K. Nishikawa

Non-Helicobacter pylori and non-NSAID peptic ulcer disease in the Japanese population.

Background Helicobacter pylori and non‐steroidal antiinflammatory drugs (NSAIDs) are recognized as the major causes of peptic ulcer disease. The status of H. pylori infection in the background population may influence the incidence of H. pylori‐negative peptic ulcer disease. Objective To examine the incidence of H. pylori‐negative peptic ulcer disease without intake of NSAIDs in Japan. Patients A total of 398 patients who had no eradication therapy for H. pylori prior to this study, including 246 patients with gastric ulcer (GU) and 152 patients with duodenal ulcer (DU), were enrolled. Methods H. pylori status was assessed by rapid urease tests, histological examinations (haematoxylin & eosin stain, Giemsa stain and/or immunostaining) and serum IgG antibody. Two biopsy specimens were taken from the antrum within 3 cm of the pyloric and two from the middle corpus of the stomach, along the greater curvature. Patients were asked a series of questions regarding risk factors, including the use of NSAIDs. The presence of gastritis, gastric atrophy and intestinal metaplasia was examined according to the updated Sydney system. Results Of the 246 patients with GU, 12 patients (4.9%) were considered to be H. pylori‐negative. Of the 152 patients with DU, two patients (1.3%) were considered to be H. pylori‐negative. Hence, a total of 14 patients were found to be H. pylori‐negative. Nine of them were taking NSAIDs. Consequently, the frequency of H. pylori‐negative ulcer without intake of NSAIDs was 1.3%. There was no significant difference in the frequencies of H. pylori‐negative patients between the GU and DU groups. Conclusion The incidence of H. pylori‐negative peptic ulcer disease without intake of NSAIDs was very low in the Japanese population. Eur J Gastroenterol Hepatol 12:635‐640

Atrophic changes of gastric mucosa are caused by Helicobacter pylori infection rather than aging: studies in asymptomatic Japanese adults.

Background.The current study was designed to evaluate the effect of aging and Helicobacter pylori infection on the gastric mucosa in asymptomatic Japanese adults.

Efficacy of triple therapy with rabeprazole for Helicobacter pylori infection and CYP2C19 genetic polymorphism

Rabeprazole is a new, potent, proton pump inhibitor. The metabolism of rabeprazole is less dependent on CYP2C19 genetic polymorphism.

A prospective evaluation of new rapid urease tests before and after eradication treatment of Helicobacter pylori, in comparison with histology, culture and 13C-urea breath test.

BACKGROUND The rapid urease test is a simple and cost-effective method to detect Helicobacter pylori in biopsy specimens. The aim of this study was to evaluate the accuracy of two new rapid urease tests, Helicocheck and PyloriTek, before and after eradication. METHODS A total of 278 patients, including 115 patients who had not undergone eradication of H pylori and 163 patients after eradication treatment, were enrolled. Eight biopsy specimens were taken from both the antrum and the body of the stomach for histology, culture, and two rapid urease tests. Assessment of H pylori infection was determined by the combination of histology, culture, and (13)C-urea breath test. RESULTS Overall sensitivity, specificity, and positive and negative predictive values of the Helicocheck before eradication were 91.0%, 100%, 100%, and 62.5%; PyloriTek, 92.0%, 100%, 100%, and 65.2%. Those of Helicocheck after eradication were, respectively, 60. 5%, 99.2%, 95.8%, and 89.2%; PyloriTek, 60.5%, 99.2%, 95.8%, and 89. 2%. For the Helicocheck, determination of the infection status of H pylori by biopsies from the gastric body had a significantly higher sensitivity than antral biopsies. After eradication, the combination of 1 antral biopsy and 1 biopsy from the body was not effective enough to improve the overall sensitivity. CONCLUSIONS Helicocheck and PyloriTek have equally satisfactory overall sensitivity before eradication treatment. However, the sensitivity of these rapid urease tests was lower after eradication than before eradication.

High-dose ecabet sodium improves the eradication rate of Helicobacter pylori in dual therapy with lansoprazole and amoxicillin

The additive effect of ecabet sodium in combination with dual therapy on Helicobacter pylori eradication was evaluated.

Attributable Risk of H. pylori in Peptic Ulcer Disease

Recent reports in the United States have found that fewer peptic ulcers are due to Helicobacter pylori than previously believed. The aim of this study is to determine if the declining prevalence of H. pylori infection in the general population can account for the apparent increase in the frequency of non-H. pylori ulcers. A total of 396 patients with peptic ulcer or ulcer scar were enrolled in this study. The pre-1950 population consisted of 149 patients with gastric ulcers and with 44 duodenal ulcers. The post-1950 population consisted of 96 patients with gastric ulcers and 107 with duodenal ulcers. The frequency of H. pylori-negative gastric ulcers was 5.4% in patients born before 1950 and 4.2% in patients born after 1950, and the frequency of H. pylori-negative duodenal ulcers was 0% and 1.9%, respectively. There are no statistical differences between the two populations in gastric and duodenal ulcers. H. pylori seropositivity was 74.9% in asymptomatic volunteers born before 1950 and 20.7% in those born after 1950 (P < 0.01) in the general population. The attributable risk of H. pylori infection in peptic ulcer diseases was not affected by the prevalence of H. pylori infection in the general population in Japan. This suggests that the apparent increase in frequency of non-H. pylori ulcers in the United States is not simply due to the declining prevalence of infection. Other explanations for non-H. pylori ulcers should be sought.

Effects of lansoprazole plus amoxycillin on the cure of Helicobacter pylori infection in Japanese peptic ulcer patients

Aim: The effect of lansoprazole plus amoxycillin on curing Helicobacter pylori infection and peptic ulcer recurrence was evaluated.

Immunological Helicobacter pylori urease analyzer based on ion-sensitive field effect transistor

Abstract Immunological Helicobacter pylori ( H. pylori ) urease analyzer (HPUA), based on a solid-phase tip coated with a monoclonal antibody toward H. pyloris urease and ion-sensitive field effect transistor (ISFET), was developed. In this system, H. pylori urease adsorbed on the solid-phase tip, after a 15-min immunological reaction with gastric mucus sample solution, was measured with a urease analyzer composed of a flow-through cell for urea solution equipped with the measuring and reference ISFETs. The pH change (ΔpH) of urea solution after 55 s of the enzymatic reaction inside the tip was measured by withdrawing about 1 μl of the urea solution toward the upstream of the tip, where the measuring ISFET is installed. It was confirmed that the present system could detect 0.2 mIU/ml of H. pylori urease. Clinical evaluations of the system were performed for 119 patients using urea breath test (UBT) as a gold standard, resulting in the sensitivity=33/36=92% and specificity=81/83=98%, respectively.

Recurrence of peptic ulcer after successful eradication of Helicobacter pylori infection in the Japanese popultion: A prospective follow-up study

Background: Successful eradication of 11. pylori reduces the rate of duodenal ulcer (DU) relapses. Only a few studies in patients with gastric ulcer (GU) have been reported. Aim: To determine the recurrence rates of GUs or DUs after cure of H. pylori infection. Patients and Methods: A total of 236 patients who had successful eradication therapy, including 133 patients with GU, 89 patients with DU and 14 patients with gastro-duodenal ulcer (GDU), were enrolled in this study. Patients using nonsteroidal anti-inflammatory drugs (NSAIDs) at entry or taking maintenance antisecretory therapy after healing of ulcers were excluded. They were followed up endoscopically at 1, 3, 6 and every 12 months after the completion of eradication therapy and at any time when an ulcer symptom recurred, for assessment of ulcer healing and cure of 1-1. pylori infection. (mean follow-up period (range): 1.5 year (0.5 4.5 years)) Biopsy specimens were taken from both the antrum and corpus. H. pylori status was assessed by rapid urease tests, histological examination (hematoxyllin and eosin stain and Giemsa stain), culture and 13C-urea breath test. Results:

Studies on gastric mucosal cell injury induced by Helicobacter pylori.

The cause of gastric cell injury induced by Helicobacter pylori was investigated in vitro using gastric mucosal cells derived from male Japanese white rabbits. To evaluate the contribution of the potent urease activity of H. pylori to gastric mucosal cell injury, the supernatant of the H. pylori bacterial pellet, solubilized with N-octyl-glucoside, was added to the gastric mucosal cell suspension. Cell injury was assessed by lactate dehydrogenase (LDH) release into the extracellular fluid. Treatment of cells with H. pylori extracts together with urea resulted in high levels of LDH release, suggesting definite gastric mucosal cell injury, and elevation of ammonia concentration was also observed. In contrast, incubation with H. pylori extracts alone or urea solution alone did not result in increased LDH release or elevated ammonia concentrations. The degree of LDH release from gastric mucosal cells due to H. pylori extracts in the presence of urea was similar to that induced by administration of the same amount of exogenous ammonia. The addition of acetohydroxamic acid, a potent specific urease inhibitor, remarkably inhibited ammonia production, the elevation of pH of extracellular fluid, and LDH release in a dose-dependent manner. These results suggest that ammonia produced by potent urease activity of H. pylori in the presence of urea plays an important role in the pathogenesis of gastric mucosal cell injury.