Endoscopic gastritis, serum pepsinogen assay, and Helicobacter pylori infection

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.

Keywords: Atrophy; Endoscopy; Gastritis; Helicobacter pylori; Pepsinogens.

Figure 1.

Endoscopic findings of the background gastric mucosa according to the gastric carcinogenesis pathway. Upon Helicobacter pylori infection, the gastric mucosa shows changes indicating active infection, such as multiple hemorrhagic spots, nodules, and thickening of the gastric rugae. During this stage, the risk of diffuse-type gastric cancer is increased, the intragastric environment becomes hyperacidic, and there is an increase in serum pepsinogen (PG) levels. When active inflammation subsides and the infection progress to a chronic stage, the background gastric mucosa shows atrophy and metaplasia. This long-term, slow process increases the risk of intestinal-type gastric cancer, the intragastric environment becomes hypoacidic, and there is a decrease in serum PG levels.

Figure 2.

(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.

Figure 3.

(A) Endoscopic findings in subjects with active Helicobacter pylori infection. (B) Nodular gastritis on the anterior-greater side of the proximal antrum. Multiple small nodules are visible on the antrum, extending up to greater curvature side of the corpus. The nodules consist of submucosal elevated lesions, and thus, there is no color change in nodular gastritis. (C) Follow-up findings of enlarged nodules on the proximal antrum to low-body in the same patient. The previously noted tiny, regular nodules have increased in size. The nodules were irregular and had grown from 12 months prior. (D) Finding of hemorrhagic spots on the fundus in nodular gastritis patient at initial endoscopy (B). Multiple tiny reddish spots, so-called diffuse redness, can be seen on the fundus and greater curvature side of the corpus. (E) Hypertrophic gastric folds. Thickened gastric rugae with whitish, sticky exudates indicate active H. pylori infection. PG, pepsinogen.

Figure 4.

(A) Endoscopic findings in subjects with chronic Helicobacter pylori infection. Therefore, the serum pepsinogen (PG) I level is decreased only when the fundus is damaged by atrophic changes. Based on these findings, gastric corpus atrophy is defined as a serum PG I/II ratio of < 3.0 and a PG I level of < 70 ng/mL, and is widely used for gastric cancer screening for the detection of high risk individuals. (B) Closed-type atrophic gastritis. Visible transparent vessels can be seen on the anterior-lesser curvature side of the low-body to the angle. An atrophic border is present. (C) Open-type atrophic gastritis. Visible transparent vessels are extended up to the cardia without an atrophic border. (D) Metaplastic gastritis. Multiple large, irregular whitish elevations are present on the distal part of the antrum. This is a common endoscopic finding in subjects with atrophic gastritis on the corpus. (E) Diffuse, irregular whitish changes in metaplastic gastritis. Intestinal metaplasia can have a variety of appearances, such as whitish, nodular elevations. Geographic and hyperemic changes can be also found in metaplastic gastritis.

Figure 5.

Different endoscopic findings of nodular gastritis, metaplastic gastritis, and erosive gastritis. (A) Nodular gastritis. On the distal part of the antrum, multiple elevated nodules are seen without color change. The nodules are regular in size and shape. (B) Metaplastic gastritis. Intestinal metaplasia can be confused when hyperemic mucosa is augmented by whitish surrounding mucosa. The elevations are irregular in size, shape, and color. (C) Erosive gastritis. Elevated hyperemic erosions are scattered on the antrum.

Figure 6.

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.