The Effect Of Helicobacter Pylori Infection On The Level Of Serum Gastrin In Different Gastric Disease Patients

From 1983, Marshall and Warren first time found Helicobacter pylori(H. pylori), to now scientists are focus on the relationship between H. pylori and chronic gastritis. A lot of epidemiological data show the infection of H. pylori is relative with gastric precancerous change and gastric cancer closely. Forman et al found that in the group, in which the infection rate of H. pylori is 100%, the risk rate of gastric cancer is six fold higher than no H. pylori infection group. 1994, H. pylori was listed by WHO as pathogenic bacterium of H. pylori and I grade carcinogenic factor. But the carcinogenic mechanism of H. pylori is still unknown.Gastrin is the first known gut peptide hormone. The coding gene is located at 17g and 4.1kb. the existence form of human gastrin is amidation gastrin , including G-17 and G-34 et al. G-17, 80%-90%, is the GA gastrin with full physiological function and the normal gastrin we known.. G-34, 5%-10%, is duodenum gastrin. The main functions of gastrin are increasing the secretion of gastric acid, inducing mucosa cell growth, increasing blood flow of gastric mucosa, increasing the repair of gastric mucosa and playing role in the gastric inflammation. Recently, scientists are no more interesting in the normal function of gastrin, but the proliferation, inhibition of tumor cell apoptosis and the function with Cycloxygenase-2 in the process of gastric cancer development.Bout development of gastric cancer, Correa et al raised a model,"normal gastric mucosa→superficial gastritis→atrophic gastritis→atypical hyperplasia→gastric cancer". During this process, the hormone level keeps change. Studying the relationship between this change and gastric cancer has a good significance. But now, the study about infection of H. pylori and serum gastrin level is absence of systematic and allround problem. And do not discover during the dynamic state process of canceration.We used ELISA and HE staining technique to grade the groups and measure the serum gastrin change. The standard of H. pylori infection is: serum anti- H. pylori IgG antibody≥44 unit is positive; above"++"is positive in the histological detection; serum anti- H. pylori IgG antibody between 32 to 44 unit and"+"positive in the histological detection are positive; other conditions are negative. To study the dynamic change of serum gastrin in the health persons, H. pylori negative Superficial gastritis, atrophic gastritis, atypical hyperplasia, cancer patients and H. pylori positive Superficial gastritis, atrophic gastritis, atypical hyperplasia, cancer patients, we hope to find mechanism of H. pylori inducing cancer to suppose the clinical work.The result are: the serum G-17 level of H. pylori positive Superficial gastritis is higher than H. pylori negative Superficial gastritis remarkably; the serum G-17 level of H. pylori positive atrophic gastritis, atypical hyperplasia and cancer are higher than H. pylori negative atrophic gastritis, atypical hyperplasia and cancer. The result indicates: the serum gastrin level of H. pylori infection patients is higher. H. pylori is a important factor to serum gastrin level; The increasing gastrin level induced by H. pylori maybe one of the carcinogenesis mechanism. The reason that H. pylori increases serum gastrin level is: urease of H. pylori resolves urea produce ammonia to increase the pH on the mucosa surface, which interrupters the normal feedback suppression of gastric acid to gastrin; vacuole toxin of H. pylori can induce parietal cell damage, which can decrease the secretion of gastric acid and stimulate G cells produce gastrin; H.pylori can suppress the releasing of growth inhibition hormone which can inhibit gastrin inducing secretion of gastric acid; H. pylori can stimulate mucosa cells release a serious of cytokines which can induce G cells secreting gastrin and proliferation.We found that serum G-17 level of H. pylori positive Superficial gastritis ,atrophic gastritis, atypical hyperplasia and cancer is higher than health persons remarkably. Serum G-17 level of H. pylori positive Superficial gastritis ,atrophic gastritis and atypical hyperplasia is increasing by turns and the level is decreasing from atypical hyperplasia to cancer. This indicates that H. pylori can increase the level of gastrin to induce the cancer. The mechanism of it maybe: H. pylori infection can induce Superficial gastritis and increase serum gastrin level; when the process comes to atrophic gastritis, the ability of H. pylori increasing gastrin is stronger than that of the decreasing number of G cells inducing the decreasing gastrin, so the serum gastrin level can keep increasing. At the stage of atypical hyperplasia, pathological changes is too superficial to damage G cells, so the serum gastrin level keeps increasing. At the stage of cancer, most gastrin can bind to the receptors on the tumor cells to induce cells proliferation, so the level of serum gastrin is dereasing.In one word, H. pylori infection can increase the level of serum gastrin, which can induce mucosa cells proliferation in the process of cancerization, to lead to cancer in the end. Meanwhile, because of the infection of H. pylori effecting the serum level of gastrin, it should be considered in clinical detection.