Helicobacter Pylori FlaA, FlaB, DupA, HomA, HomB Status In Zunyi And Relationship With Gastroduodenal Diseases

Objective:To investigate the distribution of Helicobacter pylori(H.pylori) gene, flaA, flaB, dupA (jhp0917, jhp0918), homA and homB, in patients with chronic gastritis (CG), gastric ulcer (GU), duodenal ulcer (DU), and gastric carcinoma (GC) in Zunyi, and analyze the relationship of H.pylori genotype with chronic gastritis, gastric ulcer, duodenal ulcer, and gastric carcinoma.Methods:From May2011to October2011,206patients with H.pylori infection determined by rapid urease test (RUT) in the endoscopy center, Affiliated Hospital of Zunyi Medical College, were evaluated. Total DNA was extracted from biopsy specimens which were taken from gastric antrum. H.pylori infection was further confirmed through the examination of urease C of gastric mucosal biopsy specimens by polymerase chain reaction (PCR). H.pylori gene, flaA, flaB, jhp0917, jhp0918, homA, and homB genes were determined by PCR, and detected the amplification products by agarose gel electrophoresis. Datas were analyzed with the SPSS17.0software package. The relationship of H.pylori genotype and gastroduodenal diseases was analyzed by Chi-square test and Fisher’s exact.Results:(1) Among206patients,180patients was further confirmed as H.pylori infection by PCR of urease C. The overall prevalence rates of flaA, flaB, jhp0917, jhp0918, homA, and homB in180cases of H.pylori-infected patients were98.3%,99.4%,36.1%,42.8%,26.1%and67.2%, respectively.(2) The detective rate of flaA was97.1%,98.1%,100%, and100%in chronic gastritis, gastric ulcer, duodenal ulcer, and gastric carcinoma group, respectively. The detective rate of flaB was98.5%,100%,100%, and100%, respectively. The detective rate of jhp0917was33.8%,26.9%,51.0%, and27.3%, respectively. The detective rate of jhp0918was44.2%,30.8%,55.1%, and36.4%, respectively. The detective rate of homA was20.6%,21.2%,28.8%, and27.3%, respectively. The detective rate of homB was51.5%,75.0%,85.7%, and45.5%, respectively. Pairwise comparisons were taken in chronic gastritis, gastric ulcer, duodenal ulcer and gastric cancer group, we can arrive at some conclusion as follows. There were no significant differences in flaA and flaB genes in any two groups (P>0.05). There were significant differences in jhp0917and jhp0918genes between gastric ulcer and duodenal ulcer (P<0.05). There were significant differences in homA genes between chronic gastritis and duodenal ulcer (P<0.05). There were significant differences in homB genes between chronic gastritis and gastric ulcer or duodenal ulcer (P<0.05). There were significant differences in homB genes between duodenal ulcer and gastric carcinoma (P<0.05).(3) Among180patients,59were positive and92were negative for both jhp0917and jhp0918. Pairwise comparisons were taken in chronic gastritis, gastric ulcer, duodenal ulcer and gastric cancer group, we can arrive at a conclusion as following. There were significant differences in dupA genes between gastric ulcer and duodenal ulcer (P<0.05).(4) In addition to homA-and homB-negative specimens, there is no specimens carried both homA and homB. That is, homA-positive in one specimen, then homB must be negative, and vice versa.Conclusion:(1) H.pylori gene-positive rate was in descending order as follows:flaB, flaA, homB, jhp0918, jhp0917, homA.(2) flaA and flaB are very common in patients with chronic gastritis, gastric ulcer, duodenal ulcer, and gastric carcinoma.(3) The presence of dupA, homA, homB gene in duodenal ulcer was higher than that in chronic gastritis, gastric ulcer, gastric carcinoma, which might be implicated in the formation of duodenal ulcer.