The Role of Duodenal Inflammation in Functional Dyspepsia.

Abstract

Functional dyspepsia (FD) is common and significantly impairs quality of life. Symptoms of FD are considered to originate from the gastroduodenal region, classified by the Rome criteria as disorders of brain-gut interaction without structural alteration. However, it is now apparent that FD is a number of syndromes, the epigastric pain syndrome (bothersome epigastric pain or epigastric burning) and the postprandial distress syndrome (with bothersome postprandial fullness or early satiation) and there are wide-ranging symptoms and severity. The origin of these troublesome symptoms is now considered to be a result of disrupted gastroduodenal neuropathophysiology. The complexity of the syndrome indicates that there must be different triggers, supported by the limited efficacy of the many treatments available. Current research based on evidence by association suggests that duodenal contents, including the duodenal microbiome, pathogens, and allergy may be triggers of FD. Recent studies have also shown that systemic responses of increased circulating lymphocytes and elevated proinflammatory cytokines and subtle inflammation in the duodenum may accompany the onset and persistence of symptoms. This inflammatory phenotype is characterized by innate inflammation, an eosinophil infiltrate in the duodenum in FD in those with postprandial distress syndrome. Routine histopathology practice does not quantify these cells so the status of FD is not yet appreciated as an inflammatory condition. Thus functional is becoming inflammatory and this breakthrough in understanding that functional does not necessarily mean no, but subtle pathology, may improve therapeutic options, which are currently aimed at symptom relief rather than targeted at underlying pathology.