Takekazu Kaji

Symptom relief in patients with reflux esophagitis: Comparative study of omeprazole, lansoprazole, and rabeprazole

Background and Aim:  Rabeprazole has a faster onset of antisecretory activity than omeprazole and lansoprazole. The aim of the present study was to clarify whether there is any difference in the speed of symptom relief in patients with reflux esophagitis following the administration of these three proton pump inhibitors (PPI).

Diagnostic accuracy of a new non‐invasive enzyme immunoassay for detecting Helicobacter pylori in stools after eradication therapy

Helicobacter pylori eradication therapy has been commonly performed for patients with peptic ulcer. An inexpensive, reliable, non‐invasive test would be useful for evaluation of the effectiveness of eradication therapy.

T Cell-Mediated Cytotoxicity via Fas/Fas Ligand Signaling in Helicobacter pylori-Infected Gastric Corpus

Helicobacter pylori infection induces T helper‐1 immune responses in inflamed mucosa. However, the role of T cell‐mediated cytotoxicity in the induction of epithelial apoptosis is still unclear. The aim of this study was to investigate the involvement of the Fas/Fas ligand (Fas/Fas‐L) system in the H. pylori‐infected gastric corpus.

Efficacy of ecabet sodium for Helicobacter pylori eradication triple therapy in comparison with a lansoprazole-based regimen

: The cytoprotective agent, ecabet sodium, inhibits urease activity and growth of Helicobacter pylori.

Intragastric distribution of Helicobacter pylori during short-term omeprazole therapy: study using Carnoy's fixation and immunohistochemistry for detection of bacteria.

There is controversy about the effect of acid‐suppressive therapy on Helicobacter pylori density and the severity of histological gastritis in the corpus.

Helicobacter pylori Infection Accelerates Gene Expression of Glicentin in the Gastric Mucosa: Its Association with Intestinal Metaplasia of the Stomach

BACKGROUND Glicentin is an intestinal polypeptide hormone which seems to promote intestinal metaplasia (IM) in the gastric mucosa. The aim of this study was to clarify whether Helicobacter pylori infection accelerates glicentin gene expression. METHOD Glicentin mRNA was investigated by reverse-transcription polymerase chain reaction using gastric biopsies from 47 patients examined endoscopically and denying IM. RESULTS IM was observed in 18 (38.3%) cases histologically, but not in the other 29 (62.7%). Glicentin mRNA was significantly correlated with histological IM (P < 0.01) and was positively correlated with H. pylori infection (P < 0.05). CONCLUSION Our results indicate that H. pylori infection is associated with the induction of glicentin in the gastric mucosa, thus supporting the hypothesis that H. pylori infection accelerates IM of the stomach.

Scanning Electron Microscope Examination of Pancreatic Ducts in Stroke-Prone Spontaneously Hypertensive Rats (SHRSP)

SummaryConclusionIschemic injury to the pancreatic ductal cells causes stasis of pancreatic juice, which in turn induces chronic pancreatitis.BackgroundThe pathogenesis of chronic ischemic pancreatitis is still unclear.MethodsIn 12-, 24-, and 36-wk-old, male stroke-prone spontaneously hypertensive rats (SHRSP), which have sclerotic arterioles with a marked narrowing lumen in the pancreas, pancreatic tissue was examined using light and scanning electron microscopy. Corrosion casts of pancreatic ducts and blood vessels were examined using scanning electron microscopy.ResultsDuctular proliferation, tortuous ductal channels, crater-like depressions of ductal inner surfaces, and long cilia of ductal cells were found to be sporadically distributed throughout the pancreatic tissue. Similar pancreatic abnormalities had been found in previous studies using WBN/Kob rats that exhibited pancreatic juice stasis. A few interlobular ducts in the pancreatic tissue of the SHRSP had an inner surface that was gyrus-like in appearance, a feature not found in WBN/Kob rats.

Diagnostic accuracy of a new non-invasive enzyme immunoassay for detecting Helicobacter pylori in stools after eradication therapy

Background: Helicobacterpylori (H pylori) eradication therapy has been commonly performedfor patients with peptic ulcer. An inexpensive, reliable, non-invasive test would be very useful for evaluation of the effectiveness of eradication therapy. In the course of investigations into techniques for detecting H pylori infection after eradication therapy, the diagnosticpotentialof a new non-invasive enzymeimmunoassay (HpSA)for H pylori antigen in stools was evaluated. Methods: One hundred and fifteen pepticulcerpatientswithH pylori infection(84 male,31 female; age range 22-81 years,mean54) receiveda courseof eradicationtherapy.Fourweeks after the end of the therapy, stool sampls were collectedfrom all patients and testedusing the HpSA.The diagnosticaccuracyof the HpSA EIA was evaluated in comparison with the the results of l3C-urea breath test (13C_ UBT). Results: After the eradication therapy, the H pylori status was negative in 106 (92%) cases and positive in 9 (8%), as assessed by 13C-UBT. On the other hand, HpSA stool test results were negativein 105 (91 %) cases and positive in 10 (9%). When the l3C-UBT was used as a gold-standard, the HpSA stool test showed 2 false positive and 1 false negative results, and the sensitivity and specificity were 89% and 98%, respectively, aftereradicationtherapy.The positiveand negativepredictive values of HpSA were 80% and 99%, respectively. Furthermore, a positive correlation (r=0.671, p<O.Oool) was found between the results of the 13C-UBT and the HpSA EIA. Conclusion: The HpSA stool test is potentiallyuseful for the diagnosisof H pylori infection4 weeksafter the end of eradicationtherapy. 2702