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Relationship between Helicobacter pylori infection and serum pepsinogen levels in patients with chronic gastritic diseases or gastric cancer

Tao Wei, Ning Zhang, Yang Li

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Abstract

Objective To investigate the impact of Helicobacter pylori (H. pylori) on the level of serum pepsinogen (PG) subgroup (PG Ⅰ and PG Ⅱ) in patients with chronic gastric diseases and gastric cancer. Methods A total of 263 patients with symptoms of digestive tract diseases treated in the gastroenterology department of the Affiliated Hospital of Ningxia Medical University from October 2010 to April 2011 (67 cases of gastric cancer, 104 cases of atrophic gastritis, and 92 cases of peptic ulcer) were enrolled for the study. Eighty-eight healthy people were entered as normal control. The H. pylori status was determined by rapid urease test, and the level of serum pepsinogen (PG Ⅰ and PG Ⅱ) was measured by enzyme-linked immunosorbent assay (ELISA). Results The positive rate of HP infection for peptic ulcer was the highest (71.7%), whereas that of atrophic gastritis, gastric cancer and normal control was 63.5%, 56.7% and 55.6%, respectively, there was no significant difference between groups (P > 0.05). Compared with the normal control, serum PG Ⅰ level and PG Ⅰ/PG Ⅱ ratio were lower in atrophic gastritis patients, whereas that of PG Ⅱ elevated; PG Ⅰ/PG Ⅱ ratio of peptic ulcer patients was lowered, whereas their PGⅠ and PG Ⅱ elevated (P < 0.05 or PP < 0.01). PG Ⅰ and PG Ⅰ/PGⅡ ratio of gastric cancer patients were lower than those of normal control; however, PG Ⅱ was higher (PP < 0.01). In atrophic gastritis patients, gastric cancer patients and normal control, serum PG Ⅰ and PG Ⅱ levels showed no significant difference between HP+ and HP- patients (P > 0.05). Serum PG Ⅰ, PG Ⅱ and PG Ⅰ/PG Ⅱ ratio in patients with atrophic gastritis plus intestinal metaplasia, and those plus dysplasia were not significant different from those in patients with atrophic gastritis alone (P > 0.05), while the PG Ⅰ/PG Ⅱ ratio was higher when compared with that in patients with gastric cancer (PP < 0.01). In patients with atrophic gastritis alone, atrophic gastritis plus metaplasia, and atrophic gastritis plus dysplasia, serum level of PG Ⅰ and PG Ⅱ, and PG Ⅰ/PG Ⅱ ratio showed no significant difference between HP+ patients and HP- patients (P > 0.05). Conclusion H. pylori infection has little relation with changes in serum pepsinogen level in patients with chronic gastric diseases or gastric cancer.

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What this paper is about

Objective To investigate the impact of Helicobacter pylori (H. pylori) on the level of serum pepsinogen (PG) subgroup (PG Ⅰ and PG Ⅱ) in patients with chronic gastric diseases and gastric cancer. Methods A total of 263 patients with symptoms of digestive tract diseases treated in the gastroenterology department of the Affiliated Hospital of Ningxia Medical University from October 2010 to April 2011 (67 cases of gastric cancer, 104 cases of atrophic gastritis, and 92 cases of peptic ulcer) were enrolled for the study. Eighty-eight healthy people were entered as normal control. The H. pylori status was determined by rapid urease test, and the level of serum pepsinogen (PG Ⅰ and PG Ⅱ) was measured by enzyme-linked immunosorbent assay (ELISA). Results The positive rate of HP infection for peptic ulcer was the highest (71.7%), whereas that of atrophic gastritis, gastric cancer and normal control was 63.5%, 56.7% and 55.6%, respectively, there was no significant difference between groups (P > 0.05). Compared with the normal control, serum PG Ⅰ level and PG Ⅰ/PG Ⅱ ratio were lower in atrophic gastritis patients, whereas that of PG Ⅱ elevated; PG Ⅰ/PG Ⅱ ratio of peptic ulcer patients was lowered, whereas their PGⅠ and PG Ⅱ elevated (P < 0.05 or PP < 0.01). PG Ⅰ and PG Ⅰ/PGⅡ ratio of gastric cancer patients were lower than those of normal control; however, PG Ⅱ was higher (PP < 0.01). In atrophic gastritis patients, gastric cancer patients and normal control, serum PG Ⅰ and PG Ⅱ levels showed no significant difference between HP+ and HP- patients (P > 0.05). Serum PG Ⅰ, PG Ⅱ and PG Ⅰ/PG Ⅱ ratio in patients with atrophic gastritis plus intestinal metaplasia, and those plus dysplasia were not significant different from those in patients with atrophic gastritis alone (P > 0.05), while the PG Ⅰ/PG Ⅱ ratio was higher when compared with that in patients with gastric cancer (PP < 0.01). In patients with atrophic gastritis alone, atrophic gastritis plus metaplasia, and atrophic gastritis plus dysplasia, serum level of PG Ⅰ and PG Ⅱ, and PG Ⅰ/PG Ⅱ ratio showed no significant difference between HP+ patients and HP- patients (P > 0.05). Conclusion H. pylori infection has little relation with changes in serum pepsinogen level in patients with chronic gastric diseases or gastric cancer.

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Available abstract

Objective To investigate the impact of Helicobacter pylori (H. pylori) on the level of serum pepsinogen (PG) subgroup (PG Ⅰ and PG Ⅱ) in patients with chronic gastric diseases and gastric cancer. Methods A total of 263 patients with symptoms of digestive tract diseases treated in the gastroenterology department of the Affiliated Hospital of Ningxia Medical University from October 2010 to April 2011 (67 cases of gastric cancer, 104 cases of atrophic gastritis, and 92 cases of peptic ulcer) were enrolled for the study. Eighty-eight healthy people were entered as normal control. The H. pylori status was determined by rapid urease test, and the level of serum pepsinogen (PG Ⅰ and PG Ⅱ) was measured by enzyme-linked immunosorbent assay (ELISA). Results The positive rate of HP infection for peptic ulcer was the highest (71.7%), whereas that of atrophic gastritis, gastric cancer and normal control was 63.5%, 56.7% and 55.6%, respectively, there was no significant difference between groups (P > 0.05). Compared with the normal control, serum PG Ⅰ level and PG Ⅰ/PG Ⅱ ratio were lower in atrophic gastritis patients, whereas that of PG Ⅱ elevated; PG Ⅰ/PG Ⅱ ratio of peptic ulcer patients was lowered, whereas their PGⅠ and PG Ⅱ elevated (P < 0.05 or PP < 0.01). PG Ⅰ and PG Ⅰ/PGⅡ ratio of gastric cancer patients were lower than those of normal control; however, PG Ⅱ was higher (PP < 0.01). In atrophic gastritis patients, gastric cancer patients and normal control, serum PG Ⅰ and PG Ⅱ levels showed no significant difference between HP+ and HP- patients (P > 0.05). Serum PG Ⅰ, PG Ⅱ and PG Ⅰ/PG Ⅱ ratio in patients with atrophic gastritis plus intestinal metaplasia, and those plus dysplasia were not significant different from those in patients with atrophic gastritis alone (P > 0.05), while the PG Ⅰ/PG Ⅱ ratio was higher when compared with that in patients with gastric cancer (PP < 0.01). In patients with atrophic gastritis alone, atrophic gastritis plus metaplasia, and atrophic gastritis plus dysplasia, serum level of PG Ⅰ and PG Ⅱ, and PG Ⅰ/PG Ⅱ ratio showed no significant difference between HP+ patients and HP- patients (P > 0.05). Conclusion H. pylori infection has little relation with changes in serum pepsinogen level in patients with chronic gastric diseases or gastric cancer.

Key concepts: Gastroenterology, Atrophic gastritis, Internal medicine, Medicine, Intestinal metaplasia, Helicobacter pylori, Pepsin, Cancer

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