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Aim: To determine the clinical characteristics of elderly patients of hemorrhagic gastroduodenal ulcer on low-dose aspirin (LDA) therapy., Methods: A total of 1105 patients with hemorrhagic gastroduodenal ulcer treated in our hospital between January 2000 and March 2016 were grouped by age and drugs used, and these groups were compared in several factors. These groups were compared in terms of length of hospital stay, presence/absence of hemoglobin (Hb) decrease, presence/absence of blood transfusion, Forrest I, percentage of Helicobacter pylori infection, presence/absence of underlying disease, and percentage of severe cases., Results: The percentage of blood transfusion (62.6% vs 47.7 %, P < 0.001), Hb decrease (53.8% vs 40.8%, P < 0.001), and the length of hospital stay (23.5 d vs 16.7 d, P < 0.001) were significantly greater in those on drug therapy. The percentage of blood transfusion (65.3% vs 47.8%, P < 0.001), Hb decrease (54.2% vs 42.1%, P < 0.001), and length of hospital stay (23.3 d vs 17.5 d, P < 0.001) were significantly greater in the elderly. In comparison with the LDA monotherapy group, the percentage of severe cases was significantly higher in the LDA combination therapy group when elderly patients were concerned (16.1% vs 34.0%, P = 0.030). Meanwhile, among those on LDA monotherapy, there was no significant difference between elderly and non-elderly (16.1% vs 16.0%, P = 0.985)., Conclusion: A combination of LDA with antithrombotic drugs or non-steroidal anti-inflammatory drugs (NSAIDs) contributes to aggravation. And advanced age is not an aggravating factor when LDA monotherapy is used., Competing Interests: Conflict-of-interest statement: All authors declare no conflicts-of-interest related to this article.

Background: Low-dose lansoprazole has not been intensively evaluated for its efficacy in the prevention of recurrent gastric or duodenal ulcers in patients receiving long-term non-steroidal anti-inflammatory drug (NSAID) therapy for pain relief in such diseases as rheumatoid arthritis, osteoarthritis, and low back pain., Methods: This multi-center, prospective, double-blind, randomized, active-controlled study involving 99 sites in Japan was designed to compare the efficacy of lansoprazole (15 mg daily) with gefarnate (50 mg twice daily). Patients with a history of gastric or duodenal ulcers who required long-term NSAID therapy were randomized to receive lansoprazole 15 mg daily (n = 185) or gefarnate 50 mg twice daily (n = 181) and followed up for 12 months or longer prospectively., Results: The cumulative incidence of gastric or duodenal ulcer at days 91, 181, and 361 from the start of the study was calculated by the Kaplan-Meier method as 3.3, 5.9, and 12.7%, respectively, in the lansoprazole group versus 18.7, 28.5, and 36.9%, respectively, in the gefarnate group. The risk for ulcer development was significantly (log-rank test, P < 0.0001) lower in the lansoprazole group than in the gefarnate group, with the hazard ratio being 0.2510 (95% CI 0.1400-0.4499). A long-term follow-up study showed an acceptable safety profile for low-dose lansoprazole therapy, with diarrhea as the most frequent adverse event., Conclusion: Lansoprazole was superior to gefarnate in reducing the risk of gastric or duodenal ulcer recurrence in patients with a definite history of gastric or duodenal ulcers who required long-term NSAID therapy.

Background: Helicobacter pylori eradication therapy alone is not sufficient to heal all gastric ulcers., Aim: To verify the efficacy of treatment with irsogladine maleate between the termination and assessment of treatment for eradicating H. pylori in a double-blind study., Methods: Three hundred and twenty-two patients with a single H. pylori-positive gastric ulcer were given eradication treatment, then assigned randomly to a treatment group [given 4 mg/day irsogladine maleate (n = 150)] or a control group [given a placebo (n = 161)]. The gastric ulcer healing rates were compared after 7 weeks of treatment., Results: The healing rate was significantly higher in the irsogladine maleate group (83.0%) than in the placebo group (72.2%; chi2 test, P = 0.0276). In the subgroup analysis of cases of eradication failure, the gastric ulcer healing rate was significantly higher in the irsogladine maleate group (57.9%) than in the placebo group (26.1%; chi2 test, P = 0.0366)., Conclusions: Irsogladine maleate was effective for treating gastric ulcer after H. pylori eradication. The high healing rates observed in patients with or without successful eradication demonstrate the usefulness of irsogladine maleate treatment regardless of the outcome of eradication.

Peptic ulcer disease (PUD) is one of the main lesions responsible for upper gastrointestinal (GI) bleeding, as well as esophageal varices and Mallory-Weiss tear. Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs)/aspirin are the major responsible causes. In cases of upper GI bleeding, urgent endoscopy is performed after stabilization of vital signs. There are several modalities for controlling bleeding in PUD, such as ethanol injection or hypertonic saline with epinephrine. Recurrent bleeding occurs in 20% of patients after endoscopic therapy. The combination of endoscopic intervention and a proton pump inhibitor (PPI) is necessary to achieve hemostasis of active bleeding. It has been reported that high-dose omeprazole (80 mg bolus injection, then 8 mg/h continuous infusion for 72 h, then 40 mg/day orally for 1 week) can reduce recurrent bleeding, the need for surgery and mortality from hemorrhagic shock in patients with high-risk peptic ulcer bleeding, as compared with standard-dose omeprazole. The metabolism of PPIs is dependent upon P450 2C19 genotypes and the clinical usefulness of genotypic analysis remains to be determined.

Both Helicobacter pylori (H. pylori) infection and non-steroidal anti-inflammatory drug (NSAID) administration independently and significantly increase the risk of peptic ulceration and ulcer bleeding as its complication. Because of increasing ratio of the senior generation in Japan, the relative role of NSAID including low-dose aspirin as an anti-platelet therapy, will be more important in the pathogenesis of peptic ulcerations. In order to prevent peptic ulcerations, one of the major adverse events of NSAID, a series of selective COX-2 inhibitors has been developed and some of them have been widely used clinically. However, long-term use of a COX-2 inhibitor may be associated with higher risk of cardiovascular events and strokes. Herein, we focus on prophylaxis and treatment of NSAID-associated gastric ulcerations.

The guideline for gastric ulcer treatment in Japan recommends eradication of Helicobacter pylori (H. pylori) for the first choice. Recently, it is well known that some patients develop gastro-esophageal reflux disease (GERD) after successful eradication. H. pylori infection may play a protective role against GERD by impairing gastric acid secretion. Acid secretion is influenced by the distribution of gastritis in the stomach. Antrum-predominant gastritis is associated with gastric hypersecretion. Patients with corpus-predominant gastritis have decreased acid secretion. The latter is common in Japan and at high risk of GERD after eradication. To arise GERD, both acid secretion and reflux of acid caused by hiatus hernia or gastro-esophageal dysmotility are needed. Although most of GERD developed after eradication are mild, severe GERD are also experienced at times. Recent view of GERD and H. pylori infection is described.

Migration of epithelial cells (restitution) is an essential step in the repair of gastric mucosal lesions. Although a variety of growth factors are reported to facilitate gastric epithelial restitution, the intracellular mechanisms of this process are not fully understood. In this study we investigated the effects of hepatocyte growth factor (HGF) on restitution of normal rat gastric epithelial RGM-1 cell monolayers after injury and examined whether cyclooxygenase-2 (COX-2) is involved in HGF-mediated epithelial restitution. Restitution of RGM-1 monolayers was assessed using a round wound restitution model. Application of HGF (5 ng/ml) significantly facilitated the restitution of RGM-1 monolayers after artificial wounding. HGF also induced expression of COX-2 protein in RGM-1 cells, and wounding itself induced COX-2 expression in the cells located at the edge of the wound. Inhibition of COX-2 activity by NS-398, a specific COX-2 inhibitor, significantly delayed the HGF-mediated restitution. These results suggest the involvement of COX-2 in the action of HGF on gastric epithelial restitution.