Pylori-positive Cases Research Articles

<i>Helicobacter pylori</i>感染からみた幽門側切除後残胃―胃内逆流胆汁酸との関連を含めて―

Helicobacter pylori (H. pylori) infection in cases of after distal gastric resection was studied. We also examined relation among H. pylori and residual superficial gastritis, bile acid refluxed into the stomach. 1) A rate of H. pylori infection in postoperative stomach shows 51.1%, which was lower than that of digestive ulcer, gastric carcinoma and control group. In cases of residual stomach, a concentration of chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA) refluxed into the stomach were remarkably higher than thoes of digestive ulcer and control group. I considered the rate of H. pylori infection in postoperative stomach is low because of highly concentrated CDCA and UDCA is not adequate for habitation of H. pylori. 2) There were no correlation among pathological inflammation, activity and superficial gastritis in postoperative stomach. Inflammation and activity were frequent in H. pylori positive cases than negative cases. 3) A frequency of H. pylori infection in cases of after distal gastric resection by gastric carcinoma within 5 years was lower than 50.0%. A rate of infection increased 72.7% in patients who were operated over 5 years ago.

An endoscopic study on relationship betweenHelicobacter pylori infection and endoscopic gastric ulcer scars

A two-year endoscopic follow-up study of 45 gastric ulcer patients was conducted in order to ascertain the relationship between Helicobacter pylori infection, the transformation of ulcer scar patterns, and ulcer relapse during maintenance therapy. Endoscopic findings of gastric ulcer scar patterns, which established the quality of ulcer scars, were classified as follows: Sa, with a central depression, Sb, with a coarse regenerating mucosal pattern up to the center, and Sc, with a fine pattern. The proportion of ulcer relapses was 62% among 29 H. pylori-positive patients and 0% among 16 H. pylori-negative patients. In regard to the relationship between H. pylori infection and scar patterns, 94% of the H. pylori-negative patients displayed Sc scar patterns, while all the H. pylori-positive patients showed various scar patterns, ie, Sa in 38%, Sb in 28%, and Sc in 10%. Ulcer relapses in the H. pylori-positive cases were limited to the Sa and Sb groups (100% and 88%, respectively). In conclusion, our results indicate that H. pylori infection plays an important role in the transformation of the ulcer scar patterns which relate to ulcer relapse.

Helicobacter pylori colonization in children with gastritis and peptic ulcer. I. The colonization rate and effects of colonization on mucin content and mucosal inflammation in the antrum

The incidence of Helicobacter pylori infection and effects of H. pylori colonization on mucin content and mucosal inflammation of the antral mucosa were studied quantitatively in 55 Japanese children with suspected gastritis and peptic ulcers (aged 6-16 years, mean 12.3 years). H. pylori was detected, using Warthin-Starry stain, in nine of the 22 cases (41%) with antral histological gastritis, but in none of the 33 histologically normal cases. Five out of seven duodenal ulcer cases showed histological gastritis, and all five cases were H. pylori positive. Severity of gastritis, evaluated by means of gastritis score, was significantly higher in H. pylori positive gastritis cases than in H. pylori negative gastritis cases (5.4 +/- 1.0 vs 3.1 +/- 0.3, P < 0.001). A PAS-AB index, a proportion of the periodic acid Schiff-alcian blue (PAS-AB) positive mucin area to the total epithelial area, was significantly lower in H. pylori positive cases than in H. pylori negative cases, irrespective of the existence of histological gastritis (23.5 +/- 7.6% vs 40.4 +/- 5.5%, 43.5 +/- 4.2%, P < 0.001). The decreased mucin content of gastric mucosa is likely to lead to weakening of an important defensive factor of gastric mucosa. These findings suggest that H. pylori plays an important role in gastritis and peptic ulcers in children, especially in cases with duodenal ulcer.

Is Helicobacter pylori a causal agent in gastric carcinoma?

The aim of this study is to clarify the relationship between Helicobacter pylori (H. pylori) infection and gastric carcinoma. 94 patients with gastric carcinoma and 111 patients with chronic gastritis were involved in this study. They were classified into 3 age groups: Group A (40 years and under), Group B (41-59), Group C (60 years and over). Serum samples were tested for H. pylori IgG antibodies by ELISA and for pepsinogen (PG) by RIA. The ratio of PG I/PG II was used as a marker for atrophic gastritis. Results were as follows. In the incidence of H. pylori antibodies, there was no significant differences between gastric carcinoma and chronic gastritis in any of the groups. In the quantity of H. pylori antibodies, there was no significant difference between gastric carcinoma and chronic gastritis in any of the groups. The ratio of PG I/PG II was significantly decreased in H. pylori positive cases when compared to H. pylori negative cases in each group with chronic gastritis and group A and B with gastric carcinoma. The ratio of PG I/PG II in gastric carcinoma was significantly lower than that of chronic gastritis. As conclusion, from the point of view of the prevalence of H. pylori, it is suggested that H. pylori is not a direct causal agent in the pathogenesis of gastric carcinoma.

Significance of Helicobacter Pylori Infection in Human Peptic Ulcers

Abstract: Experimental studies have suggested that the continuous administration of 0.02% NH, solution, induced by Helicobacter pylori (H, Pylori), leads to a glandular atrophy of the gastric mucosa, and adversely affects healing of acetic acid ulcers in rats, because of the suppression of cell kinetics of the regenerative epithelial cells and connective tissues at ulcer margins. To visualize the distribution of H. pylori in human gastric mucosa, a phenol red dye spraying endoscopy was performed in 45 patients with gastric ulcers, and 43 patients with duodenal ulcers, who were medicated with a full dose of H2‐blocker until ulcer healing, and with half doses thereafter. In the H. pylori negative cases, 8 (88.9%) of 9 gastric ulcers healed within 3 months after medication, with no relapse discernible up to 6 months after healing of the preceding ulcer. The relapse rate was 25% up to 12 months after ulcer healing. In contrast, only 22 (66.1%) of 36 gastric ulcers healed within 3 months after medication in the H. pylori positive cases. The relapse rate was 12.5% up to 3 months, 30.4% UP to 6 months and 63.6% up to 12 months after ulcer healing. In addition, all 6 duodenal ulcers healed within 2 months after medication in the H. pylori negative cases, with no relapse discernible up to 12 months after healing of the preceding ulcer. In contrast, in the H. pylon positive cases, 20 (53.1%) of 37 duodenal ulcers healed within 2 months, and the relapse rate was 14.3%, 33.3%, and 66.7% up to 3, 6 and 12 months respectively after healing of the preceding ulcer. These data suggest that H. pylori is likely to interfer with ulcer healing, and promotes peptic ulcer relapse.

Effect of Oral Bismuth Subsalicylate on Campylobacter pylori and on Healing and Relapse Rate of Peptic Ulcer

A controlled, open clinical trial was performed to compare the effect of oral bismuth subsalicylate (600 mg three times daily) with that of cimetidine (800 mg/d) on Campylobacter pylori, ulcer healing, and rate of ulcer relapse in 49 patients with peptic ulcer. At the first endoscopic examination (to confirm the diagnosis) and at the second (after 4 weeks of treatment), biopsy specimens were taken from the gastric antrum; the presence of C. pylori in culture and the rate of ulcer healing were determined. The rate of ulcer relapse was determined by a 9-month follow-up examination. After cessation of treatment a significant rate of healing was seen in both treatment groups: 73% in the bismuth group and 65% in the cimetidine group. Ulcer healing was confirmed by endoscopic examination. Before therapy the number of C. pylori-positive cases (61%) was identical from the two groups; however, after 4 weeks of treatment, 75% of the previously culture-positive cases in the bismuth group reverted to negative (a statistically significant change), whereas only 40% of those in the cimetidine group reverted (not statistically significant). The rate of clearance of C. pylori was statistically significant for the 29 patients with healed ulcers and correlated strongly with ulcer healing in the bismuth group only. The rate of relapse after 9 months of follow-up was 13% in the group treated with bismuth subsalicylate--a figure significantly lower than the 54% rate of relapse in the group treated with cimetidine.