Interestingly, a positive correlation between CagA antibody titer and the extent score of the atherosclerotic disease was also found. Moreover, patients infected with CagA-positive strains had a more extensive coronary artery disease (CAD) compared with those infected with PD98059 in vivo CagA-negative strains and, at multivariate analysis, anti-CagA antibody titer was the only predictor of the extent of coronary atherosclerosis [2]. Another study by Agrawal et al. [3] conducted on diabetic patients with or without H. pylori infection

reported a higher prevalence of H. pylori infection in patients with diabetes mellitus (DM). Moreover, H. pylori-positive diabetic patients showed a higher prevalence of CAD than H. pylori-negative diabetic subjects. Nevertheless, this is still a debated topic. In fact, these data were not confirmed by the study of Schimke et al. [4], in which CagA positivity was not shown to be a risk factor for chronic vascular complications in patients with type 2 diabetes. Concerning the pathogenic mechanisms by which H. pylori may eventually concur to the pathogenesis of ischemic heart disease (IHD), two studies were published last year. The first one aimed at investigating whether

CagA-positive H. pylori strains may influence serological levels of high sensitivity C-reactive protein, total cholesterol, low-density protein (LDL), oxidized LDL (oxLDL), and apolipoprotein B. Interestingly, the levels of all those markers were significantly increased in CagA-positive patients compared with negative; moreover, buy Gefitinib CagA-positive patients showed a more severe coronary atherosclerosis [5]. The second study presents a meta-analysis of all studies published in the field of H. pylori infection, platelet aggregation, and thrombosis [6]. Results showed that some H. pylori strains are able to bind to the von Willebrand factor, to interact with glycoprotein Ib, and to induce platelet aggregation in humans. The final hypothesis is that H. pylori may Protein tyrosine phosphatase eventually affect IHD by

eliciting thrombosis [6]. The consistency of a role of H. pylori infection in the pathogenesis of DM as well as in the gastric abnormalities of patients with diabetes has been analyzed and critically discussed. Several controversies emerge from the epidemiological data. The clinical consequence of H. pylori infection in terms of metabolic control seems to be low. Regarding interventional studies, the bacterial eradication rate is significantly lower in patients with DM than in controls [7]. The difference in the H. pylori eradication rate observed between adults and children affected by diabetes could be due to the fact that the latter have no history of repeated infectious diseases and antibiotic treatments, leading to less antibiotic-resistant H. pylori strains. Ojetti et al. showed that a higher H.