Correlation of NOD2 genotypes with Helicobacter pylori infection in a South‐European country

Abstract

Outcome of Helicobacter pylori (H. pylori) infection in a specific individual is unpredictable and results from interaction of multiple variables, including host genetic factors. This study aimed to investigate if NOD2 mutations increased the risk of H. pylori infection and if it has any relationship with bacterial genotype or gastric histopathological modifications. This prospective study involved 86 patients (54 females; mean age, 48.7 ± 13.6 years) with positive 13 C-urea breath test (UBT) and a sex and age-matched control group of 266 individuals, 64 of them with negative UBT. The three main NOD2 mutations (L1007fsinsC, R702W, and G908R) were obtained for all patients and controls. Fifty-one infected patients were submitted to endoscopy with gastric biopsies. H. pylori was isolated, and genotypes were determined by PCR. Histopathological features were graded according to the updated Sydney system. Overall, NOD2 mutations were found in 14 patients (16.3%) and in 31 controls (11.7%) (OR = 1.40, 95% CI = 0.78-2.50; P = .264). Genotype frequencies for L1007fsinsC (1.2% vs 0.8%), R702W (11.6% vs 7.6%) and G908R (5.8% vs 3.4%) were not statistically different between the two groups. A significant positive association was observed between NOD2 polymorphisms and peptic ulcer but only in univariate analysis. There were no other correlations with clinical variables, gastric histological patterns and H. pylori genotypes. NOD2 mutations are not associated with increased prevalence of H. pylori infection or more severe gastric histopathological modifications induced by this bacterium. However, such host polymorphisms could influence clinical manifestations.

Mutations in Helicobacter pylori infected patients with chronic gastritis, intestinal type of gastric cancer and familial gastric cancer

“…This phenomenon may occur in chronic gastritis caused by H.pylori , leading to an increased risk of gastric cancer, but the available data are inconclusive. This is due to the study of different groups of patients with various inflammatory lesions of the gastric mucosa, small numbers, analysis of different variants of the NOD2 gene and incomplete information on H.pylori infection [ 66 ]. The main limitation of most studies on the association of NOD2 gene mutations with gastric cancer was the lack of data concerning H.pylori infection status.…”

“…The main limitation of most studies on the association of NOD2 gene mutations with gastric cancer was the lack of data concerning H.pylori infection status. Such a situation is presented in the article by de Almeida [ 66 ], in which the R702W rs2066844, G908R rs2066845 and L1007fsinsC rs2066847 variants of the NOD2 gene were analysed, mainly in patients with non-ulcer dyspepsia without cases of gastric dysplasia and gastric cancer, with the authors pointing to the potential involvement of other genetic factors that can modify the immune response.…”