부산대학교 도서관

Simple Summary: Virulence factor genes in Helicobacter pylori (H. pylori) strains promote changes in the gastric epithelial mucosa that are associated with the risk of developing neoplastic lesions, and in Peru, H. pylori infection prevalence is greater than 45% and the gastric cancer incidence rate is the highest in the Americas. The aim of our cross-sectional study was to explore the association between clinical strain virulence genotypes of H. pylori from Peruvian patients with gastric intestinal metaplasia compared to chronic non-atrophic gastritis cases. We observed that the prevalence of the genotypes cagA+/vacAs1m1 and cagA+/vacAs1am1 was 2.42 and 1.67 times higher in cases with intestinal metaplasia compared to chronic non-atrophic gastritis cases, respectively. Our findings revealed that H. pylori strains circulating in our environment have a higher frequency of genotypes documented as risk variants for neoplastic lesions, highlighting that in Peruvian patients with H. pylori infection, the risk genotypes are related to intestinal metaplasia clinical stage. We explored the clinical-stage association of gastric intestinal metaplasia (IM) compared to cases of chronic non-atrophic gastritis (CNAG) and its relationship with virulence genotypes of Helicobacter pylori (H. pylori) clinical isolates from patients with dyspepsia in Peru. This study was cross-sectional and included 158 H. pylori clinical isolates; each isolate corresponded to a different Peruvian patient, genotyped by polymerase chain reaction to detect cagA gene and EPIYA motifs, the vacA gene (alleles s1, s2, i1, i2, d1, d2, m1, m2 and subtypes s1a, s1b and s1c), the iceA gene (alleles 1 and 2), and the babA gene (allele 2). We observed that 38.6% presented with IM and that all clinical isolates were CagA positive. The EPIYA-ABC motif was predominant (68.4%), and we observed a high frequency for the vacA gene alleles s1 (94.9%), m1 (81.7%), i1 (63.9%), and d1 (70.9%). Strains with both iceA alleles were also detected (69.6%) and 52.2% were babA2 positive. In addition, it was observed that the cagA+/vacAs1m1 (PR: 2.42, 1.14 to 5.13, p < 0.05) and cagA+/vacAs1am1 (PR: 1.67, 1.13 to 2.45, p < 0.01) genotypes were associated with IM. Our findings revealed the cagA and vacA risk genotypes predominance, and we provided clinically relevant associations between Peruvian patients with H. pylori infection and IM clinical stage. [ABSTRACT FROM AUTHOR]