The Helicobacter pylori vaca S1 genotype and the cagE gene are associated with gastroduodenal disease

Prevalence of Helicobacter pylori vacA, cagA, cagE, iceA, babA2 Genotypes and Correlation with Clinical Outcome in Turkish Patients with Dyspepsia

“…In the present study, 51 of 91 (59.3%) cases possessed the cagE gene and its prevalence was significantly higher among subjects with DU and GC compared to them with NUD (Table 2), a finding which is in agreement with previous studies reporting a significant association between the cagE gene and DU [44][45][46][47]. A very important result of our study was that the cagE gene was found to be an independent marker of both DU and GC in multivariate regression analysis.…”

Ethnicity and H. Pylori as Risk Factors for Gastric Cancer in Malaysia: A Prospective Case Control Study

“…With respect to Cag A status using PCR in situ hybridization, we reported a high Cag A prevalence among all three major races in Malaysia (Malay 76.6%, Chinese 86.4%, Indian 86.8%). However, the Cag E prevalence was significantly lower among Chinese (39.0%) compared to the Indians (81.6%) and Malays (70.0%), which appears paradoxical, as some studies have suggested that the Cag E gene is a more reliable virulence marker (21). Other virulence factors have to be studied to see if there were indeed bacterial strain differences between races, which could account for the discordant GCA prevalence between the Chinese and Indians.…”

cagEIs a Virulence Factor Associated withHelicobacter pylori–Induced Duodenal Ulceration in Children

“…Similarly, preliminary data from study of adults also show that the presence of the cagE gene in infecting strains of H. pylori is associated with duodenal ulceration. For instance, in a study by Fallone et al [30], 31 (37%) of 84 patients with gastroduodenal disease (including both peptic ulceration and gastric cancer) were infected with cagE-positive strains, compared with only 20.7% of 92 patients with gastritis alone ( ) . P = .02…”

“…Fifty-one (91%) of 56 strains isolated from patients with duodenal ulcers were cagEpositive, whereas 13 (76%) of 17 H. pylori isolates obtained from patients with gastritis alone were cagE-positive (not significant). A potential confounding factor that could explain the differing results in these studies [30,31] is the geographic location of the patient cohort under study. It is clear that Helicobacter isolates in humans from different regions of the world are dissimilar, with high interstrain variability [24,32].…”