View clinical trials related to Functional Dyspepsia.
Filter by:This study aims to evaluate, in patients with functional dyspepsia, a model example of medical care based upon the biopsychosocial model (called: the therapeutic encounter) compared with standard medical care based upon the biomedical model (called: medical consultation).
Double-blind randomized controlled trials of 8 weeks mirtazapine 15 mg daily or placebo, followed by 8 weeks of open-label mirtazapine 15 mg daily
Pathogenesis of functional dyspepsia is poorly understood. Gastrointestinal motor abnormalities, Helicobacter pylori infection, impaired gastric accommodation to a meal, hypersensitivity of the afferent nerves of the gut, psychological disturbances and central nervous system dysfunction have been proposed. Pharmacological treatments for patients with functional dyspepsia remain unsatisfactory. Only small benefits relative to placebo have been found with histamine H2 receptor antagonists, proton pump inhibitor and Helicobacter pylori eradication. Itopride is a dopamine antagonist with acetylcholinesterase inhibitory actions. This agent is currently indicated for patients with various upper GI symptoms. This study is aimed to evaluate the effect of Itopride on gastric emptying(by 13-C Octanoic acid breath Test), accommodation (by Gastric Scintigraphy SPECT and slow nutrient drinking test)and symptoms in FD patients
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.