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Novel concepts in the pathophysiology and treatment of functional dyspepsia
  1. Lucas Wauters1,2,
  2. Nicholas J Talley3,4,
  3. Marjorie M Walker5,
  4. Jan Tack1,2,
  5. Tim Vanuytsel1,2
  1. 1Gastroenterology and Hepatology, University Hospitals Leuven, Leuven, Belgium
  2. 2Translational Research in Gastrointestinal Disorders, KU Leuven, Leuven, Belgium
  3. 3Faculty of Health and Medicine, University of Newcastle, Newcastle, New South Wales, Australia
  4. 4School of medicine and public Health, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
  5. 5Anatomical Pathology, University of Newcastle, Newcastle, New South Wales, Australia
  1. Correspondence to Professor Nicholas J Talley, Health, University of Newcastle, Callaghan, NSW 2305, Australia; Nicholas.Talley{at}newcastle.edu.au

Abstract

Emerging data increasingly point towards the duodenum as a key region underlying the pathophysiology of functional dyspepsia (FD), one of the most prevalent functional GI disorders. The duodenum plays a major role in the control and coordination of gastroduodenal function. Impaired duodenal mucosal integrity and low-grade inflammation have been associated with altered neuronal signalling and systemic immune activation, and these alterations may ultimately lead to dyspeptic symptoms. Likely luminal candidates inducing the duodenal barrier defect include acid, bile, the microbiota and food antigens although no causal association with symptoms has been convincingly demonstrated. Recognition of duodenal pathology in FD will hopefully lead to the discovery of new biomarkers and therapeutic targets, allowing biologically targeted rather than symptom-based therapy. In this review, we summarise the recent advances in the diagnosis and treatment of FD with a focus on the duodenum.

  • duodenal mucosa
  • functional dyspepsia
  • functional bowel disorder
  • intestinal permeability
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Footnotes

  • Contributors LW drafted the manuscript. JT revised the manuscript. MMW revised the manuscript. NJT drafted and revised the manuscript. TV drafted and revised the manuscript.

  • Funding LW and TV are supported by the Flanders Research Foundation (FWO Vlaanderen) through a doctoral fellowship and a senior clinical research mandate, respectively. JT is supported by a Methusalem grant of KU Leuven. NJT is supported by an NHMRC Level 3 Investigator Grant and is lead investigator of an NHMRC Centre of Research Excellence.

  • Competing interests NT: Consultancy: Allergan, IM Health Sciences, Takeda, Theravance, Danone, Sanofi. JT: Consultancy: AlfaWassermann, Allergan, Danone, Shire, Takeda, Theravance, Tsumura and Zeria Pharmaceuticals; Speaker fees: Abbott, Allergan, Shire, Takeda and Zeria Pharmaceuticals. TV: Speaker fees: Abbott. Research Grant: Danone.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

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