View clinical trials related to Gastric Ulcer.
Filter by:The purpose of this study is to assess the efficacy of esomeprazole (D961H) 20 mg versus placebo once daily for up to 24 weeks of treatment involving patients with a history of gastric and/or duodenal ulcers receiving daily nonsteroidal anti-inflammatory drug (NSAID) therapy by evaluating presence or absence of gastric and/or duodenal ulcers throughout the treatment period (24 weeks) in terms of efficacy on prevention of gastric and/or duodenal ulcers
This study uses an open-label design and will be conducted in approximately 60 sites aiming to enroll a total number of 200 subjects to ensure that at least 100 subjects will have 12 months exposure to PN400 (VIMOVO).
This study uses a randomized, double-blind, controlled design to demonstrate that PN400 (esomeprazole and naproxen) is more effective in reducing the occurrence of gastroduodenal ulcers, dyspepsia, and heartburn in subjects at risk for developing NSAID-associated gastric ulcers compared to naproxen alone.
The purpose of this study is to evaluate the safety of rabeprazole 20mg/day in polymedicated patients and to examine the necessity of adjusted dosage in both therapies (rabeprazole and concomitant drug). Proton pump inhibitors (PPI) act in the final step of the gastric secretion. PPI's block ATP-ase H+/K+ in gastric parietals cells. It has been described that inhibition of acid secretion has produced the recovery of the gastroesophageal pathology in a high percentage of the patients resistant to conventional drugs. In this context, the objective of the study is to evaluate the safety of rabeprazole as a concomitant treatment and examine the clinical practice the interaction with drugs whose absorption has gastric pH dependence.
The purpose of this study is to compare the effect of esomeprazole 20 or 40 mg once daily versus placebo on the occurrence of peptic ulcers during 26 weeks in subjects on continuous low-dose acetylsalicylic acid.
This study is being done to see if Nexium I.V. can reduce and control stomach acid in mechanically ventilated, critically ill patients in an Intensive Care Unit setting.
The purpose of this study is to assess the efficacy of esomeprazole 20 mg dosed once daily and ranitidine 150 mg dosed twice daily through 4 weeks of treatment for the healing of gastric ulcers in patients receiving daily non-steroidal anti-inflammatory drug (NSAID)therapy.
Recently, cytokine polymorphisms are considered to play an important role in the pathogenesis of peptic ulcer and gastric cancer. We intended to clarify the association between polymorphisms of pro-inflammatory and anti-inflammatory cytokines, and the susceptibility to gastric cancer, gastric ulcer and duodenal ulcer in Japan, and to detect the individuals who have higher risks for gastrointestinal disease development.
Helicobacter pylori (H. pylori) eradication increases the serum pepsinogen (PG) I/PG II ratio and the percentage change in PG I/PG II ratios was found to be a useful marker of H. pylori eradication (e.g., the PG method). We studied whether the PG method could be an early diagnostic marker of H. pylori eradication even in patients persistently treated with a proton pump inhibitor. Sixty-two H. pylori-positive patients underwent H. pylori-eradication therapy, followed by treatment with a PPI to cure ulcers. Serum levels of PG I and PG II were measured before, at the end of, and at 4 weeks after the eradication therapy. At more than one month after the end of treatments, 13C-urea breath test (UBT) was performed. The cut-off values of percentage changes in PG I/PG II ratios for the diagnosis of eradication of H. pylori were set in proportion to PG I/PG II ratios before eradication in accordance with our previous report. Using the results of UBT as the standard, the percentage change in serum PG I/PG II ratios is useful as an early diagnostic marker for judgment of H. pylori eradication irrespective of PPI treatment.
Proton pump inhibitors (PPIs) are mainly metabolized in the liver by CYP2C19, one of the cytochrome P450 isoenzymes, which shows a genetic polymorphism associated with enzyme activities. The most essential role of a PPI in H. pylori eradication therapy is to make antibiotics more stable and bioavailable in the stomach by raising intragastric pH to neutral levels. Most patients who have failed in the eradication of H. pylori infection by triple therapy with a PPI, amoxicillin (AMPC) and clarithromycin (CAM) at standard doses have extensive metabolizer (EM) genotypes of CYP2C19 and/or are infected with CAM-resistant strains of H. pylori. Four-times daily dosing of a PPI could achieve complete gastric acid inhibition. Dual therapy with 4-times daily dosing of a PPI and AMPC could yield sufficient re-eradication rates in patients with EM genotype of CYP2C19. Metronidazole (MNZ)-based re-eradication therapy, such as triple PPI/AMPC/MNZ therapy, also achieved high eradication rates and has been recommended as the second line therapy in Japan. But carcinogenic actions of MNZ have been unclear. The purpose of this study is to compare the re-eradication rates of H. pylori infection by the dual high-dose PPI/AMPC therapy and triple PPI/AMPC/MNZ therapy, and to validate the efficacies of these re-eradication regimens as second line eradication therapies.