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Endoscopic gastritis, serum pepsinogen assay, and Helicobacter pylori infection

View Article: PubMed Central - PubMed

ABSTRACT

Endoscopic findings of the background gastric mucosa are important in the Helicobacter pylori-seroprevalent population. It is strongly correlated not only with the risk of gastric cancer, but also with the excretion ability of gastric mucosa cells. In noninfected subjects, common endoscopic findings are regular arrangement of collecting venules, chronic superficial gastritis, and erosive gastritis. In cases of active H. pylori infection, nodularity on the antrum, hemorrhagic spots on the fundus, and thickened gastric folds are common endoscopic findings. The secreting ability of the gastric mucosa cells is usually intact in both noninfected and actively infected stomachs, and the intragastric condition becomes hyperacidic upon inflammation. Increased serum pepsinogen II concentration correlates well with active H. pylori infection, and also indicates an increased risk of diffuse-type gastric cancer. In chronic inactive H. pylori infection, metaplastic gastritis and atrophic gastritis extending from the antrum (closed-type chronic atrophic gastritis) toward the corpus (open-type chronic atrophic gastritis) are common endoscopic findings. The intragastric environment is hypoacidic and the risk of intestinal-type gastric cancer is increased in such conditions. Furthermore, there is a decrease in serum pepsinogen I concentration when the secreting ability of the gastric mucosa cells is damaged. Serologic and endoscopic changes that occur upon H. pylori infection are important findings for estimating the secreting ability of the gastric mucosa cells, and could be applied for the secondary prevention of gastric cancer.

No MeSH data available.


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(A) Endoscopic findings in subjects without Helicobacter pylori infection. Pepsinogen (PG) I is produced exclusively by chief cells and mucus neck cells on the fundus. PG II is secreted throughout the stomach and also from the Brunner’s gland of the duodenal bulb. (B) Normal endoscopic finding of the angle in noninfected subject. The regular arrangement of the collecting venules on the angle indicate normal gastric mucosa. (C) Normal finding of the corpus in the same subject. The regular arrangement of the collecting venules extends up to the on the cardia and fundus. (D) Chronic superficial gastritis. Several hyperemic streaks are noticed on greater curvature side of the antrum. (E) Erosive gastritis. Multiple raised, hyperemic erosions are visible on the antrum.
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f2-kjim-2016-166: (A) Endoscopic findings in subjects without Helicobacter pylori infection. Pepsinogen (PG) I is produced exclusively by chief cells and mucus neck cells on the fundus. PG II is secreted throughout the stomach and also from the Brunner’s gland of the duodenal bulb. (B) Normal endoscopic finding of the angle in noninfected subject. The regular arrangement of the collecting venules on the angle indicate normal gastric mucosa. (C) Normal finding of the corpus in the same subject. The regular arrangement of the collecting venules extends up to the on the cardia and fundus. (D) Chronic superficial gastritis. Several hyperemic streaks are noticed on greater curvature side of the antrum. (E) Erosive gastritis. Multiple raised, hyperemic erosions are visible on the antrum.

Mentions: The ability to secrete gastric acid and other gastric hormones is intact in subjects without H. pylori infection. The background gastric mucosa exhibits regular arrangements of the collecting venules when a subject has never been infected with H. pylori (Fig. 2). In hyperacidic conditions, multiple hyperemic erosions or linear streaks can occur on the antrum, which may lead to erosive gastritis (EG) or chronic superficial gastritis (CSG).


Endoscopic gastritis, serum pepsinogen assay, and Helicobacter pylori infection
(A) Endoscopic findings in subjects without Helicobacter pylori infection. Pepsinogen (PG) I is produced exclusively by chief cells and mucus neck cells on the fundus. PG II is secreted throughout the stomach and also from the Brunner’s gland of the duodenal bulb. (B) Normal endoscopic finding of the angle in noninfected subject. The regular arrangement of the collecting venules on the angle indicate normal gastric mucosa. (C) Normal finding of the corpus in the same subject. The regular arrangement of the collecting venules extends up to the on the cardia and fundus. (D) Chronic superficial gastritis. Several hyperemic streaks are noticed on greater curvature side of the antrum. (E) Erosive gastritis. Multiple raised, hyperemic erosions are visible on the antrum.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5016293&req=5

f2-kjim-2016-166: (A) Endoscopic findings in subjects without Helicobacter pylori infection. Pepsinogen (PG) I is produced exclusively by chief cells and mucus neck cells on the fundus. PG II is secreted throughout the stomach and also from the Brunner’s gland of the duodenal bulb. (B) Normal endoscopic finding of the angle in noninfected subject. The regular arrangement of the collecting venules on the angle indicate normal gastric mucosa. (C) Normal finding of the corpus in the same subject. The regular arrangement of the collecting venules extends up to the on the cardia and fundus. (D) Chronic superficial gastritis. Several hyperemic streaks are noticed on greater curvature side of the antrum. (E) Erosive gastritis. Multiple raised, hyperemic erosions are visible on the antrum.
Mentions: The ability to secrete gastric acid and other gastric hormones is intact in subjects without H. pylori infection. The background gastric mucosa exhibits regular arrangements of the collecting venules when a subject has never been infected with H. pylori (Fig. 2). In hyperacidic conditions, multiple hyperemic erosions or linear streaks can occur on the antrum, which may lead to erosive gastritis (EG) or chronic superficial gastritis (CSG).

View Article: PubMed Central - PubMed

ABSTRACT

Endoscopic findings of the background gastric mucosa are important in the Helicobacter pylori-seroprevalent population. It is strongly correlated not only with the risk of gastric cancer, but also with the excretion ability of gastric mucosa cells. In noninfected subjects, common endoscopic findings are regular arrangement of collecting venules, chronic superficial gastritis, and erosive gastritis. In cases of active H. pylori infection, nodularity on the antrum, hemorrhagic spots on the fundus, and thickened gastric folds are common endoscopic findings. The secreting ability of the gastric mucosa cells is usually intact in both noninfected and actively infected stomachs, and the intragastric condition becomes hyperacidic upon inflammation. Increased serum pepsinogen II concentration correlates well with active H. pylori infection, and also indicates an increased risk of diffuse-type gastric cancer. In chronic inactive H. pylori infection, metaplastic gastritis and atrophic gastritis extending from the antrum (closed-type chronic atrophic gastritis) toward the corpus (open-type chronic atrophic gastritis) are common endoscopic findings. The intragastric environment is hypoacidic and the risk of intestinal-type gastric cancer is increased in such conditions. Furthermore, there is a decrease in serum pepsinogen I concentration when the secreting ability of the gastric mucosa cells is damaged. Serologic and endoscopic changes that occur upon H. pylori infection are important findings for estimating the secreting ability of the gastric mucosa cells, and could be applied for the secondary prevention of gastric cancer.

No MeSH data available.


Related in: MedlinePlus