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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.


Related in: MedlinePlus

Different prognoses in two Helicobacter pylori-infected subjects. (A) Endoscopic findings of a 55-year-old man. A single, raised erosion is present on the greater curvature side of the pylorus. A serum anti-H. pylori immunoglobulin G (IgG) assay was positive on the day of endoscopic examination. The serum pepsinogen (PG) I level was 25.8 ng/mL, the PG II level was 12.2 ng/mL, and the PG I/II ratio was 2.1 (normal values: PG I > 70.0 ng/mL, PG II < 15.0 ng/mL, PG I/II ratio > 3.0). Pathology test results revealed chronic gastritis with marked intestinal metaplasia, and Giemsa staining was negative. (B) Forty-three months after the initial tests. The patient revisited our clinic for follow-up testing. The serum anti-H. pylori IgG assay was still positive, and the serum PG I level and PG I/II ratio had decreased (PG I 24.0 ng/mL, PG II 13.0 ng/mL, PG I/II ratio 1.8). Pathology test results and Giemsa staining were not altered. (C) Endoscopic findings of a 62-year-old man. The serum anti-H. pylori IgG assay was positive, and the serum PG assay finding was also positive (PG I 28.6 ng/mL, PG II 14.5 ng/mL, PG I/II ratio 2.0). Active gastritis with foveolar hyperplasia and regenerated glands were found on the biopsy, and Giemsa staining was positive. (D) Follow-up endoscopy 1 year after successful H. pylori eradication. The serum anti-H. pylori IgG test became negative, and the serum PG I/II ratio had increased (PG I 29.0 ng/mL, PG II 10.4 ng/mL, PG I/II ratio 2.7). Pathology test results revealed chronic gastritis without H. pylori-like microorganisms, and Giemsa staining was negative.
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f6-kjim-2016-166: Different prognoses in two Helicobacter pylori-infected subjects. (A) Endoscopic findings of a 55-year-old man. A single, raised erosion is present on the greater curvature side of the pylorus. A serum anti-H. pylori immunoglobulin G (IgG) assay was positive on the day of endoscopic examination. The serum pepsinogen (PG) I level was 25.8 ng/mL, the PG II level was 12.2 ng/mL, and the PG I/II ratio was 2.1 (normal values: PG I > 70.0 ng/mL, PG II < 15.0 ng/mL, PG I/II ratio > 3.0). Pathology test results revealed chronic gastritis with marked intestinal metaplasia, and Giemsa staining was negative. (B) Forty-three months after the initial tests. The patient revisited our clinic for follow-up testing. The serum anti-H. pylori IgG assay was still positive, and the serum PG I level and PG I/II ratio had decreased (PG I 24.0 ng/mL, PG II 13.0 ng/mL, PG I/II ratio 1.8). Pathology test results and Giemsa staining were not altered. (C) Endoscopic findings of a 62-year-old man. The serum anti-H. pylori IgG assay was positive, and the serum PG assay finding was also positive (PG I 28.6 ng/mL, PG II 14.5 ng/mL, PG I/II ratio 2.0). Active gastritis with foveolar hyperplasia and regenerated glands were found on the biopsy, and Giemsa staining was positive. (D) Follow-up endoscopy 1 year after successful H. pylori eradication. The serum anti-H. pylori IgG test became negative, and the serum PG I/II ratio had increased (PG I 29.0 ng/mL, PG II 10.4 ng/mL, PG I/II ratio 2.7). Pathology test results revealed chronic gastritis without H. pylori-like microorganisms, and Giemsa staining was negative.

Mentions: The ability of gastric mucosa cells to heal from an H. pylori infection depends on the period of bacterial regression. If H. pylori is eradicated before the point of no return, gastric mucosa regains its secreting ability, and serum PG concentrations start to increase (Fig. 6). This is rare in cases of spontaneous regression of H. pylori infection, in which most damage to the gastric mucosa is irreversible.


Endoscopic gastritis, serum pepsinogen assay, and Helicobacter pylori infection
Different prognoses in two Helicobacter pylori-infected subjects. (A) Endoscopic findings of a 55-year-old man. A single, raised erosion is present on the greater curvature side of the pylorus. A serum anti-H. pylori immunoglobulin G (IgG) assay was positive on the day of endoscopic examination. The serum pepsinogen (PG) I level was 25.8 ng/mL, the PG II level was 12.2 ng/mL, and the PG I/II ratio was 2.1 (normal values: PG I > 70.0 ng/mL, PG II < 15.0 ng/mL, PG I/II ratio > 3.0). Pathology test results revealed chronic gastritis with marked intestinal metaplasia, and Giemsa staining was negative. (B) Forty-three months after the initial tests. The patient revisited our clinic for follow-up testing. The serum anti-H. pylori IgG assay was still positive, and the serum PG I level and PG I/II ratio had decreased (PG I 24.0 ng/mL, PG II 13.0 ng/mL, PG I/II ratio 1.8). Pathology test results and Giemsa staining were not altered. (C) Endoscopic findings of a 62-year-old man. The serum anti-H. pylori IgG assay was positive, and the serum PG assay finding was also positive (PG I 28.6 ng/mL, PG II 14.5 ng/mL, PG I/II ratio 2.0). Active gastritis with foveolar hyperplasia and regenerated glands were found on the biopsy, and Giemsa staining was positive. (D) Follow-up endoscopy 1 year after successful H. pylori eradication. The serum anti-H. pylori IgG test became negative, and the serum PG I/II ratio had increased (PG I 29.0 ng/mL, PG II 10.4 ng/mL, PG I/II ratio 2.7). Pathology test results revealed chronic gastritis without H. pylori-like microorganisms, and Giemsa staining was negative.
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f6-kjim-2016-166: Different prognoses in two Helicobacter pylori-infected subjects. (A) Endoscopic findings of a 55-year-old man. A single, raised erosion is present on the greater curvature side of the pylorus. A serum anti-H. pylori immunoglobulin G (IgG) assay was positive on the day of endoscopic examination. The serum pepsinogen (PG) I level was 25.8 ng/mL, the PG II level was 12.2 ng/mL, and the PG I/II ratio was 2.1 (normal values: PG I > 70.0 ng/mL, PG II < 15.0 ng/mL, PG I/II ratio > 3.0). Pathology test results revealed chronic gastritis with marked intestinal metaplasia, and Giemsa staining was negative. (B) Forty-three months after the initial tests. The patient revisited our clinic for follow-up testing. The serum anti-H. pylori IgG assay was still positive, and the serum PG I level and PG I/II ratio had decreased (PG I 24.0 ng/mL, PG II 13.0 ng/mL, PG I/II ratio 1.8). Pathology test results and Giemsa staining were not altered. (C) Endoscopic findings of a 62-year-old man. The serum anti-H. pylori IgG assay was positive, and the serum PG assay finding was also positive (PG I 28.6 ng/mL, PG II 14.5 ng/mL, PG I/II ratio 2.0). Active gastritis with foveolar hyperplasia and regenerated glands were found on the biopsy, and Giemsa staining was positive. (D) Follow-up endoscopy 1 year after successful H. pylori eradication. The serum anti-H. pylori IgG test became negative, and the serum PG I/II ratio had increased (PG I 29.0 ng/mL, PG II 10.4 ng/mL, PG I/II ratio 2.7). Pathology test results revealed chronic gastritis without H. pylori-like microorganisms, and Giemsa staining was negative.
Mentions: The ability of gastric mucosa cells to heal from an H. pylori infection depends on the period of bacterial regression. If H. pylori is eradicated before the point of no return, gastric mucosa regains its secreting ability, and serum PG concentrations start to increase (Fig. 6). This is rare in cases of spontaneous regression of H. pylori infection, in which most damage to the gastric mucosa is irreversible.

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