Sensitivity of biopsy site in evaluating regression of gastric atrophy after Helicobacter pylori eradication treatment.

BACKGROUND: Helicobacter pylori infection is a major cause of the progress of gastric glandular atrophy, a high-risk background factor in the development of gastric cancer. Regression of gastric atrophy is critical to prevention of cancer by H. pylori eradication treatment. However, it is controversial whether gastric atrophy regresses after H. pylori eradication. AIM: To determine the most sensitive and appropriate biopsy site for evaluation of regression of atrophy after treatment. SUBJECTS AND METHODS: Thirty-eight patients who showed regression of gastric atrophy in histology after treatment were investigated. Four biopsy specimens from the lesser and greater curvatures in the antrum and corpus were evaluated before and after treatment according to the Updated Sydney System. RESULTS: Regression of atrophy after treatment was seen in 30 of 38 biopsy specimens from the lesser curvature of the corpus (79%), and this site was most sensitive. Odds ratio of this site to the others was 8.28. Regression of atrophy in this site was observed at 12.2 months in the younger patients and 15.9 months in the elder patients. CONCLUSION: Biopsy sampling from the lesser curvature of the corpus is the most sensitive and appropriate for evaluation of regression of gastric atrophy after H. pylori eradication treatment.

Ten-year prospective follow-up study on the relationship between Helicobacter pylori infection and progression of atrophic gastritis, particularly assessed by endoscopic findings.

AIM: To ascertain the progression of atrophic gastritis due to Helicobacter pylori infection, we conducted a 10-year prospective follow-up study with annual endoscopy of the stomach. METHODS: Prospective endoscopic observation was started in 53 subjects in 1989 and 1990 after informed consent was obtained. The progression of atrophic gastritis was evaluated mainly by the endoscopic pattern of atrophy. Histological assessment was performed on biopsy specimens taken from the lesser curvature of the lower corpus. By 2000, 43 patients (20 males, 23 females, mean age 56.7 years at entry) had completed at least 10 years of endoscopic follow-up. RESULTS: Eight H. pylori-negative patients with normal fundic mucosa showed no change endoscopically or histologically. In 35 H. pylori-positive patients, the progression of histological atrophy was observed in 46% and intestinal metaplasia was observed in 49%. Fifteen of 35 H. pylori-positive cases exhibited a cephaloid shift of the endoscopic atrophic border. The cephaloid shift of the atrophic area occured suddenly. The cumulative progression rate of atrophic patterns was 6% after 2 years, 22% after 4 years, 34% after 6 years and 43% after 10 years. These atrophic changes were related to neutrophil infiltration. CONCLUSION: The progression of atrophic gastritis is a result of chronic active gastritis caused by H. pylori infection.

[Intestinal metaplasia and Helicobacter pylori infection, their relationship and effects of eradication therapy].

Intestinal metaplasia is characterized by Goblet cells and Peneth cells in histological examination. It is frequently observed in gastric mucosa with atrophic gastritis and easily diagnosed using Methylene blue stain in endoscopy. Intestinal metaplasia is seemed to occur during the progression of atrophic gastritis. From our prospective endoscopic follow-up study over 8 years, progression of intestinal metaplasia in gastric body is observed in 44.4% out of 27 H. pylori positive patients. Progression of atrophy is also observed in 37.0% of cases. Development of intestinal metaplasia is also assured in other clinical investigations and experimental studies using Mongolian Gerbils. However, reversibility of intestinal metaplasia after H. pylori eradication is under discussion still now. In our study, we can not observe the regression of intestinal metaplasia even 2 years after successful H. pylori eradication.

Preliminary study on a novel quadruple eradication therapy with a mucoprotective drug, sofalcone, for Helicobacter pylori infection.

To assess the effects of the mucoprotective drug sofalcone, which has direct and indirect effects on Helicobacter pylori in vitro, the eradication rate, adverse effects, and the quality of healing peptic ulcers were evaluated. Each study patient was given 500 mg t.i.d. amoxicillin and 200 mg t.i.d. clarithromycin. In addition, three different treatment regimens were compared: a standard dose (20 mg q.d.) of the proton pump inhibitor omeprazole (OAC), a double dose (20 mg b.i.d.) of omeprazole (Ox2AC), and a standard dose of omeprazole and a standard dose (100 mg t.i.d.) of sofalcone (OACS). Thirty-one H. pylori-positive patients were treated with OAC, 37 with Ox2AC, and 41 with OACS therapy. With an intention-to-treat analysis, the eradication rates were 74.2% for OAC, 86.2% for Ox2AC, and 85.0% for OACS therapy. The incidence of side effects was 9.6% for patients given OAC therapy, 86.5% for Ox2AC, and only 7.5% for OACS-treated patients, which was significantly lower than the incidence in the Ox2AC group. High-quality peptic ulcer scars were observed after eradication therapy which included solfacone. Although it is necessary to conduct a randomized double-blind study to obtain definitive conclusions, our results indicate that this novel quadruple eradication therapy with solfacone is an efficacious regimen with a high eradication rate and positive effects on ulcer healing, combined with a low incidence of adverse events.

Isolation of four novel tachykinins from frog (Rana catesbeiana) brain and intestine.

In a survey for unknown bioactive peptides in frog (Rana catesbeiana) brain and intestine, we isolated four novel peptides that exhibit potent stimulant effects on smooth muscle preparation of guinea pig ileum. By microsequencing and synthesis, these peptides were identified as Lys- Pro- Ser- Pro- Asp- Arg- Phe- Tyr- Gly- Leu- Met- NH2 (ranatachykinin A), Tyr- Lys- Ser- Asp- Ser- Phe- Tyr- Gly- Leu- Met- NH2 (ranatachykinin B), His- Asn- Pro- Ala- Ser- Phe- Ile- Gly- Leu- Met- NH2 (ranatachykinin C) and Lys- Pro- Ans- Pro- Glu- Arg- Phe- Tyr- Ala- Pro- Met- NH2 (ranatachykinin D). Ranatachykinin (RTK) A, B and C conserve the C- terminal sequence, Phe- X- Gly- Leu- Met- NH2, which is common to known members of the tachykinin family. On the other hand, RTK-D has a striking feature in its C-terminal sequence, Phe- Tyr- Ala- Pro- Met- NH2, which has never been found in other known tachykinins, and may constitute a new subclass in the tachykinin family.

Isolation and sequence determination of frog C-type natriuretic peptide.

A new bioactive peptide was isolated from frog brain using a bioassay for chick rectum relaxant activity. Amino acid sequence of this peptide was determined to be Gly-Tyr-Ser-Arg-Gly-Cys-Phe-Gly-Val-Lys-Leu-Asp-Arg-Ile-Gly-Ala-Phe-Ser- Gly- Leu-Gly-Cys, in which two cysteines were linked by a disulfide bond. The peptide was found to belong structurally to the natriuretic peptide family and to exert diuretic-natriuretic activity as well as hypotensive activity when injected into rats. The peptide showed a high homology to recently identified porcine C-type natriuretic peptide (CNP) and a pharmacological spectrum highly similar to porcine CNP. Thus, the peptide was designated frog C-type natriuretic peptide (frog CNP). Frog CNP may participate in the central control of body fluid homeostasis, since its tissue concentration is high in brain.