Roczniki Akademii Medycznej w Bialymstoku (1995) · 2004
Gastric acid and salivary bicarbonate. Is there a relationship in duodenal ulcer patients?
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Namiot Z, Stasiewicz J, Markowski A R, Namiot D B, Jaroszewicz W, Kemona A, Górski J
Аннотация
PURPOSE: Since saliva protects the oesophageal and oral mucosa against hydrogen ions, the aim of the study was to establish the relationship between the secretion of gastric acid and salivary bicarbonate.
MATERIAL AND METHODS: The study involved 43 Helicobacter pylori positive duodenal ulcer patients receiving: 1. omeprazole alone (O), 2. omeprazole and amoxicillin (OA) or 3. omeprazole, amoxicillin and tinidazole (OAT). In each study group the examination was performed twice, before and at the end of a two-week treatment, both under basal conditions and during a gastric secretory test with pentagastrin. Concentrations of gastric hydrogen ions and salivary bicarbonate were evaluated by the titration method.
RESULTS: In all therapeutic groups analysed separately, the secretion of gastric acid as well as salivary bicarbonate decreased at the end of the treatment, however only in OA and OAT groups the differences in bicarbonate reached statistical significance. As the changes in the concentration and output of both salivary bicarbonate and gastric acid had the same direction, the three therapeutic groups (O, OA, OAT) were subjected to combined analysis. It showed that under basal conditions and during stimulation with a gastric catheter or catheter and pentagastrin, bicarbonate concentration and output were higher before than at the end of the treatment. However, no direct correlation between gastric acid secretion and salivary bicarbonate was found in groups subjected to either separate or combined analysis.
CONCLUSIONS: The results of our study provide evidence for the partial involvement of hydrogen ions of gastric origin in the regulation of salivary bicarbonate secretion in duodenal ulcer patients.
MATERIAL AND METHODS: The study involved 43 Helicobacter pylori positive duodenal ulcer patients receiving: 1. omeprazole alone (O), 2. omeprazole and amoxicillin (OA) or 3. omeprazole, amoxicillin and tinidazole (OAT). In each study group the examination was performed twice, before and at the end of a two-week treatment, both under basal conditions and during a gastric secretory test with pentagastrin. Concentrations of gastric hydrogen ions and salivary bicarbonate were evaluated by the titration method.
RESULTS: In all therapeutic groups analysed separately, the secretion of gastric acid as well as salivary bicarbonate decreased at the end of the treatment, however only in OA and OAT groups the differences in bicarbonate reached statistical significance. As the changes in the concentration and output of both salivary bicarbonate and gastric acid had the same direction, the three therapeutic groups (O, OA, OAT) were subjected to combined analysis. It showed that under basal conditions and during stimulation with a gastric catheter or catheter and pentagastrin, bicarbonate concentration and output were higher before than at the end of the treatment. However, no direct correlation between gastric acid secretion and salivary bicarbonate was found in groups subjected to either separate or combined analysis.
CONCLUSIONS: The results of our study provide evidence for the partial involvement of hydrogen ions of gastric origin in the regulation of salivary bicarbonate secretion in duodenal ulcer patients.