Purpose of review Structural causes are absent in more than 50% of patients with symptoms referred to the gastroduodenal region when routine diagnostic tests are applied. New knowledge holds the prospect that targeted therapy may more optimally manage subsets of these patients with functional dyspepsia.
Recent findings An understanding of gut-to-brain and brain-to-gut pathways in functional dyspepsia is expanding. Minimal mucosal inflammation with eosinophils (and in some cases mast cells) characterized by ultrastructural changes in the duodenum appears to be present in a substantial subgroup of functional dyspepsia patients as identified now by investigators globally. Although antibiotic therapy targeting Helicobacter pylori appears to be effective in a small proportion of functional dyspepsia patients, eradication therapy may be more effective in functional dyspepsia patients with microscopic duodenal inflammation, a potentially important finding needing to be confirmed. This may suggest that the effects of antibiotics for functional dyspepsia are not simply mediated by the eradication of gastric H. pylori, but have other antibacterial effects (e.g., on the duodenal microbiome). Abnormal visceral sensory function plays a key role not only in the manifestations of functional dyspepsia but also in peptic ulcer disease.
Summary The pathophysiologic concepts underlying functional dyspepsia and related treatment approaches are shifting from a focus on H. pylori, acid suppression or modulation of motility toward new models. New evidence suggests that minimal duodenal inflammation plays a role in symptom generation in at least a proportion of patients with otherwise unexplained symptoms. This is a paradigm shift and ultimately may change the treatment of many patients with functional gastrointestinal disorders.