Study On Antral Gastritis And Inflammatory Mediators Of Duodenal Ulcer With Helicobacter Pyloryi And Those Of Duodenal Ulcer After Eradication H.pylori

Objectives Although convincing evidence exists that Helicobacter pylon has a pathogenic role in the development of duodenal ulcer, the pathophysiology of H pylon-induced duodenal ulceration is unsettled. There have been three related theory for explanation of mechanisms by which H pylon! may contribute to the development of duodenal ulceration . They are gastric metaplasia theory, gastrin-acid theory and immunologic damage theory respectively, but all cannot explain the mechanisms completely. In recent years, mediator wash down theory has been paid attention gradually. The main point of this theory is that H. pylon! indirectly contributes to ulceration via the production of inflammatory mediators that wash down to the duodenum during gastric emptying. Our research is to study differences between antral gastritis and inflammatory mediators of duodenal ulcers with H pylon and those of duodenal ulcers after eradicating H pylon!, and to study the significance of 3 eradicating H pylon in treatment of duodenal ulcer. Materials and methods Gastric antral biopsy specimens were taken from seventy patients with duodenal ulcers for examination of histology and Warthin-Starry staining and inflammatory mediators(interleukin-8, tumor necrosis factor a , superoxide dismutase and malondialdehyde). Interleukin-8 and tumor necrosis factor a were examined using Enzyme linked immunosorbent assay(ELISA), and superoxide dismutase and malondialdehyde were examined using colorimetric method. Among 70 patients, Gastric antral biopsy specimens from 25 cases after eradicating H. pylon! were taken above examinations again. Statistics analysis: Measurement data were compared by (test, and x2 test was used for enumeration data comparisons. Kendall and Pearson rank correlation were used to test for associations between variables. Results Degrees of acute and chronic antral gastritis in the antrum were significantly greater in H. pylon positive than in H pylon negative mucosa, and expressions of inflammatory mediators in the antrum were also significantly greater in H pylon! positive than in H. pylon! negative mucosa(IL-8 t2.629, P<0.05; TNF a t=4.740, P<0.001; SOD 1=2.135, P<0.05; MDA 1=4.619, P<0.00l). Degrees of acute and chronic antral gastritis were associated with grades of H pylon in the antrum(acute inflammation T=O.565, P<0.001; chronic inflammation T=0.614, P<0.001), and expressions of inflammatory mediators correlated with grades of H pylon in the antrum too. What抯 more, expressions of inflammatory mediators correlated with 4 degrees of acute and chronic antral gastritis respectively. After eradicating IL pylon, acute and chronic antral gastritis both improved obv ously(acute inflammation ,~=11.430, P=:0.01; chronic inflammation 113.000, P= 0.005) and expressions of inflammatory mediators decreased significantly. Conclusions It is probable that products of H pylon are directly responsible for recruitment of inflammatory cells into the gastric mucosa, and inflammatory mediators may play an important role between H pylon-associated gastritis and duodenal ulcer. Eradicating IL pylon can improve degree of antral gastritis significantly, and can r...