Mucosal gastrin cells and serum gastrin levels in children with Helicobacter pylori infection.

PURPOSE Impaired control of gastric juice secretion is observed in chronic gastritis due to Helicobacter pylori (H. pylori) infection. G cells are stimulated by such cytokines as tumor necrosis factor (TNF-alpha), interferon gamma (IFN-gamma) and interleukin-8 (IL-8). The number of D cells producing somatostatin decreases simultaneously. An increase in gastrin levels could also depend on alkalization in G cell environment caused by bacterial urease. The aim of the study was to evaluate G cell counts in the antrum and gastrin levels in the serum of children with H. pylori infection and after bacterium eradication. MATERIAL AND METHODS The study was performed in 106 patients. Children were divided into 3 groups with regard to the presence and course of H. pylori infection. Fifty nine children (55.7%) had chronic gastritis in the course of H. pylori infection with a positive titre of antibodies in IgG class against H. pylori; 29 children (27.3%) with past H. pylori infection, without bacterium colonization and gastritis but with a positive titre of antibodies in IgG class against H. pylori; 18 children (17%) with functional disorders of the gastrointestinal tract but without H. pylori infection. RESULTS The quantitative analysis of gastrin cells in the antral mucosa of children performed by immunohistochemical method showed the highest gastrin cell count in group I with H. pylori infection (112.1 +/- 58.9 cell/mm2) and in group II with past H. pylori infection (105.3 +/- 73.1 cell/mm2). The serum gastrin level (92.9 +/- 41.6 microU/ml) was the highest in children with H. pylori infection. In controls, it was 70.0 +/- 15.3 microU/ml and could be compared to the results of children with past H. pylori infection. CONCLUSIONS 1. The H. pylori infection plays a significant role in the stimulation of G cells increase and gastrin release in the blood serum in children. 2. The eradication of H. pylori infection is probably a main factor in gastric secretion down-regulation during gastritis in children.