Jiro Kagawa

Efficacy of triple therapy comprising rabeprazole, amoxicillin and metronidazole for second‐line Helicobacter pylori eradication in Japan, and the influence of metronidazole resistance

Background : The widespread use of eradication therapy for Helicobacter pylori in Japan has led to an increase in antibiotic‐resistant strains and the problem of re‐treatment in cases of eradication failure.

Eradication rates of clarithromycin-resistant Helicobacter pylori using either rabeprazole or lansoprazole plus amoxicillin and clarithromycin

Background : The resistance of Helicobacter pylori to clarithromycin has become one of the primary reasons for eradication failure.

Is the Recurrence of Helicobacter pylori Infection After Eradication Therapy Resultant from Recrudescence or Reinfection, in Japan

Background. Reinfection of Helicobacter pylori after eradication is rare in developed countries but most often occurs within 1 year. In the present study, we attempted to differentiate between reinfection and recrudescence of H. pylori strains between 6 months and 6 years after successful eradication in Japan, a country with a high prevalence of H. pylori infection.

Influence of anti-ulcer drugs used in Japan on the result of (13)C-urea breath test for the diagnosis of Helicobacter pylori infection.

BackgroundThe 13C-urea breath test (UBT) is a simple test for the diagnosis of Helicobacter pylori infection, but several factors have been reported to affect the results of this test. In this study, the effects of the anti-ulcer drugs used in Japan on the results of the UBT were determined.MethodsThe subjects of the study were 64 adult volunteers who tested positive for H. pylori infection by the serum antibody method. Eight classes of anti-ulcer drugs used in Japan were administered at their usual doses to these subjects: lansoprazole, a proton pump inhibitor (PPI); nizatidine, an H2-receptor antagonist (H2RA); and polaprezinc, ecabet sodium, rebamipide, teprenone, cetraxate hydrochloride, and sucralfate, all mucoprotective agents. The study drugs were randomized for administration to the subjects, and each of the drugs was administered for 14 consecutive days. The UBT was performed on days 0, 14, and 21.ResultsThe mean Δ13C‰ in the lansoprazole group was significantly decreased on day 14, to below 10‰, in 4 of 16 subjects, and in 1 of the 4 subjects, the test result was negative, with the Δ13C‰ falling to 1.7‰. The value returned to baseline 1 week after the discontinuation of lansoprazole. The other drugs administered had no significant effect on the result of the UBT, except that the mean Δ13C‰ showed a tendency to decrease after the administration of ecabet sodium and rebamipide.ConclusionsAdministration of a PPI may produce a false-negative UBT result, while other anti-ulcer drugs, for the most part, have little effect on the result of the UBT when used alone.

Enterocromaffin-Like Cell Tumor Induced by Helicobacter pylori Infection in Mongolian Gerbils

Background. Gastric carcinoids are strongly associated with chronic atrophic gastritis A, and it is suggested that hypergastrinemia plays a critical role in development of gastric carcinoids. Since Helicobacter pylori infection causes hypergastrinemia, it is held that H. pylori infection produces gastric carcinoids. We followed the histological changes of H. pylori‐infected stomachs of Mongolian gerbils for a long time.

ANALYSIS OF P53 MUTATIONS AND HELICOBACTER PYLORI INFECTION IN HUMAN AND ANIMAL MODELS

Background. p53 gene mutations are believed to play a critical role in the development of gastric carcinoma. We examined the relation betweenHelicobacter pylori infection andp53 gene mutations of the gastric mucosa in human and animal models.Methods. To detect the originalp53 DNA sequences of the Japanese monkey and Mongolian gerbil, thep53 genes of these animals were amplified using the nested polymerase chain reaction method with primers for the humanp53 gene. Direct DNA sequencing of exons 5, 6, 7, and 8 of thep53 genes was performed by the dyedeoxy terminator method for gastric mucosa of humans, the Japanese monkey, and the Mongolian gerbil. The expression ofp53 was examined immunohistochemically in a Japanese monkey model.Results. Mutations of thep53 gene were identified in 52.4% of humanH. pylori-positive mucosa and in 100% of monkeyH. pylori-positive mucosa. However, no mutations of thep53 gene were found in theH. pylori-positive gastric mucosa of Mongolian gerbils. There were no mutations inH. pylori-negative gastritis mucosa of humans, monkeys, or Mongolian gerbils. Nuclear staining of p53 was seen in the glandular cells of theH. pylori-infected mucosa of Japanese monkeys, especially in the neck region of the glands.Conclusions. These findings demonstrate that theH. pylori infection can inducep53 point mutations in humans and the Japanese monkey and appear to be involved in the pathway leading to dysplasia or carcinoma. However, our direct DNA sequencing method showed nop53 mutations in the Mongolian gerbil model at present. Further studies with this model are needed.

Analysis of p53 mutations and Helicobacter pylori infection in human and animal models

BACKGROUND p53 gene mutations are believed to play a critical role in the development of gastric carcinoma. We examined the relation between Helicobacter pylori infection and p53 gene mutations of the gastric mucosa in human and animal models. METHODS To detect the original p53 DNA sequences of the Japanese monkey and Mongolian gerbil, the p53 genes of these animals were amplified using the nested polymerase chain reaction method with primers for the human p53 gene. Direct DNA sequencing of exons 5, 6, 7, and 8 of the p53 genes was performed by the dideoxy terminator method for gastric mucosa of humans, the Japanese monkey, and the Mongolian gerbil. The expression of p53 was examined immunohistochemically in a Japanese monkey model. RESULTS Mutations of the p53 gene were identified in 52.4% of human H. pylori-positive mucosa and in 100% of monkey H. pylori-positive mucosa. However, no mutations of the p53 gene were found in the H. pylori-positive gastric mucosa of Mongolian gerbils. There were no mutations in H. pylori-negative gastritis mucosa of humans, monkeys, or Mongolian gerbils. Nuclear staining of p53 was seen in the glandular cells of the H. pylori-infected mucosa of Japanese monkeys, especially in the neck region of the glands. CONCLUSIONS These findings demonstrate that the H. pylori infection can induce p53 point mutations in humans and the Japanese monkey and appear to be involved in the pathway leading to dysplasia or carcinoma. However, our direct DNA sequencing method showed no p53 mutations in the Mongolian gerbil model at present. Further studies with this model are needed.