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<p>Recent studies have suggested that <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection might be a risk factor for atherosclerosis. Since the bacterium has not been isolated from atherosclerotic lesions, a direct role in atherogenesis is not plausible. We examined associations of plasma total homocysteine (tHcy) and serum folate, independent risk factors for atherosclerosis, with <i>H. pylori </i>infection and subsequent gastric atrophy among 174 patients (78 males and 96 females) aged 20 to 73 years, who visited an <i>H. pylori</i> eradication clinic of Nagoya University from July 2004 to October 2005. Polymorphism genotyping was conducted for <i>methylenetetrahydrofolate reductase</i> (<i>MTHFR</i>) C677T and <i>thymidylate synthase</i> (<i>TS</i>) 28-bp tandem repeats by PCR with confronting two-pair primers and PCR, respectively. <i>H. pylori</i> infection and gastric atrophy were not significantly associated with hyperhomocysteinemia (tHcy &#8805; 12 nmol/ml), when adjusted by sex, age, smoking, alcohol, and genotypes of <i>MTHFR</i> and <i>TS</i>. The adjusted odds ratio of gastric atrophy for low folate level (&#8804; 4mg/ml) was 0.21 (95% confidence interval = 0.05-0.78). The associations of tHcy with serum folate and <i>MTHFR</i> genotype were clearly observed in this dataset. The present study demonstrated that folate and <i>MTHFR</i> genotype were the deterministic factors of plasma tHcy, but not <i>H. pylori</i> infection and subsequent gastric atrophy, indicating that even if <i>H. pylori</i> infection influences the risk of atherosclerosis, the influence may not be through the elevation of homocysteine.</p>