| Objective: Helicobacter pylori(Hp) has been closely associated with the onset and progression of chronic active gastritis, peptic ulcer and gastric cancer since its first separation in 1983. Mainly located in the stomach, particularly in the antral mucosa, Hp induces gastric mucosal lesions upon changes of the host internal environment. Meanwhile, chemotaxis of neutrophils induced by Hp and its metabolites causes inflammatory cell infiltration, and the released free oxygen species lead to damage and degeneration of epithelial cells. Long-term inflammation results in disappearance of normal gastric mucosal structure, atrophic gastritis, and even gastric cancer, i.e. chronic non atrophic gastritis-atrophic gastritis-intestinal metaplasia-atypical hyperplasia-gastric cancer. A variety of gastrointestinal hormones are involved in regulation of gastric acid secretion and protection of gastric duodenal mucosa. Therefore, we studied the relationship among gastrointestinal hormones gastrin(Gas), somatostatin(SS) and pepsinogen(PG: PGI, PGII) by detecting their levels in blood serum from Hp-infected patients with gastroduodenal diseases, and by staining the regions with lesions. The relationship between gastrointestinal hormones and gastric mucosal lesions was also analyzed, which benefited diagnosis of early gastric cancer.Method: A total of 135 Hp-positive patients diagnosed by gastroscopy and pathological examinations were selected. They were aged 21-75 years old, consisting of 58 females and 77 males. There were 41 cases of chronic atrophic non gastritis(CANG), 20 cases of chronic atrophic gastritis(CAG), 22 cases of gastric ulcer(GU), 24 cases of duodenal ulcer(DU), and 26 cases of gastric cancer(never received antibiotics, bismuth agents, or acid suppressive agents within 2 weeks, and never took hormones or nonsteroidal anti-inflammatory drugs; patients with heart, liver and renal insufficiencies and endocrine diseases were excluded). Thirty-three healthy subjects who received physical examinations in our hospital at the same time were chosen as Hp-negative control. Fasting blood(5 ml) was drawn and centrifuged, from which blood serum was collected. ELISA assay was used to detect the levels of Gas, SS, PGI and PGII. Biopsy was performed after staining under gastroscopy, and sections were prepared and subjected to Giemsa staining.Result: 1. Compared to normal control, the serum level of Gas in patients with chronic atrophic gastritis was significantly lower(P<0.01), whereas those in chronic non atrophic gastritis, peptic ulcer and gastric cancer groups were significantly higher(P<0.01).2. Compared to normal control, the serum level of somatostatin decreased following disease progression, i.e. chronic non atrophic gastritis-peptic ulcer-chronic atrophic gastritis-gastric cancer(P<0.01).3. The levels of PGI 、PGII and PGI/PGII( PGR) in chronic non atrophic gastritis group were no difference compared to those of normal control(P>0.05),while the levels were decreased significantly in chronic atrophic gastritis group and gastric cancer group compared to those of normal control(P<0.01),peptic ulcer group had significantly higher PGI and PGR levels than those of normal control(P<0.01).4. Contrast the detection rate of gastric cancer: test PGI and PGR, chromoendoscopy, and combined of two methods, we found that combined of serum detection and chromoendoscopy has the highest detection rate for gastric cancer. Conclusion: 1.Various gastrointestinal hormones in serum changed after Hp infection through multiple mechanisms.2. The changes of gastrointestinal hormones reflected the degree of gastric mucosal lesions.3. The changes of gastrin and somatostatin levels may predict the occurrence of gastric cancer.4. PGI and PGR may be eligible serum markers for chronic atrophic gastritis.5.Associate with the level of gastrointestinal hormones with Hp infection and chromoendoscopy can offer the theory evidence for gastric cancer early diagnosis. |
PDF Full Text Request