Targeting the abnormalities of gastroduodenal functions in functional dyspepsia

The current definition of functional dyspepsia changes the previous concept of absence of organic disease to the presence of a functional alteration of the upper gastrointestinal tract. From a theoretical point of view, the alteration of any major gastrointestinal function may induce dyspeptic symptoms. However, both asymptomatic subjects with some gastrointestinal functional alteration and dyspeptic patients without a demonstrable dysfunction are not unusual. This may be explained at least in part by the more recent concept of visceral sensitivity. The potential role of acid secretion in the pathogenesis of functional dyspepsia as well as the positive effect of antisecretory drugs in a proportion of patients may be based on an increased gastric acid secretion and duodenal acid overload, a hypersensitivity to acid and/or the development of acid-mediated gastrointestinal motor abnormalities. Helicobacter pylori infection may play a role in this context. Both interdigestive and postprandial gastrointestinal motility, mainly a delayed gastric emptying and an altered intragastric distribution of nutrients, have been described to be disturbed in up to half of the patients with functional dyspepsia. This may also be an explanation for the high frequency of intestinal bacterial overgrowth in these patients. Most probably, visceral hypersensitivity should be present for motor alterations to induce symptoms. This is the basis for future development of new drugs in the management of this functional syndrome. The role of H. pylori in the pathogenesis of functional dyspepsia is a matter of discussion, but a proportion of patients benefit from eradication therapy and, therefore this therapeutic approach should be taken into account.