Heterogeneity of cag genotypes of Helicobacter pylori in the esophageal mucosa of dyspeptic patients and its relation to histopathological outcomes

Abstract

A high prevalence of Helicobacter pylori in the esophageal mucosa of dyspeptic Venezuelan patients has been reported. We aimed to assess the genetic composition of the cag genotypes of H. pylori and its relation to histopathological outcomes in the gastroesophageal mucosa. The presence of cagA, cagE, and virB11 cag pathogenicity island (PAI) genes was detected by PCR in 80 of 150 H. pylori-positive dyspeptic patients in both mucosae. Alterations of the gastroesophageal mucosa were assessed by histological techniques. The frequency of intact, partial, and deleted cag-PAI genes in the stomach of dyspeptic patients was found to be 57.5%, 21.3%, and 21.3%, respectively, whereas in the esophagus, frequencies were 33.8%, 33.8%, and 32.5% respectively. The genetic composition in the stomach was 57.5% cagA-positive, 20.0% cagA-negative, 75.0% cagE, and 77.5% virB11, whereas in the esophagus the distribution was 36.3% cagA-positive, 30.0% cagA-negative, 61.3% cagE, and 63.8% virB11. The gene with the largest difference between the two mucosae was cagA, with 58.8% in the stomach and 37.5% in the esophagus; cagE and virB11 were less variable. The correlation among single and/or mixed cag genotypes with histopathological outcomes in both mucosae from the same patient was higher for intact single cag-PAI genotypes, showing severe alterations. H. pylori may coexist in similar proportions without dominance of one cag genotype, suggesting a heterogeneous distribution in the esophagus. The cagE and virB11 genes can be used as markers of cag-PAI in the esophagus. The single cag-PAI genotype in both mucosae confers an increased risk of developing histological damage.