Mika Yuki

Predominant nocturnal acid reflux in patients with Los Angeles grade C and D reflux esophagitis

Nocturnal gastric acid breakthrough (NAB) is defined as an intragastric pH < 4.0 lasting more than 1 h during the night in patients taking a proton pump inhibitor (PPI). Gastroesophageal reflux disease (GERD) patients with nocturnal gastroesophageal acid reflux accompanied by NAB are thought to be refractory to PPI treatment. The aim of this study was to endoscopically identify the patients with predominant nocturnal gastroesophageal acid reflux.

Prevalence of functional dyspepsia and its relationship with Helicobacter pylori infection in a Japanese population.

Aim: To investigate the prevalence of functional dyspepsia and Helicobacter pylori infection and their relationship in a Japanese population.

Cardiovascular risk factors in subjects with Helicobacter pylori infection.

Background. It has been proposed that Helicobacter pylori infection is related to cardiovascular disease, although this has not been fully investigated. The aim of this study was to investigate whether H. pylori in‐fection is associated with cardiovascular risk factors.

Comparative evaluation of urine-based and other minimally invasive methods for the diagnosis of Helicobacter pylori infection.

Background: Diagnostic methods have recently been developed for detecting anti-Helicobacter pylori antibody in urine and H. pylori antigen in stool samples. Our aim was to evaluate the usefulness of noninvasive urine-based methods for the diagnosis of H. pylori infection. Methods: The study subjects were 100 asymptomatic Japanese volunteers. We investigated the diagnostic efficacy of various noninvasive diagnostic methods; five serological tests (Immunis anti-pylori, HM-CAP, EIAgen Helicobacter pylori IgG, Helico G, and GAP-IgG), one test for antigen in stool (HpSA enzyme immunoassay [EIA]), and two tests for antibody in urine (Urinelisa and Rapirun) by using the urea breath test (UBT) as the gold standard. Results: Fifty subjects were diagnosed as positive for H. pylori infection by the UBT. The serological tests showed good sensitivity, specificity, and accuracy. The diagnostic values of the feces-based test (HpSA EIA) were lower than that of the serological tests. The sensitivities of the two urine-based methods in frozen urine samples were markedly lower than those of the other tests. However, the use of unfrozen samples markedly improved the diagnostic accuracy of these urine-based tests, which was then superior to that of the feces-based method. Conclusions: This study clearly showed that urine-based tests were useful for the diagnosis of H. pylori infection. However, the use of frozen urine samples was not appropriate for the detection of anti-H. pylori antibody.

Influence of Helicobacter pylori infection on the prevalence of reflux esophagitis in Japanese patients

Reflux esophagitis is caused by esophageal motor dysfunction in patients with sufficient gastric acid secretion. Helicobacter pylori causes atrophic gastritis and influences gastric acid secretion. Hiatus hernia (HH) of the esophagus causes motor dysfunction in the lower esophagus. Therefore, this study aimed to test whether H. pylori infection, gastric mucosal atrophy and HH are predictive factors for reflux esophagitis.

Nocturnal gastric acid breakthrough during the administration of rabeprazole and ranitidine in Helicobacter pylori-negative subjects: effects of different regimens

Background. Nocturnal gastric acid breakthrough (NAB) is defined as nocturnal intragastric pH less than 4 for more than 1 h during proton pump inhibitor (PPI) administration. A bedtime dose of an H2 receptor antagonist (H2RA) inhibites NAB, but the efficacy of the H2RA decreases with continuous administration. We carried out the present study to investigate the effect of 14-day H2RA administration on NAB. Methods. Ten male volunteers without Helicobacter pylori infection received four different 14-day regimens of rabeprazole and ranitidine (study a, morning dose of 20 mg rabeprazole; study b, morning dose of 20 mg rabeprazole with a single bedtime dose of 150 mg ranitidine only on the last day; study c, continuous 20 mg morning dose of rabeprazole and 150 mg at bedtime; study d, morning and evening doses of 10 mg rabeprazole). Ambulatory 24-h gastric pH monitoring was conducted on the last day of each regimen. Results. NAB in studies a, b, c, and d was observed in 9, 1, 4, and 4 subjects, respectively, and the longest periods of nocturnal gastric pH at less than 4.0 were 102.5, 14.0, 37.5, and 52.5 min, respectively (study b vs study c, P < 0.05). Conclusions. The continuous inhibitory effect of ranitidine combined with rabeprazole on nocturnal gastric acid secretion declined during 14-day-long administration in H. Pylori-negative subjects. Split dosing of rabeprazole was more effective than the single morning dose for inhibiting nocturnal gastric acid secretion.

Pulse-wave velocity and cardiovascular risk factors in subjects with Helicobacter pylori infection

Background: Helicobacter pylori infection has been reported to correlate with the onset of cardiovascular diseases. However, the relationship between H. pylori infection and the development of arteriosclerosis has not been fully investigated. We performed a cross‐sectional study to clarify the possible role of H. pylori infection in the development of arteriosclerosis.

Is a computerized bowel sound auscultation system useful for the detection of increased bowel motility

pylori positive status indicated a weak correlation (r 0.267, p 0.05) between the bacterial burden of gastric mucosa and the GUA ratio. However, we failed to find any significant correlation between the GUA ratio and colonization density of H. pylori in children with peptic ulcers (r 0.454, p 0.05) and in the H. pylori positive children without ulcers (r 0.174, p 0.05). Significant correlation was observed between GUA ratio and gastric inflammation score (r 0.406, p 0.01) in the total H. pylori positive group. However, the GUA ratio did not correlate with gastritis severity in the patients with peptic ulceration (r 0.358, p 0.05) and in the H. pylori negative patients (r 0.02, p 0.05). Nevertheless, there was a significant positive correlation between GUA ratio and the gastritis score in the ulcer-free group of children with H. pylori positive status (r 0.416, p 0.05). It is well known that H. pylori produce large amounts of the enzyme urease. Unusually high urease activity of H. pylori may allow consideration of urease as a specific marker of the infection (1, 2). The standard biopsy-dependent urease tests are very specific but moderately sensitive because of patchy dissemination of H. pylori on the gastric mucosa (4). Noninvasive C urea breath tests have great sensitivity and safety, but they are very expensive techniques. In the present study we propose a sensitive, cheap, and biopsy-independent minimally invasive method for rapid H. pylori detection. The present procedure is more suitable for pediatric practice because it is a safer technique than the standard local biopsy-dependent methods. The presented data on the diagnostic importance of the GUA ratio are comparable with the results obtained by the noninvasive C urea breath test (5). Therefore, the GUA measurement method is an excellent surrogate marker that reflects the total urease activity in the stomach but does not predict density of the bacterial load on the gastric mucosa. Finally, the current findings are mainly in agreement with our previous data on the lack of a relationship between the H. pylori urease activity and duodenal ulceration in childhood (2, 6).

Prognosis following endoscopic injection sclerotherapy for esophageal varices in adults: 20-year follow-up study

Objective. Endoscopic injection sclerotherapy (EIS) is beneficial in the management of active hemorrhaging and prevention of recurrent bleeding from esophageal varices. However, its long-term efficacy and safety are poorly defined. The aim of this study was to determine long-term cumulative survival and clarify negative predictive factors for survival following EIS in patients with esophageal varices. Material and methods. Between 1981 and 1987, 72 patients were prospectively enrolled in a post-EIS follow-up program. Variceal rebleeding, recurrence, and survival were recorded in follow-up examinations conducted for up to 20 years. Results. The mean follow-up period was 86.9 months. The cumulative survival rates were 65.2%, 53.6%, 26.1%, and 11.6% at 36, 60, 120, and 240 months, respectively, with liver failure the most common cause of death. Esophageal varices were eradicated in 93.1% of the patients following EIS and no recurrence of varices was seen beyond 7 years. Significant negative predictive factors for survival rate shown by Coxs proportional multivariate hazard model analysis were older age, advanced liver damage, presence of hepatocellular carcinoma, and occurrence of rebleeding. Conclusions. Long-term survival, rebleeding, and recurrence rates following EIS were clarified. Furthermore, our results clearly demonstrate negative predictive factors for survival after EIS.

Effect of a gastrin/cholecystokinin B receptor antagonist, S-0509, on the omeprazole-induced proliferation of gastric mucosa in rats

Hypergastrinemia is known to cause hyperplasia of the gastric mucosa, especially in gastric enterochromaffinlike (ECL) cells. In some clinical conditions causing hypergastrinemia, such as long-term gastric-acid inhibition and gastric-mucosa atrophy, hyperplastic ECL cells may develop into gastric carcinoid tumors. A newly developed gastrin-receptor antagonist, S-0509, has been reported to block gastrin-induced stimulation of gastric-acid secretion. We therefore investigated whether S-0509 inhibits the omeprazole- and gastrin-stimulated hyperproliferation of gastric mucosa, especially of ECL cells. Daily administration of omeprazole and gastrin in male Sprague-Dawley rats induced marked hypergastrinemia and increased proliferation of gastric-mucosa cells. The numbers of ECL cells and of ECL cells producing messenger RNA for regenerating gene, a potent growth factor for gastric-mucosa cells, were also augmented by long-term administration of omeprazole and gastrin. Coadministration of S-0509 with omeprazole or gastrin almost completely inhibited the omeprazole- and gastrin-induced changes in gastric mucosa, including mucosal thickening and ECL hyperplasia. S-0509 did not induce gastric-mucosa atrophy, even when administered for as long as 4 weeks. In summary, we have found that a newly developed gastrin receptor antagonist, S-0509, inhibits omeprazole- and gastrin-induced mucosal hyperplasia, especially ECL-cell hyperplasia, in rats.