Active clinical trials for "Gastritis"

All children from 1day to 18years of age, diagnosed with peptic ulcer disease due to H pylori at Pakistan Institute of Medical Sciences, Islamabad, from July 2020 to December 2021 will be included in the study. After informed written consent from parents/ guardians patients' bio data along with history and examination will be recorded on a proforma. They will be allocated into two groups, group A and group B randomly based on treatment regimen offered. Group A: Amoxicillin AMO + Clarithromycin CLA + Proton pump inhibitor PPI) Group B: Amoxicillin AMO+ Metronidazole MET+ Proton pump inhibitor PPI The history will include presenting symptoms along duration, remission of symptoms after therapy and clinical outcome will also be recorded.

This is a prospective, randomized, double - blind study of 200 male and female volunteers with gastritis diagnosed at the Oswaldo Cruz University Hospital Gastroenterology Outpatient Clinic from October 2019 to July 2020. . Hypothesis: As a non-inferiority study, the hypothesis is that the use of oral Aroeira (Schinus terebinthifolius raddi), associated with amoxicillin and clarithromycin, for the treatment of patients diagnosed with gastritis and dyspeptic symptoms has similar efficacy and safety (non-inferior) and/or superior efficacy and safety to traditional therapy based on the use of omeprazole-associated antibiotic therapy.

The purpose of this study is to determine whether treatment with esomeprazole alone is able to heal patients with lymphocytic gastritis

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.

Helicobacter pylori (H. pylori) gastritis is a common bacterial infection among the elderly population. H. pylori infection causes chronic progressive gastric inflammation, peptic ulcer disease and gastric cancer. Gastric cancer is a significant contributor of cancer-related mortality. The eradication of H. pylori reduces the incidence of gastric cancer. However, the efficacy of H. pylori eradication has decreased dramatically because of antibiotic resistance. This study aims to (i) compare the eradication rates of H. pylori by triple therapy with vonoprazan for the treatment of H. pylori gastritis) (TTV regimen), with triple therapy with conventional proton pump inhibitor (PPI) (TTP regimen) in a multi-racial Asian cohort, (ii) evaluate the prevalence of antibiotic (klacid/amoxicillin/levofloxacin/tetracycline) resistance in H. pylori infected patients, and (iii) assess the safety of the TTV regimen. Diagnosed H. pylori-infected patients (n=252) will be enrolled and randomized 1:1 to TTV or TTP regimen. Gastric biopsies will be cultured and antibiotic sensitivity evaluated using E-test/agar dilution method. The safety of TTV regimen will be assessed using adverse effect questionnaire. This study may potentially impact on prescribing policies and management of H. pylori infections for improved therapeutic outcome.

Research purpose To elucidate the effect mechanism and clinical effective of weifuchun in the prevention and treatment of chronic atrophic gastritis and precancerous lesions of gastric cancer. From genes related to cell differentiation, proliferation, apoptosis, tumor invasion and metastasis, genes related to immune inflammation and immune escape and other possible aspects to elucidate the effective and mechanism of weifuchun's treatment on chronic atrophic gastritis, reversing precancerous lesions of gastric cancer.

Recently studies showed that the eradication rate of H. pylori fail to exceed 80% and even falls into an unacceptable range. A major cause of treatment failure is associated with antibiotic resistance and poor patient compliance. However, the refractory infection of H. pylori is still existing, although patients have good compliance and receive standardized treatment. This phenomenon is likely attributed to the different ratio of sensitive and resistance in H. pylori, the difference of Amoxicillin resistance between in vivo and in vitro, the difference between phenotype and genotype or the influence of micro-environment in the stomach. In order to solve the refractory infection of H. pylori, investigators performed a muti-center study together with other 14 institutions. In this study, investigators will select the patients with refractory infection of H. pylori after two standardized treatment from patients with first eradication therapy of H. pylori infection. Then, investigators will perform a high-throughput sequencing for patients in groups. Finally, investigators will compare the differences between the patients with first successful eradication and patients with refractory infection of H. pylori, such as drug resistance gene mutation, phenotype and genotype, the mechanisms of Amoxicillin resistance and micro-environment in stomach.

The investigators performed a double-blind parallel study in a group of Subjects Showing Erosive Gastritis who were given Hizikia Fusiformis Extract over a period of 4 weeks. Endoscopic observations were performed before and 4 weeks after the treatment, and the cure and improvement rates were investigated.

H. pylori infection plays a very important role in gastric carcinogenesis, progressing from chronic gastritis through atrophic gastritis, intestinal metaplasia, dysplasia and finally cancer. It is difficult to diagnose H. pylori related gastritis and gastric atrophy on the basis of endoscopic findings. Histology is currently considered to be the gold standard for detecting H. pylori infection. The reliability of detecting H. pylori infection histologically depends on the site, number, and size of gastric biopsy specimens. The blind biopsy sampling of normal appearing mucosa has the risk of missing pathology and sampling errors. Most studies conclude that as well as on expertise in staining and visualizing the bacteria. Considerable error also occurs in identifying gastric atrophy using blind biopsy sampling, and neither the original nor the revised version of the Sydney system reliably identifies more than half the cases in patients with confirmed gastric atrophy.

Atrophic gastritis with hypochlorhydric milieu is a risk factor for gastric cancer. Microbes colonizing the acid-free stomach oxidize ethanol into acetaldehyde, a group 1 carcinogen. The aim is to assess gastric production of acetaldehyde and its inert condensation product, non-toxic 4-methyltiazolidine-2-carboxylic acid (MTCA), after alcohol intake under treatment with slow-release L-cysteine or placebo. Patients with biopsy-confirmed atrophic gastritis, low serum pepsinogen and high gastrin-17 are studied. On separate days, patients will be randomly assigned to receive 200 mg slow-release L-cysteine or placebo, then have intragastric instillation of 15% (0.3 g/kg) ethanol. After intake, gastric concentrations of acetaldehyde, ethanol, L-cysteine and MTCA are analysed for 4 hours. Expected results show mitigated exposure of the gastric mucosa to acetaldehyde.