J Neurogastroenterol Motil  
Role of the Duodenum in the Pathogenesis of Functional Dyspepsia: A Paradigm Shift
Hye-kyung Jung1 and Nicholas J Talley2*
1Department of Internal Medicine, College of Medicine, Ewha Womans University, Seoul, Korea; and 2University of Newcastle and Hunter Medical Research Institute, Newcastle, NSW, Australia
Correspondence to: Nicholas J Talley, MD, PhD
Hunter Medical Research Institute, University of Newcastle, Kookaburra Circuit, Newcastle, NSW 2258, Australia
Tel: +61-249215855, Fax: +61-240420034, E-mail: nicholas.talley@newcastle.edu.au
Received: March 26, 2018; Accepted: May 4, 2018; Published online: May 23, 2018.
© The Korean Society of Neurogastroenterology and Motility. All rights reserved.

cc This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Functional dyspepsia (FD) is a common disorder characterized by chronic epigastric pain or burning, or bothersome postprandial fullness or early satiation, without a definitive organic cause. The pathogenesis of FD is likely heterogeneous. Classically, motor disorders, visceral hypersensitivity, and brain-gut interactions have been implicated in the pathophysiology of FD, but recently an important role for chronic low-grade inflammation and post-infectious gastroenteritis in FD has been reported and confirmed. Duodenal low-grade inflammation is frequently observed in FD in those with and without documented previous gastroenteritis. Duodenal eosinophils and in some cases mast cells may together or separately play a key role, and immune activation (eg, circulating homing small intestinal T cells) has been observed in FD. Low-grade intestinal inflammation in patients with FD may provoke impairment in motor-sensory abnormalities along the gastrointestinal neural axis. Among FD patients, the risk of developing dyspeptic symptoms after a bout of gastroenteritis is 2.54 (95% CI, 1.76-3.65) 6 months after acute gastroenteritis. Gut host and microbial interactions are likely important, and emerging data demonstrate both quantitative and qualitative changes of duodenal mucosal and fecal gut microbiota in FD. Food antigens (eg, wheat proteins) may also play a role in inducing duodenal inflammation and dyspepsia. While causation is not established, the hypothesis that FD is a disorder of microscopic small intestinal inflammation in a major subset is gaining acceptance, opening the possibility of novel treatment approaches that may be able to alter the natural history of the disorder.
Keywords: Duodenum; Dyspepsia; Eosinophils; Inflammation


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