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Purpose: Erosive esophagitis frequently develops after successful Helicobacter pylori eradication. Since salivary secretion of epidermal growth factor (EGF) plays a crucial role in the pathogenesis of gastroesophageal reflux disease, the current study objective was to find out whether erosive esophagitis development after Helicobacter pylori eradication is associated with the secretion of EGF in saliva., Materials and Methods: A total of 115 H. pylori infected patients (positive results of CLO-test, histology and serology) with a duodenal ulcer were recruited for the study. Gastroscopic examinations and saliva collections were performed twice, prior to H. pylori eradication and one year after its cessation. The salivary EGF was determined using a radioimmunological method., Results: Salivary EGF secretion was lower in H. pylori infected subjects with erosive esophagitis than without (0.82+/-0.66 vs 1.70+/-3.49 ng/min, p=0.021). However, a year after successful H. pylori eradication, salivary EGF did not differ between the groups (2.17+/-2.06 vs 1.79+/-2.06 ng/min); the lack of difference was due to high peptide secretion in patients who developed erosive esophagitis after eradication., Conclusion: Erosive esophagitis development following H. pylori eradication is not the result of decreased salivary EGF secretion.

Purpose: Erosive esophagitis frequently develops after successful Helicobacter pylori eradication. Since salivary secretion of epidermal growth factor (EGF) plays a crucial role in the pathogenesis of gastroesophageal reflux disease, the current study objective was to find out whether erosive esophagitis development after Helicobacter pylori eradication is associated with tile secretion of EGF in saliva. Materials and methods: A total of 115 H. pylori infected patients (positive results of CLO-test, histology and serology) with a duodenal ulcer were recruited for the study. Gastroscopic examinations and saliva collections were performed twice, prior to H. pylori eradication and one year after its cessation. The salivary EGF was determined using a radioimmunological method. Results: Salivary EGF secretion was lower in H. pylori infected subjects with erosive esophagitis than without (0.82±0.66 vs 1.70±3.49 ng/min. p=0.021). However, a year after successful H. pyfori eradication, salivary EGF did not differ between the groups (2.17±2.06 vs 1.79±2.06 ng/min); the lack of difference was due to high peptide secretion in patients who developed erosive esophagitis after eradication. Conclusion: Erosive esophagitis development following H. pylori eradication is not the result of decreased salivary EGF secretion. [ABSTRACT FROM AUTHOR]