The EGFR expression in gastric mucosa of children infected with Helicobacter pylori.

PURPOSE: Epidermal growth factor receptor (EGFR) modulates balance between proliferation and apoptosis in gastric mucosa of the gastrointestinal tract. The aim of the study was to evaluate immunohistochemically the EGFR expression in epithelial and gland cells of antral mucosa in children infected with Helicobacter pylori (H. pylori). MATERIAL/METHODS: The study included 44 children, aged from 5 to 18 years (mean age 13+/-3.4 years) with dyspeptic symptoms, of whom 30 (68.2%) children were infected with H. pylori, 14 (31.8%) children constituted controls. Endoscopic and histopathological assessment of antral mucosa samples was performed according to the Sydney System. Samples taken from gastroscopy were prepared to evaluate EGFR expression in epithelial and gland cells of antrum mucosa according to the manual of a detection kit of EnVision+System-HRP (DAKO). RESULTS: In children H. pylori infected, the EGFR expression in epithelial cells of antral mucosa equaled on average 82.5+/-15 cells/mm2 and ranged from 45.0 to 98.0 cells/mm2 as well as differed statistically significantly when compared to controls (10.2+/-5.0 cells/mm2) (p<0.001). In children with H. pylori infection, the EGFR expression in gland cells of antral mucosa ranged from 2.0 to 85.0 cells/mm2 (mean 25.7+/-22.6 cells/mm2); was lower and differed statistically significantly from controls (54.2 +/- 29.6 cells/mm2) (p<0.001). In children H. pylori infected, there was a statistically significant difference (p<0.001) between the EGFR expression in epithelial and in gland cells of antral mucosa. CONCLUSION: The increased EGFR expression in epithelial cells in comparison with gland cells of antral mucosa in children with H. pylori infection may suggest its role in regeneration processes of gastric mucosa.

Helicobacter pylori eradication as prevention against chronic peptic ulcer disease in children.

The changes caused by Helicobacter pylori are a slow, progressing inflammatory process developing from several to dozen years. H. pylori infection leads to an inflammatory response in the gastric mucosa with granulocyte infiltrates in an acute form of the inflammation, and lymphocytes, plasmatic, macrophages and eosinophils in a chronic form inducing the development of gastric and duodenal ulcers and gastric cancer in some patients. The frequency and the type of morphological changes in the gastric mucosa were analyzed in children with positive IgG against H. pylori and the incidence of gastric and duodenal ulcers in family members of children examined was evaluated in our study. Gastritis was reported in 68.8% of children with positive IgG against H. pylori. Gastric ulcer was confirmed in 37.1% of families of children included in the study. Duodenal ulcers were found in 22.9% of families. The results obtained, indicate the usefulness of long-term observation and clinical follow-up of children with chronic gastritis of H. pylori ethiology taking into consideration bacterium eradication as prophylaxis of peptic ulceration.