Dyspepsia is a complex of symptoms referable to the gastroduodenal region of the gastrointestinal tract and includes epigastric
pain or burning, postprandial fullness, or early satiety. Approximately 80% of individuals with
dyspepsia have no structural explanation for their symptoms and have functional
dyspepsia. Functional
dyspepsia affects up to 16% of otherwise healthy individuals in the general population. Risk factors include psychological comorbidity, acute
gastroenteritis, female sex, smoking, use of non-steroidal anti-inflammatory drugs, and Helicobacter pylori
infection. The pathophysiology remains incompletely understood, but it is probably related to disordered communication between the gut and the brain, leading to motility disturbances, visceral
hypersensitivity, and alterations in gastrointestinal microbiota, mucosal and immune function, and CNS processing. Although technically a normal endoscopy is required to diagnose functional
dyspepsia, the utility of endoscopy in all patients with typical symptoms is minimal; its use should be restricted to people aged 55 years and older, or to those with concerning features, such as
weight loss or
vomiting. As a result of our incomplete understanding of its pathophysiology, functional
dyspepsia is difficult to treat and, in most patients, the condition is chronic and the natural history is one of fluctuating symptoms. Eradication
therapy should be offered to patients with functional
dyspepsia who test positive for Helicobacter pylori. Other
therapies with evidence of effectiveness include
proton pump inhibitors, histamine-2 receptor antagonists, prokinetics, and central
neuromodulators. The role of psychological
therapies is uncertain. As our understanding of the pathophysiology of functional
dyspepsia increases, it is probable that the next decade will see the emergence of truly disease-modifying
therapies for the first time.