View clinical trials related to Dyspepsia.
Filter by:The goal of this study is to determine if Visceral Manipulation (VM) is effective in treating Functional Dyspepsia in addition to drug therapy. Null hypothesis is that VM does not influence FD symptoms.
There has been recent interest into the potential role of mucosal barrier defects in the pathophysiology of functional gastrointestinal disorders (FGIDs). There has been evidence of increased intestinal permeability in patients of IBS,and abnormal tissue resistance in NERD. Although the mucosa of Functional dyspepsia (FD) patients is endoscopically and histologically "normal," it contains ultrastructural changes, activated immune cells, along with evidence of an increased release of mediators leading to gastric dysfunction. There is now consistent evidence indicating that mucosal barrier defects allow the passage of an increased load of bacteria, antigens and toxins which, in turn evoke activation of mucosal immune responses involved in the FD symptom.
Aspirin can prevent ischemic vascular disease but is commonly complicated by dyspepsia in 30% of patients. Patients, who have aspirin related dyspepsia, commonly underwent upper endoscopy to exclude peptic ulcer disease or gastric cancers. For those without significant lesions in the stomach and duodenum (non-ulcer dyspepsia), the best approach in the management is unclear. The objective of this study is to compare the efficacy of esomeprazole and famotidine in the control of dyspeptic symptom. After giving consent, patients will be randomised to receive either esomeprazole 20 mg daily or famotidine 40 mg daily in a double blinded manner. The patient will be followed-up at the 2nd and 4th week. The study will be completed at the 4th week. The primary analysis will be the efficacy in the control of dyspepsia symptom between the two groups.
The primary purpose of the study is to determine the effect of esomeprazole compared to placebo in patients from general practice who have previously been treated with proton-pump-inhibitors (PPI) and who have no upper endoscopic findings.
Helicobacter pylori is a major human pathogen that infects over half of the world population. Infection initiates a series of changes in the gastric mucosa, beginning with gastritis and leading in some patients to peptic ulcer disease, mucosa-associated lymphomas, and gastric adenocarcinoma. It is believed that host factors, in particular, the T cell-mediated immune responses may play an important role in the pathogenesis of diseases induced by H. pylori infection. Recent results revealed that there were higher IFN-γ secreting cells in gastric infiltrating T cells isolated from H. pylori infected patients than in uninfected patients, suggesting that the TH1 response and degree of IFN-γ production is associated with disease severity. Meanwhile, recent studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. In this project, we are trying to further investigate role of host T cell mediated immune response in pathogenesis of Helicobacter infection by characterization of the expression of chemokine receptors on gastric infiltrating lymphocytes. We are going to investigate the mechanisms involving in chemokine/chemokine receptor interaction in recruitment of gastric infiltrating lymphocytes and pathogenesis of gastric mucosa damage in Helicobacter infection. This study will be helpful for understanding the mechanisms of activation and recruitment of gastric-infiltrating lymphocytes during gastric inflammation.