The Changes of Ammonia and Epidermal Growth Factor Concentration in Gastric Juice before and after the Helicobacter pylori Eradication

Jang, Jae Young; Chang, Young Woon; Choi, Sun Young; Kim, Nam Hoon; Lim, Keun Woo; Jung, Yong Hee; Han, Yo Seb; Dong, Seok Ho; Kim, Hyo Jong; Kim, Byung Ho; Lee, Joung Il; Chang, Rin

Abstract

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection is the cause of peptic ulcer diseases, and gastric cancer. Hydrolysis of urea generating ammonia may cause cytotoxic effects on the gastric epithelium. The ammonia may induce the synthesis of epidermal growth factor (EGF) in gastric epithelium as an adaptive cytoprotective mechanism. The first aim was to examine the concentration of ammonia and EGF in gastric juice before and after H. pylori eradication in functional dyspepsia patients. The second aim was to examine the correlation among ammonia concentration, EGF concentration, and inflammatory score of gastritis. METHODS: The concentration of ammonia and EGF were measured by ELISA. The grade and severity of gastritis were measured according to the updated Sydney system. RESULTS: The concentration of ammonia in gastric juice was much higher in the H. pylori positive subjects (10,787 +/- 6,584 micro mol/L) than in the negative subjects (2,339 +/- 1,158 micro mol/L, p<0.0001). The concentrations of EGF in gastric juice was much higher in the positive subjects (1,462 +/- 393 pg/mL) than in the negative subjects (1,088 +/- 499 pg/mL, p<0.005). The concentration of ammonia and EGF in gastric juice showed significant correlation (r=0.63, p<0.0001). The concentrations of ammonia and histologic severities showed significant correlation (r=0.41, p<0.0001). Moreover, the level of EGF in gastric juice and histologic severities showed positive correlation (r=0.20, p<0.005). CONCLUSIONS: As the concentration of ammonia in gastric juices increased, the concentration of EGF was also increased in functional dyspepsia with H. pylori infection. The concentration of EGF in gastric juice may play a role in the adaptive cytoprotection in H. pylori- induced gastritis.