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Gastroenterology. 2018 Jan;154(2):277-288. doi: 10.1053/j.gastro.2017.09.047. Epub 2017 Oct 14.

Pathophysiology of Gastroesophageal Reflux Disease.

Author information

1
Translational Research Center for Gastrointestinal Disorders, University of Leuven, Belgium. Electronic address: jan.tack@kuleuven.be.
2
Division of Gastroenterology and Hepatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Abstract

The pathogenesis of gastroesophageal reflux disease (GERD) is complex and involves changes in reflux exposure, epithelial resistance, and visceral sensitivity. The gastric refluxate is a noxious material that injures the esophagus and elicits symptoms. Esophageal exposure to gastric refluxate is the primary determinant of disease severity. This exposure arises via compromise of the anti-reflux barrier and reduced ability of the esophagus to clear and buffer the refluxate, leading to reflux disease. However, complications and symptoms also occur in the context of normal reflux burden, when there is either poor epithelial resistance or increased visceral sensitivity. Reflux therefore develops via alterations in the balance of aggressive and defensive forces.

KEYWORDS:

Acid Exposure; Esophageal Motility; Esophageal Sensitivity; Hiatal Hernia; Transient Lower Esophageal Sphincter Relaxations

PMID:
29037470
DOI:
10.1053/j.gastro.2017.09.047
[Indexed for MEDLINE]

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