Functional Dyspepsia, 2016

Nicholas J. Talley; Marjorie M. Walker; Gerald Holtmann

Disclosures

Curr Opin Gastroenterol. 2016;32(6):467-473. 

In This Article

A Comprehensive Disease Model

In a review in the New England Journal of Medicine[1] that builds on current studies and previous syntheses,[30] a disease model is presented that potentially explains the gastrointestinal and extra-intestinal manifestations of PDS. In a genetically predisposed individual, infection or an allergen induces a TH2 response that induces eosinophil and, in some cases, mast cell infiltration and degranulation in the duodenum, further impairing duodenal permeability and allowing antigen presentation in the mucosa and submucosa. Damaged nerve fibers send signals to the central nervous system that may be experienced as symptoms. Nutrients entering the inflamed duodenum increase nerve firing, leading to feedback and abnormal gastroduodenal function with induction of early satiety, Release of cytokines and homing small bowel T cells further alter gastroduodenal function and induce systemic symptoms. This hypothesis and all its elements are testable. On the other hand, EPS likely has a different pathway and, for example, may be induced by chronic H. pylori infection, perhaps via antral predominant gastritis that increases gastric acid secretion, leading to excessive bathing of the duodenum with acid. Acid may activate duodenal sensory nerves and induce pain.

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