“…However, the vitamin C level of gastric juice was inversely related to the severity of chronic or active inflammation or histological H. pylori density as shown previously in other studies [6][7][8][9][10]. Our study populations were asymptomatic young, relatively healthy medical students who volunteered for endoscopy during the course of problem-based learning in chronic gastritis, one of the very common medical disorders in Chinju, Korea.…”
Section: Discussionsupporting
confidence: 70%
“…But this secretion is impaired with the onset of H. pylori-induced acute gastritis and remains impaired in H. pylori-associated chronic gastritis [4,5]. Several studies revealed that vitamin C levels of gastric juice decreased in patients with H. pylori infection [6][7][8][9][10] and returned to normal after H. pylori eradication [11][12][13]. However, most studies have been performed in a small number of volunteers or in patients with gastroduodenal disorders.…”
“…However, the vitamin C level of gastric juice was inversely related to the severity of chronic or active inflammation or histological H. pylori density as shown previously in other studies [6][7][8][9][10]. Our study populations were asymptomatic young, relatively healthy medical students who volunteered for endoscopy during the course of problem-based learning in chronic gastritis, one of the very common medical disorders in Chinju, Korea.…”
Section: Discussionsupporting
confidence: 70%
“…But this secretion is impaired with the onset of H. pylori-induced acute gastritis and remains impaired in H. pylori-associated chronic gastritis [4,5]. Several studies revealed that vitamin C levels of gastric juice decreased in patients with H. pylori infection [6][7][8][9][10] and returned to normal after H. pylori eradication [11][12][13]. However, most studies have been performed in a small number of volunteers or in patients with gastroduodenal disorders.…”
“…Ascorbic acid is actively secreted in gastric juice [20]. Its median value in subjects with a healthy stomach is 250 mmol/l and is substantially lower in subjects with H. pylori infection [21], atrophic gastritis [22] and those of black ethnicity [23].…”
Luminal NO at the gastro-oesophageal junction increases the generation of transient LOS relaxations following a meal. Chemicals generated by the acidification of salivary nitrite may contribute to gastro-oesophageal motility disorders.
“…During chronic H. pylori infection all these types of repair occur, the respective proportion of each being probably modulated by environmental, genetic and bacterial factors. [32][33][34][35] Figure 4 depicts a schematic representation of two possible scenarios of damage and repair. In the first scenario the stomach responds to injury with a continuing process of restitutio ad integrum, the gastric mucosa remains hospitable for H. pylori, and chronic active gastritis persists indefinitely without developing atrophy.…”
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