Pathogenesis and therapy for idiopathic dyspepsia

Abstract

Functional dyspepsia (FD) is one of the most common gastrointestinal disorders. This review summarizes recent progress in our understanding of the pathogenesis and therapy for FD. Although distinction among FD, irritable bowel syndrome, and reflux disease is difficult in population-based studies, separate entities can be recognized in patients who seek medical attention. The pathogenesis of FD remains unclear, but recent studies have demonstrated a role for acute gastrointestinal infection in triggering FD and in genetic polymorphisms of G-proteins in predisposing to FD. The role of abnormalities in gastric motor function, visceral hypersensitivity, and psychosocial factors in the pathophysiology of dyspeptic symptoms has been the topic of multiple studies. Treatment options for FD remain limited. Recent studies have focused on acid-suppressive drugs and on novel prokinetics. Progress in our understanding of the pathogenesis and pathophysiology of FD may lead to new or improved treatment modalities. Areas of major advances are the role of infection and genetic predisposition and studies on the role of abnormalities in gastric motility and sensitivity.

The study on the role of inflammatory cells and mediators in post-infectious functional dyspepsia

“…Functional dyspepsia is a multifactorial disorder with many potential mechanisms having been purported to play roles in symptom generation including abnormalities in gastric motor function, visceral hypersensitivity, neurotransmitter imbalance, inflammation and psychological dysfunction [3]. Helicobacter pylori (H. pylori) is present in some patients with functional dyspepsia but H. pylori eradication therapy has a positive effect in only about 10% of H. pylori positive non-ulcer dyspepsia patients [4,5].…”

Prolonged Recording of Duodenal Acid Exposure in Patients With Functional Dyspepsia and Controls Using a Radiotelemetry pH Monitoring System

“…Postulated and observed physiologic derangements include delayed gastric emptying, impaired gastric accommodation, abnormal duodenojejunal motility, gastric hypersensitivity to distension, or central nervous system dysregulation. 2 Several recent studies have examined the relationship between duodenal acid clearance and FD. In healthy subjects, duodenal acid infusion results in decreased antral contractions and increased sensitivity to balloon distension in the duodenum.…”

Randomised clinical trial: rabeprazole improves symptoms in patients with functional dyspepsia in Japan

“…The low efficacy of rabeprazole 40 mg relative to 20 mg observed in this study was considered to be caused by the multifactorial pathophysiology of FD and the lower acid secretion of patients in Asian countries relative to those in Europe and the United States . As noted previously, various mechanisms may contribute to dyspeptic symptoms, including several factors not related to acid suppression . Hence, strong acid suppression may not necessarily elicit benefit in patients with symptoms partially involving acid.…”

“…2 The pathogenesis of FD is complex and characterised by multiple pathophysiological mechanisms such as delayed gastric emptying, impaired gastric accommodation, hypersensitivity to gastric distension, abnormal clearance of duodenal acid or dysregulation of the central nervous system. 3 Among these, visceral hypersensitivity is recognised as an important pathophysiological mechanism and hypersensitivity to acid secretion is known to cause dyspeptic symptoms. 4 Although most patients with FD have normal acid output, 5 acid-suppressive therapies have been the mainstay of treatment.…”