Pathogenesis of Dyspepsia

Abstract

Functional dyspepsia (FD) is a highly prevalent and heterogeneous disorder. Although recent studies have investigated various pathophysiological mechanisms, the pathogenesis of FD remains obscure. Pathophysiological mechanisms currently proposed to be involved in FD symptom generation include delayed gastric emptying, impaired gastric accommodation to a meal, hypersensitivity to gastric distention, altered duodenal sensitivity to lipids or acid, abnormal duodenojejunal motility, and others. Pathogenetic factors implicated in the occurrence of FD include genetic susceptibility, Helicobacter pylori status, acute gastrointestinal infections and psychosocial factors. The present article provides an overview of pathogenetic factors, pathophysiologic mechanisms and their potential roles in FD.

Helicobacter pylori Infection Impacts on Functional Dyspepsia in Thailand

“…Many factors were reported as possible pathophysiological mechanisms of FD e.g. impaired gastric accommodation, delayed gastric emptying, hypersensitivity to gastric distension, altered duodenal sensitivity to lipids or acid, lack of postprandial suppression of phasic contractility in the proximal stomach (Mimidis and Tack, 2008). However, the strong mechanisms related with PDS were impaired gastric accommodation and delayed gastric emptying (Mimidis and Tack, 2008).…”

“…impaired gastric accommodation, delayed gastric emptying, hypersensitivity to gastric distension, altered duodenal sensitivity to lipids or acid, lack of postprandial suppression of phasic contractility in the proximal stomach (Mimidis and Tack, 2008). However, the strong mechanisms related with PDS were impaired gastric accommodation and delayed gastric emptying (Mimidis and Tack, 2008). H. pylori is a microaerophilic gram negative spiral bacillus that infects the gastric mucosa in 20-80% of humans throughout the world and this bacteria was reported to be the major pathologic agent in the development of FD.…”

“…The study published in 2012 demonstrated that the DQB1*0401 genotype was related to a higher risk of H. pylori infection (Zhao et al, 2012). To date, the correlations of H. pylori infection and the pathogenesis or subgroup of FD are still inconclusive (Mimidis and Tack, 2008). A systematic review demonstrated 10% risk reduction in H. pylori treatment group compared to placebo, and the number needed to treat to improve one case of FD was 14 (Moayyedi et al, 2006).…”

Postinfectious Chronic Gut Dysfunction: From Bench to Bedside

“…Putative mechanisms currently proposed include delayed gastric emptying, impaired gastric accommodation to a meal, hypersensitivity to gastric distention, altered duodenal sensitivity to lipids or acid, abnormal duodenojejunal motility, and others. Among the pathogenetic factors implicated are genetic susceptibility, Helicobacter pylori status, acute gastrointestinal infections, and psychosocial factors ( 32 ). Whether postinfectious dyspepsia pathophysiology diff ers from that of idiopathic dyspepsia is not clear.…”

Effects of the Addition of Mosapride to Gastroesophageal Reflux Disease Patients on Proton Pump Inhibitor: A Prospective Randomized, Double-blind Study

“…6,8,9 Delayed gastric emptying could influence functional gastrointestinal disorders including gastroesophageal reflux disease, peptic ulcer disease and functional dyspepsia. [10][11][12] Mosapride is a selective 5-hydroxytryptamine type 4 (5-HT 4 ) receptor agonist and has been used in patients with upper gastrointestinal disorders by shortening gastric emptying in healthy volunteers and gastroparesis. 13,14 Gastrin and cholecystokinin (CCK) are homologous gastrointestinal endocrine hormones which are known to regulate gastric acid secretion, gastric emptying, growth of gastric mucosa and intestinal motility in upper gastrointestinal tract.…”