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Background: There are still insufficient data on the frequency of seroconversion and seroreversion of Helicobacter pylori antibodies. The frequency of serochange and related factors were investigated in this study over 9 years., Subjects and Methods: Using sera from 3104 workers who underwent health checks in 1989 and again in 1998, H. pylori antibodies were measured. Those with intermediate serology were excluded from the study. Information on past history was collected using a questionnaire., Results: Of the 912 seronegative and 1286 seropositive subjects in 1989, seroconversion was observed in 57 and seroreversion in 91 subjects. Seroconversion and seroreversion rates over the 9-year period were 6.3% and 7.1%, respectively, giving rates per 1000 person-years (with 95% confidence interval) of 7.0 (5.2-8.7) and 7.9 (6.3-9.4), respectively. Subjects that reported abdominal symptoms or gastric fiberscope use showed significantly higher seroconversion rates than controls (8.7 vs. 4.5 and 9.2 vs. 1.6, respectively), which remained significant after adjustment for age and gender. Those with a history of duodenal ulcers, a smoking habit or a drinking habit showed significantly lower seroreversion rates than controls (3.5 vs. 8.9, 5.4 vs. 9.2 and 5.9 vs. 13.3, respectively). After adjustment, the association between seroreversion and smoking habit disappeared, while the associations with history of duodenal ulcers and drinking habit remained., Conclusions: Those with a history of nonspecific abdominal symptoms and those with a history of gastric fiberscope use showed higher seroconversion rates. Alcohol consumption and duodenal ulcers may inhibit the autoeradication of H. pylori, possibly through increased acid secretion.

Background: Although age-adjusted mortality from gastric cancer has been decreasing in Japan, the crude incidence of gastric cancer shows a slight increase., Methods: We have observed trends in the incidence of gastric cancer by sex and 20-year age groups over the past two decades (1976-1996). Source data were obtained from the cancer statistics materials provided by the Research Group for Population-Based Cancer Registration in Japan. Simultaneously, we observed changes in the prevalence of Helicobacter pylori infection and in serological atrophy of the gastric mucosa, and compared the results with those involving changes in the incidence of gastric cancer., Results: A slight decline was observed in all age groups over 40 years old, in both men and women, between 1986 and 1996. However, a marked decline in incidence was observed for those aged 20-39 years. The prevalence of H. pylori infection declined in both sexes between 1989 and 1998. The frequency of serological atrophy of the gastric mucosa significantly declined in all age groups between 1989 and 1996, with young age groups experiencing a more marked decrease., Conclusion: The marked decline in gastric cancer incidence observed in the young population will also begin to occur in the elderly population in the future.

Background and Aims: Body gastritis caused by Helicobacter pylori infection appears to inhibit gastric acid secretion. The aim of this study was to determine the effects of H pylori infection on gastric acid secretion and clarify its mechanisms with reference to interleukin 1beta (IL-1beta)., Methods: (1) Mongolian gerbils were inoculated orally with H pylori. Before, six, and 12 weeks after inoculation, serum gastrin levels, gastric acid output, and IL-1beta mRNA levels in the gastric mucosa were determined. Pathological changes were also determined according to the updated Sydney system. (2) Effects of recombinant human IL-1 receptor antagonist (rhIL-1ra) on gastric acid output and serum gastrin levels were also determined., Results: (1) Scores for activity and inflammation of gastritis and serum gastrin levels were significantly increased, and gastric acid output was significantly decreased six and 12 weeks after inoculation with H pylori. IL-1beta mRNA levels in the gastric mucosa were also elevated six and 12 weeks after inoculation with H pylori. (2) Acid output and serum gastrin levels in the infected groups returned to control levels after rhIL-1ra injection., Conclusions: Gastric acid secretion is decreased and serum gastrin levels are increased in Mongolian gerbils infected with H pylori. This change in gastric acid secretion appears to be mediated by IL-1beta induced by H pylori infection.

Background: Proton pump inhibitors such as omeprazole and lansoprazole are mainly metabolized by CYP2C19 in the liver. The therapeutic effects of proton pump inhibitors are assumed to depend on CYP2C19 genotype status., Objective: We investigated whether CYP2C19 genotype status was related to eradication rates of H pylori by triple proton pump inhibitor-clarithromycin-amoxicillin (INN, amoxicilline) therapy and attempted to establish a strategy for treatment after failure to eradicate H pylori., Methods: A total of 261 patients infected with H pylori completed initial treatment with 20 mg of omeprazole or 30 mg of lansoprazole twice a day, 200 mg of clarithromycin three times a day, and 500 mg of amoxicillin three times a day for 1 week. CYP2C19 genotypes of patients were determined with polymerase chain reaction-restriction fragment length polymorphism analysis. Patients without eradication after initial treatment were retreated with 30 mg of lansoprazole four times daily and 500 mg of amoxicillin four times daily for 2 weeks., Results: Eradication rates for H pylori were 72.7% (95% confidence interval, 64.4%-81.8%), 92.1% (confidence interval, 86.4%-97.3%), and 97.8% (confidence interval, 88.5%-99.9%) in the homozygous extensive, heterozygous extensive, and poor metabolizer groups, respectively. Thirty-four of 35 patients without eradication had an extensive metabolizer genotype of CYP2C19. Nineteen of those patients were infected with clarithromycin-resistant strains of H pylori. However, there were no amoxicillin-resistant strains of H pylori. Re-treatment of H pylori infection with dual high-dose lansoprazole-amoxicillin therapy succeeded in 30 of 31 patients with extensive metabolizer genotype of CYP2C19., Conclusion: The majority of patients without initial eradication of H pylori had an extensive metabolizer CYP2C19 genotype but were successfully re-treated with high doses of lansoprazole and an antibiotic to which H pylori was sensitive, such as amoxicillin, even when the patients were infected with clarithromycin-resistant strains of H pylori.

Background: Helicobacter pylori is a major cause of various gastroduodenal diseases. Some risk factors related to H. pylori infection have been reported; however, studies on the relationship between H. pylori infection and smoking or drinking habits have given conflicting results. In the present study, these relationships were investigated by collecting sera and information from 8837 subjects., Methods: Serum H. pylori immunoglobulin G antibody was measured by an enzyme-linked immunoassay. In addition to sex and age, information on smoking and drinking habits was collected by questionnaire. Age- and sex-adjusted odds ratios (95% confidence interval) of smoking and alcohol consumption were calculated for H. pylori seropositivity using logistic regression models., Results: Current smokers had a 0.82 (0.74-0.91)-fold greater risk of H. pylori seropositivity than those who had never smoked. Current cigarette consumption showed a dose-dependently negative association with H. pylori seropositivity, and the association between smoking and H. pylori infection was strong in younger subjects. Current drinkers had a 0.88 (0.79-0.98)-fold greater risk of H. pylori seropositivity than those who had never drunk alcohol. The volume of alcohol consumed showed a negative association with H. pylori seropositivity., Conclusions: In the current study, smoking was negatively associated with H. pylori infection. The risk of H. pylori seropositivity decreased linearly with cigarette consumption per day. Increased gastric acidity in the stomach through smoking may be a cause of the dose-dependently negative association between H. pylori and smoking. Drinking was negatively and dose-dependently associated with H. pylori positivity, although the effect of drinking was weaker than that of smoking.

Background: How Helicobacter pylori infection affects gastric acid secretion has not been made clear. This study aimed to elucidate the effects of H. pylori infection on H+/K+-adenosine triphosphatase (ATPase) mRNA in gastric fundic gland mucosa., Methods: Twenty patients with chronic gastritis and H. pylori infection were treated with lansoprazole and antibiotics. Before and 1 month after treatment gastroduodenoscopy was performed, and changes in the amount of H+/K+-ATPase mRNA in the fundic gland mucosa, gastric juice pH, and serum gastrin levels were determined., Results: The amount of H+/ K+-ATPase mRNA in the fundic gland mucosa was increased in patients with eradication of H. pylori, in whom significant decreases in gastric juice pH and serum gastrin levels were observed. No significant changes were observed in patients without eradication of H. pylori., Conclusions: These results suggest that one of the mechanisms by which H. pylori infection suppresses acid secretion is by the inhibition of proton pump synthesis in parietal cells.

Background: The aim of this study was to determine whether the amount of Helicobacter pylori and the extent of gastric metaplasia in the duodenal mucosa play critical roles in the pathogenesis of duodenal ulcer., Methods: Duodenal and gastric biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer, gastric ulcer or chronic gastritis. The extent of gastric metaplasia was evaluated histologically and endoscopically using the methylene blue test. In this study, we performed competitive polymerase chain reaction, a highly sensitive and quantitative method for determining the amount of H. pylori gastric and duodenal mucosa. The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in the three patient groups were compared. The correlation between the amount of H. pylori in the duodenum and gastric antrum and extent of gastric metaplasia were also determined., Results: The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in patients with duodenal ulcer were much higher than in patients with gastric ulcer or chronic gastritis. A positive correlation was found between the amount of H. pylori in the duodenum and the extent of gastric bulb and that in the antrum., Conclusions: The findings of this study indicate that H. pylori colonization in the duodenal bulb may play a critically important role in the pathogenesis of duodenal ulcer and that the amount of H. pylori in the duodenal bulb may be related to the amount of H. pylori in the gastric antrum and the extent of gastric metaplasia in the duodenal bulb.

The effects of Helicobacter pylori infection on gastric acid secretion has not been clarified. The aim of this study was to elucidate the effects of H. pylori infection on gastric juice pH in relation to gene expression of interleukin-1beta (IL-1beta), which is reported to inhibit gastric acid secretion. Gastric juice pH and serum gastrin levels were measured in patients with peptic ulcer disease. The amount of IL-1beta mRNA in gastric fundic gland mucosa was also measured by a competitive reverse transcription-polymerase chain reaction method. These parameters were determined before and after treatment with lansoprazole and amoxicillin. Before treatment a significant positive relation was observed between the amount of IL-1beta mRNA in gastric fundic gland mucosa and gastric juice pH. After treatment significant decreases in the amount of IL-1beta mRNA, gastric juice pH, and serum gastrin levels were observed in patients with eradication of H. pylori, whereas no significant changes were observed in patients without eradication. These results suggest that H. pylori infection induces IL-1beta and suppresses acid secretion, resulting in increases in gastric juice pH and serum gastrin levels. Eradication of H. pylori decreases IL-1beta induction, resulting in an increase in gastric juice acidity and normalization of serum gastrin levels.

Background: Omeprazole is metabolized by S-mephenytoin 4'-hydroxylase (CYP2C19) in the liver. In persons with a poor-metabolizer genotype for CYP2C19, the therapeutic efficacy of omeprazole may be increased., Objective: To investigate whether CYP2C19 genotype status is associated with cure rates for Helicobacterpylori infection and peptic ulcer achieved by using dual therapy with omeprazole and amoxicillin., Design: Prospective cohort study., Setting: University hospital and health service center in Hamamatsu, Japan., Patients: 62 patients with peptic ulcer and H. pylori infection., Intervention: Omeprazole and amoxicillin., Measurements: CYP2C19 genotype status and cure rates for H. pylori infection and peptic ulcer., Results: Cure rates for H. pylori infection were 28.6% (95% CI, 13.1% to 48.7%), 60% (CI, 38.6% to 83.0%), and 100% (CI, 66.4% to 100%) in the rapid-, intermediate-, and poor-metabolizer groups, respectively. Healing rates for both duodenal and gastric ulcer in the three groups were roughly parallel with cure rates for H. pylori infection., Conclusion: The results of the genotyping test for CYP2C19 seem to predict cure of H. pylori infection and peptic ulcer in patients who receive dual therapy with omeprazole and amoxicillin.

Helicobacter pylori is present in infected patients not only on the gastric epithelial cell surface but also in gastric mucus. We developed a competitive polymerase chain reaction (cPCR) method for quantitative measurement of H. pylori in gastric mucus. The aim of this study was to determine the number of H. pylori in gastric mucus before and after anti-H. pylori treatment. Patients with duodenal ulcer were treated with lansoprazole alone (n = 11) or lansoprazole and amoxycillin (n = 12). The amount of H. pylori in gastric mucus was measured over time by a cPCR assay. Helicobacter pylori infection was also tested for using histology, culture, and the rapid urease test (RUT). Although most patients treated with lansoprazole alone had become H. pylori-negative by the end of treatment when tested by histology, RUT, and culture, a large number of H. pylori organisms were found in the gastric mucus at that time by cPCR. These patients returned to being H. pylori positive 1 to 12 months later on the basis of histology, RUT, and culture. However, cPCR results indicated eradication of H. pylori by the end of treatment in eight of the 12 patients treated with lansoprazole and amoxicillin, and these patients remained H. pylori negative on histology, RUT, culture, and cPCR 1 to 12 months later. Testing for H. pylori in gastric mucus is thus useful for precise determination of the success or failure of H. pylori eradication therapy.

Background: How Helicobacter pylori infection affects gastric acid secretion is still unclear., Methods: Gastric juice pH, ammonia concentration in gastric juice, serum gastrin level, and grade of gastritis in accordance with the Sydney System were determined for patients with gastric ulcer (GU) and duodenal ulcer (DU) before and after treatment with lansoprazole and amoxicillin, and results were compared with those of H. pylori-negative controls., Results: Scores for H. pylori density, atrophy, metaplasia, and activity of gastritis in the corpus were higher in patients with GU, especially those with proximally located GU, than in those with DU. Gastric juice pH was significantly higher in GU patients than in DU patients and controls. After H. pylori eradication, gastric juice pH and serum gastrin levels in both GU and DU patients were significantly decreased to control levels. In patients without eradication, no significant changes in these factors were observed., Conclusions: These findings suggest that H. pylori infection and gastritis in the corpus suppress acid secretion and increase gastric juice pH, resulting in hypergastrinemia, and that eradication of H. pylori normalizes acid secretion and serum gastrin levels.

The seroprevalence of Helicobacter pylori in a group of 1,043 healthy Japanese people was compared with that of hepatitis A virus (HAV), which was used as a marker of fecal-oral exposure. No statistically significant relationship was observed between seropositivity for HAV and that for H. pylori. Therefore, the fecal-oral spread of H. pylori is of limited relevance in Japan.

Objective: Eradication of Helicobacter pylori has been gaining significance for the treatment of gastroduodenal diseases. Establishment of a precise diagnostic method for H. pylori is of great value. The aim of this study was to establish a new method for precisely judging the eradication of this bacteria., Methods: We measured serum pepsinogen I (PG I) and pepsinogen II (PG II) levels in 105 cases of peptic ulcer with H. pylori infection before and after anti-H. pylori treatment, determined percentage changes in serum PG I:PG II ratios before and 1 month after the treatment, and established cut-off values for them to distinguish success from failure of H. pylori eradication. Cut-off values for percentage changes in serum PG I:PG II ratios were tentatively set as +40%, +25%, and +10% when the serum PG I:PG II ratios before treatment were less than 3.0, not less than 3.0 but less than 5.0, and not less than 5.0, respectively., Results: With these cut-off values, the sensitivity, specificity, and validity for determination of eradication of H. pylori-on the basis of culture, histology, the rapid urease test, and a polymerase chain reaction method-were 100.0%, 93.1%, and 96.2%, respectively. These cut-off values could be applied to both gastric ulcer and duodenal ulcer., Conclusion: Our findings suggest that percentage changes in serum PG I:PG II ratios are useful as indices for distinguishing success from failure in eradication therapy for H. pylori.