Clinical significance of the presence of Cag-A and Vac-A and the presence of toll-like receptor-4 Asp299Gly and toll-like receptor-9 123T/C polymorphism in helicobacter pylori infection

Clinical Significance of the Existence of Cag-A / Vac-A and polymorphism of Toll-like Receptor -4 Asp299Gly and Toll-like Receptor-9 123T/C in childhood Helicobacter pylori infection. Abstract BACKGROUND: In this study, both H. pylori CagA and VacA genes carried by pathogenicity factors of the patient as well as the toll-like receptor (TLR-4, and 9) gene polymorphisms. Determination of the effects intended. METHODS: Presenting with dyspeptic symptoms. obtained by upper gastrointestinal endoscopy examination of gastric biopsies of 200 patients were enrolled between the ages of 5-18 that have been made. Of the patients studied retrospectively, 100 H. pylori positive and 100 H. pylori negative patients were selected by simple random sampling method. H. pylori-positive patient group I. , H. pylori negative patient group II. (control group) as described. Consent from the patients, Toll-like receptor [TLR-4 (Asp299Gly) and TLR-9 (123T / C)] polymorphisms were studied. Paraffin blocks of gastric biopsies obtained from 100 patients with a group I-CagA and Vac-A were investigated. Chi-square and logistic regression analysis results. Odds ratios and 95% confidence intervals were calculated. RESULTS: Reference complaints with heartburn in group I 70 (70%). group II, 51 (51%) were more common. (p = 0.008). Lack of personal hygiene, the use of a common plate, the use of tap water as drinking water, the parents' level of education is low and the economic situation in the evil group I was statistically significant (p <0.05). A history of peptic ulcer disease was more frequent in group I than group II (p = 0.009). Group I mentioned as premalignant symptoms atrophy and intestinal metaplasia were statistically significant (p <0.05). A 3.6-fold increased likelihood of the presence of cag A duodenitis was seen (OR: 3.6, 95% CI: 1.2-11.3). At the same time, with the presence of Cag A 5.6-fold increased frequency of duodenal ulcer (OR: 5.6, 95% CI: 0.7-40.8). There was no statistically significant difference between Vac A s and m1/m2 positive clinical findings. However, chronic inflammation in s positive in patients for a 1.3-fold, even in those m1/m2 positive activity in 7.5 times, 1.6-fold increase in the severity of the density of H. pylori found. However, s positive patients, chronic inflammation, a 1.3-fold increase in activity 7.5 times for those with positive m1/m2 and H. pylori density 1.6-fold increase in severity was found. TLR4 +896 A> G polymorphism and H. pylori positivity was not associated with. TLR4 +896 A> G polymorphism was not associated with H. pylori positivity. Only in terms of type of gastritis, erosive gastritis AG polymorphism in the heterozygous individuals had more. Especially in the presence of TLR9 C allele; duodenitis risk 4.8 fold, duodenal ulcer risk 2.5-fold and antral nodularity risk 1.5 -fold increased. In addition, histopathological aspects are evaluated, the presence of C allele, chronic inflammation 2.6-fold, atrophy 1.6-fold, intestinal metaplasia was increased 8.13-fold. CONCLUSION: Cag A, 71.3% of our patients when the positive and 3.6-fold increased the risk of duodenal ulcer in accordance with the literature. Positivity Vac A s increases of chronic inflammation at 1.3 times, 7.5 times increase in activity to cause positivity in m1/m2, these two virulent factor H. pylori infection suggests that the severity of an impact on. H. pylori infection in the pathogenesis of TLR-9 polymorphism rather than TLR-4 polymorphism is important. especially in the presence of the C allele with precancerous lesions of gastric atrophy 1.6-fold. 8.13-fold increase of intestinal metaplasia is remarkable. Further studies with larger patient groups are needed in this regard.