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.