Discussionmentioning

confidence: 99%

“…It has been reported that increases in inflammatory factors, such as CRP, WBC and fibrinogen as a consequence of HP infection, are candidates to explain the progression of arterial stiffness 29,39) . In our study, however, neither CRP nor WBC was different between AG-positive and AG-negative groups.…”

Section: Discussionmentioning

confidence: 99%

Possible Association of Atrophic Gastritis and Arterial Stiffness in Healthy Middle-Aged Japanese

Torisu

Takata

Ansai

et al. 2009

JAT

View full text Add to dashboard Cite

show abstract

“…Recently, both bacterial and viral infections have been shown to increase the level of serum fibrinogen and lipids and to result in the release of proinflammatory mediators, which can lead to the progression of arteriosclerosis. [1][2][3][4][5][6][7][8] Hepatitis B virus (HBV) and hepatitis C virus (HCV) are well-known causes of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. In patients with liver cirrhosis due to chronic infection with HBV and HCV, low levels of serum fibrinogen and lipids may have a favorable effect in the prevention of arteriosclerosis.…”

Section: Introductionmentioning

confidence: 99%

A study of arteriosclerosis in healthy subjects with HBV and HCV infection

et al. 2005

Self Cite

View full text Add to dashboard Cite

show abstract

“…Previous studies reported that the serum T-Chol, TG, or LDL concentrations in H. pylori-infected persons are significantly elevated over those in noninfected individuals (39,40). On the other hand, several authors described HDL cholesterol levels to be decreased by longterm infection with H. pylori (41)(42)(43). In the present study, H. pylori-infected animals showed similar lipid dynamics with significant elevation of TG and LDL and depression of HDL, and pitavastatin markedly up-regulated the T-Chol and TG levels in infected groups.…”

Section: Discussionmentioning

confidence: 94%

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

Toyoda

Tsukamoto²,

Takasu

et al. 2009

Cancer Prevention Research

View full text Add to dashboard Cite

Statins are commonly used lipid-lowering drugs that reduce the risk of cardiovascular morbidity and mortality. Although recent studies have pointed to chemopreventive effects of statins against various cancers, their efficacy for gastric cancer is unclear. Here, we examined the effects of pitavastatin, a lipophilic statin, on Helicobacter pylori (H. pylori)-associated stomach carcinogenesis and gastritis using Mongolian gerbil and mouse models. The animals were allocated to H. pylori + N-methyl-N-nitrosourea administration (gerbils, 52 weeks) or H. pylori infection alone groups (gerbils and mice, 12 weeks). After H. pylori infection, they were fed basal diets containing 0 to 10 ppm of pitavastatin. The incidences of H. pylori-associated gastric adenocarcinomas and degrees of chronic gastritis were not decreased by pitavastatin compared with those of control values. Expression of interleukin-1β and tumor necrosis factor-α mRNAs in the pyloric mucosa was markedly up-regulated in pitavastatin-treated animals. Furthermore, in the H. pyloriinfected groups, serum total cholesterol, triglyceride, and low-density lipoprotein levels were significantly increased by pitavastatin treatment, contrary to expectation. In the short-term study, H. pylori-infected gerbils and mice also showed significant up-regulation of serum triglyceride levels by pitavastatin, whereas total cholesterol was markedly reduced and low-density lipoprotein exhibited a tendency for decrease in noninfected animals. These findings indicate pitavastatin to be ineffective for suppressing gastritis and chemoprevention of gastric carcinogenesis in H. pylori-infected gerbils. Our serologic results also suggest that the H. pylori infection and consequent severe chronic gastritis interfere with the cholesterol-lowering effects of pitavastatin.

show abstract

Cardiovascular Risk Factors in Subjects with Helicobacter pylori Infection

Abstract: Long-term infection with H. pylori may have an important role in decreasing the serum HDLC concentration.

Cited by 48 publications

References 32 publications

Possible Association of Atrophic Gastritis and Arterial Stiffness in Healthy Middle-Aged Japanese

Possible Association of Atrophic Gastritis and Arterial Stiffness in Healthy Middle-Aged Japanese

A study of arteriosclerosis in healthy subjects with HBV and HCV infection

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

Contact Info

Product

Resources

About