电邮这篇文章 Time course of changes in the gastric juice levels of nitric oxide in patients with upper digestive tract diseases
- 作者: Esedov E.M.1, Magomedeminova A.S.1, Esedov EM1, Magomedeminova AS1
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- 期: 卷 82, 编号 2 (2010)
- 页面: 21-24
- 栏目: Editorial
- ##submission.dateSubmitted##: 09.04.2020
- ##submission.datePublished##: 15.02.2010
- URL: https://ter-arkhiv.ru/0040-3660/article/view/30536
- ID: 30536
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Aim. to study the time course of changes in the gastric juice levels of nitric oxide (NO) in patients with esophagogastroduonenal diseases (EGDD).
Subjects and methods. One hundred and seventy-four patients with EGDD were examined.
Results. In patients with chronic atrophic gastritis, the level of NO was significantly lower than the normal levels and correlated with the magnitude of mucosal atrophy. Elevated gastric juice NO levels were noted at exacerbations of gastroesophageal reflux disease (GERD), chronic nonatrophic gastritis (CNAG), and duodenal ulcer disease (DUD). At the end of a therapy course, the gastric juice levels of NO did not achieve the control values in patients with GERD, reduced to the normal values in those with CNAG, although became lower, but remained above the normal values in DUD in a remission phase.
Conclusion. The patients with EGDD were observed to have heterodirectional changes in the content of NO in gastric juice. In the patients with DUD, the remaining gastric juice NO levels above the normal values after ulcerative defect cicatrization are indicative of incomplete reparative processes in the gastric mucosa, i.e. delayed morphological remission. In chronic atrophic gastritis, the gastric juice levels of NO did not achieve normal values after treatment despite the onset of clinical remission which may be caused by a continuous gastric mucosal atrophic process.
Subjects and methods. One hundred and seventy-four patients with EGDD were examined.
Results. In patients with chronic atrophic gastritis, the level of NO was significantly lower than the normal levels and correlated with the magnitude of mucosal atrophy. Elevated gastric juice NO levels were noted at exacerbations of gastroesophageal reflux disease (GERD), chronic nonatrophic gastritis (CNAG), and duodenal ulcer disease (DUD). At the end of a therapy course, the gastric juice levels of NO did not achieve the control values in patients with GERD, reduced to the normal values in those with CNAG, although became lower, but remained above the normal values in DUD in a remission phase.
Conclusion. The patients with EGDD were observed to have heterodirectional changes in the content of NO in gastric juice. In the patients with DUD, the remaining gastric juice NO levels above the normal values after ulcerative defect cicatrization are indicative of incomplete reparative processes in the gastric mucosa, i.e. delayed morphological remission. In chronic atrophic gastritis, the gastric juice levels of NO did not achieve normal values after treatment despite the onset of clinical remission which may be caused by a continuous gastric mucosal atrophic process.
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