Influence of E266K polymorphism in the NOD1 gene on the clinical outcome of helicobacter pylori infection

Influence of E266K Polymorphism in The NOD1 Gene on The Clinical Outcome of Helicobacter Pylori InfectionObjective: The severity of Helicobacter pylori related disease varies greatly among infected individuals and seems to be influenced by both host and bacterial factors. The aim of this study is to investigate whether the presence of the NOD1 G796A polymorphism had any influence in the clinical outcomes of helicobacter pylori.Material and Method: The presence of Helicobacter pylori was investigated using the rapid urease test and histology in 500 patients who underwent upper gastrointestinal endoscopy. Serum samples from Helicobacter pylori positive patients were tested by ELISA for IgG antibodies against CagA gene. Only Helicobacter pylori positive and CagA positive patients were considered eligible for the study. In these selected group, NOD1 G796A was detected by using polymerase chain reaction/restriction fragment length polymorphism. Activity and severity of gastritis, atrophy, intestinal metaplasia and Helicobacter pylori density were assessed in body and antral biopsies. Also post-therapy controls for predicting the Helicobacter pylori persistance were done. The correlations of these parameters were determined by SPSS 15 packet program for statictical analysis.Results: 266 patients were Helicobacter pylori positive (% 53,2). CagA was positive in 140 patients (% 52,6). NOD1 796A allele carriers had higher risk for antral atrophy (OR=13,35, 95% CI=5,12-34,82) and antral intestinal metaplasia (OR=2,71, 95% CI=1,26-5,80). Carriage of the single nucleotide polymorphism of NOD1 G796A proved to be a significant risk factor for the Helicobacter pylori therapy failure (OR=4,62, 95% CI=1,67-12,79).Conclusions: Our results suggest that carriage of the NOD1 G796A mutation increases the susceptibility of gastric epithelial cells for intestinal metaplasia and atrophy when infected by CagA positive Helicobacter pylori strains. Additionally, increases the ratio of eradication failure.Key Words: Atrophy, CagA, Helicobacter pylori, intestinal metaplasia, NOD1 E266K polymorphism.