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Background: Helicobacter pylori (H. pylori) are a causative agent of digestive disease. Although a proton pump inhibitor combined with amoxicillin-clarithromycin is the accepted drug treatment for H. pylori eradication in Japan, there is no consensus treatment for hemodialysis patients., Study: Seventy-seven hemodialysis patients underwent upper digestive tract endoscopy. Biopsy specimens were taken, and histological findings, culture, and rapid urease tests were performed to confirm the presence of H. pylori. H. pylori-positive patients were then administered at random either a seven-day lansoprazole (60 mg a day)-amoxicillin (750 mg a day)-clarithromycin (400 mg a day) (LAC) regimen or a seven-day lansoprazole (60 mg a day)-clarithromycin (400 mg a day) (LC) regimen. The success of H. pylori eradication was determined from histological findings, culture, and rapid urease tests., Results: In 13 of 77 patients (13.6%), ulcers and/or ulcer scars were seen by endoscopy. Thirty-one patients (40.3%) were positive for H. pylori, and 20 patients among them were randomized to one of two regimens: one is seven-day LAC regimen (eleven patients) and the other is seven-day LC regimen (nine patients). Eradication was successful in nine of the eleven patients (72.7%) receiving the LAC regimen, but in only three of the nine patients (33.3%) who underwent the LC regimen. No serious adverse effects were observed with either regimen, and 95% of the patients reported complete compliance., Conclusion: A seven-day low dose LAC regimen is safe and effective and recommended for treatment of H. pylori infection in hemodialysis patients.

Background: Recent studies have reported that proton pump inhibitor (PPI)/amoxicillin (A) metronidazole (M) therapy for Helicobacter pylori infection provides a sufficient cure rate in Japan in patients who have failed first-line treatment with PPI/amoxicillin and clarithromycin (AC). To validate the efficacy of this regimen as second-line therapy, our experience with second-line treatment using a PPI/AM regimen was reviewed., Methods: We analyzed data on 151 patients who had been prescribed a 10-day PPI/AM re-treatment regimen after eradication failure of 1 to 2 weeks' first-line PPI/AC therapy. The PPI/AM regimen was given according to results of susceptibility testing (S+) in 31 patients. The group that had undergone susceptibility testing was further divided into two subgroups according to dosage: standard dose of omeprazole (O)/AM (n = 11) and double dose of lansoprazole (L)/AM (n = 20). The PPI/AM regimen was given without susceptibility testing (S-) to 120 patients. These patients were also divided into two subgroups according to whether they received omeprazole or lansoprazole: OAM (n = 61) and LAM (n = 59). Cure rates and adverse effects in each group were analyzed., Results: The intention-to-treat (ITT)-based cure rate with/without susceptibility testing was 93.5% (95% confidence interval [CI], 79%-99%) and 87.5% (95% CI, 80%-93%), respectively (not significant [NS]). The ITT-based cure rate in S+/S- for OAM and S+/S- for LAM was 90.9% (95% CI, 59%-100%)/82% (95% CI, 70%-91%), and 95% (95% CI, 75%-100%)/93.2% (95% CI, 84%-98%), respectively (NS). Adverse effects were seen in 26.3% and 32.5% of patients in the OAM group and the LAM group, respectively (NS)., Conclusions: The 10-day PPI/AM re-treatment regimen is safe and effective, suggesting its usefulness as second-line treatment in Japan in patients who have failed initial treatment with the PPI/AC regimen.

In the last decade, the dogma that no bacteria could grow in the acid milieu of the stomach has been destroyed by evidence that the infective agent, H. pylori, is responsible for gastric and duodenal disease. Studies on H. pylori infection suggest that some strains of intestinal bacteria may be responsible for intestinal ulceration and inflammation concomitant with inflammatory bowel diseases (IBD), i.e., ulcerative colitis and Crohn's disease. Evidence for pathophysiological roles for certain strains of luminal bacteria result from a number of IBD animal models. Recent studies on innate immunity, including toll-like receptors and NOD isoforms, suggest that bacterial infections may contribute to intestinal inflammation in genetically susceptible hosts. This brief review focuses on the bacterial pathogenesis and the role of innate immunity in the etiology of IBD's.

Background: It remains controversial whether gastric atrophy is reversible after Helicobacter pylori eradication therapy., Aim: To clarify whether gastric atrophy improves after H. pylori eradication therapy using a histologic approach., Methods: Subjects were 87 H. pylori infection-cured patients (treatment group) and 29 continuously H. pylori-infected patients (control group). The subjects in the treatment and control groups were followed for 10-49 months (mean, 22 months) and 11-50 months (mean, 22 months), respectively. Biopsy specimens were obtained from the greater curvature of the antrum and corpus at the beginning and end of the observation period; histologic analyses of these specimens were performed for detection of activity, inflammation, atrophy, and intestinal metaplasia. Results were scored without any clinical information according to the Sydney system., Results: In the treatment group, the histologic score for atrophy was improved in the corpus but not in the antrum. Intestinal metaplasia was not improved in either the antrum or the corpus. There were no significant differences during the follow-up in gastric atrophy and intestinal metaplasia in the control group., Conclusion: Gastric atrophy was improved in the corpus approximately 2 years after H. pylori eradication therapy.

In the guideline, for H. pylori the Japanese Society of Helicobacter published diagnosis and treatment in July 2000. Only peptic ulcers and low grade MALT lymphomas are recommended as an indication of H. pylori eradication and other diseases such as atrophic gastritis, post EMR state for early gastric cancer and post-operated stomach due to gastric cancer, hyperplastic polyps and non-ulcer dyspepsia, were not included. In addition, Japanese social security foundation approves only peptic ulcers for indication of H. pylori eradication treatment. However, eradication therapy for atrophic gastritis should be considered in aspect of decreasing gastric cancer risk. Since accumulated epidemiological, experimental and clinical data strongly support its positive correlation with cancer risk, patients in high risk group for gastric cancer should be included for a target eradication therapy. Indication of the treatment should be expanded to histological gastritis caused by H. pylori in our country, where prevalence of gastric cancer is very high.

Background: Evidence indicates that eradication of Helicobacter pylori leads to the disappearance of hyperplastic polyps in the stomach. However, there are some exceptions. We have compared endoscopic and serologic findings of responder and non-responder cases with hyperplastic polyps to try to identify the cause(s), other than H. pylori infection, of the formation or growth of gastric hyperplastic polyps., Methods: We retrospectively studied 33 patients whose hyperplastic polyps disappeared after eradication of H. pylori and 10 patients whose hyperplastic polyps did not disappear after eradication. The patients were examined both endoscopically and serologically before, 1-3 months after and 12-15 months after the eradication., Results: The responder and non-responder groups were similar with respect to age, sex, coexisting diseases, and histologic findings. The number and maximum size of polyps tended to be larger before treatment in the non-responder group than in the responder group. The serum gastrin level was higher in the non-responder group than in the responder group before, 1-3 months after and 12-15 months after the eradication (p=0.0096, p>0.2, p=0.0014). On histologic examination, similar reductions in the degree of inflammatory cell infiltration in the gastric mucosa of the antrum and body were seen in both the responder and non-responder groups. In the non-responders, the size and numbers of the polyps regressed in 5 of the 10 patients. The score of glandular atrophy in the antrum and the serum gastrin levels in the non-regressed cases was higher than those in the regressed cases at 1-3 and 12-15 months after eradication., Conclusion: Persistent high gastrin levels were found in the non-responder cases with gastric hyperplastic polyps., (Copyright 2003 S. Karger AG, Basel)

Although available H. pylori eradication regimens in Japan fail to cure 10-20% of patients, an optimal re-treatment therapy for eradication-failure patients has still not been established. Since patient compliance, bacterial resistance and genotypic differences in CYP2C19 influence the eradication rate, re-eradication therapy should be selected, taking them into consideration. In the West, meta-analysis of the second-line treatment of H. pylori infection showed therapies comprising ranitidine bismuth and two antimicrobials are very effective re-treatment therapies irrespective of factors influencing H. pylori eradication. However ranitidine bismuth is not available in Japan and re-eradication therapy consisting of PPI, amoxicillin and metronidazole have been often undertaken and have achieved high eradication rate, even including patients with metronidazole resistant H. pylori.

Background: Development of reflux esophagitis is one of the adverse effects that cause concern in relation to curative treatment of Helicobacter pylori infection. However, recent studies present a rather negative association between curative treatment and development of reflux esophagitis or reflux symptoms. Therefore, this issue has remained controversial. Accordingly, we investigated the long-term adverse effects of H. pylori eradication treatment in special reference to development of reflux symptoms., Patients and Methods: We conducted a case controlled study by mailing structured questionnaires on past (before curative treatment or 3 years previously) and current status. A case was an endoscopically confirmed peptic ulcer patient with confirmed cure of the infection after eradication treatment 3 years previously and a control was one who had not undergone the eradication treatment during the same period. We studied 241 pairs who matched for age, gender, and type of ulcer disease (GU, DU or GDU). Of these pairs, 81.3% were male and the mean age was 52.6 +/- 9.6 year (range 23-76)., Results: The rates of patients with improved reflux symptoms in the case and control groups were 65.4% and 30.4%, respectively, with the rate being significantly greater in the case group. On the contrary, the rates of those with worsened reflux symptoms were similar (5.1% and 7.6%). Regarding general events, the rate of patients with decreased frequency of hospital visits and of those who regularly used antiacid medications were significantly decreased in the case group. Furthermore, the case group experienced significantly fewer hospital admissions for various diseases in this 3-year period. However, a significantly greater number of case group patients than control subjects gained weight., Conclusion: Reflux symptoms as well as general well-being were significantly improved after cure of H. pylori infection.

The actual distribution of Helicobacter pylori infection and its related diseases in various Asian countries is controversial. Only limited information is available regarding this issue. We discuss the etiological role of H. pylori in gastric cancer through the Asian experience. Seroprevalence of H. pylori infection in asymptomatic subjects and the annual incidence rate of gastric cancer per 100,000 in various Asian countries are summarized from literature reviews and World Health Organization statistics, respectively. There is a large intercountry variation in incidence of gastric cancer and H. pylori seroprevalence among Asian countries. There is a strong link between H. pylori infection and gastric cancer in many countries, such as Japan. By contrast, the prevalence of H. pylori infection is high in some countries, including India and Bangladesh, but low gastric cancer rates have been reported. These disparate observations represent the Asian enigma. Factors that may influence the etiology of gastric cancer include the genetic diversity of the infecting H. pylori strains and differences in the host genetic background in various ethnic groups, including gastric acid secretion and genetic polymorphisms in proinflammatory cytokines. These factors, in addition to environmental factors, such as personal hygiene and dietary habits, reflect the multifactorial etiology of gastric cancer.