The pathogenesis of heartburn in nonerosive reflux disease: a unifying hypothesis

Gastroenterology. 2005 Mar;128(3):771-8. doi: 10.1053/j.gastro.2004.08.014.

Abstract

Heartburn is a symptom complex that has traditionally been accepted as an acid-mediated event and a reliable indicator of gastroesophageal reflux disease. Recently, however, these concepts have been questioned because patients with endoscopy-negative "heartburn" have lower response rates to acid suppression with proton pump inhibitors than do patients with endoscopy-positive "heartburn," ie, erosive esophagitis. As explanation for this, 3 different mechanisms have been proposed to explain the occurrence of heartburn in the endoscopy-negative setting. They are: esophageal visceral hypersensitivity, sustained esophageal contractions, and abnormal tissue resistance. In this report, we review the observations in support of each concept and propose a means for reconciling them under one hypothesis: abnormal tissue resistance. Essential to this review and to the conclusions drawn about the pathogenesis of heartburn in nonerosive reflux disease is a reaffirmation of the definition of reflux-associated "heartburn" as an acid-mediated event requiring "relief by antacids" as a necessary component of the history.

Publication types

  • Review

MeSH terms

  • Endoscopy, Digestive System
  • Epithelium / metabolism
  • Esophageal Diseases / complications
  • Esophagus / metabolism
  • Esophagus / physiopathology
  • Gastroesophageal Reflux / complications*
  • Gastroesophageal Reflux / metabolism
  • Gastroesophageal Reflux / pathology
  • Gastroesophageal Reflux / physiopathology
  • Heartburn / etiology*
  • Humans
  • Models, Biological*
  • Muscle Contraction
  • Muscle, Smooth / physiopathology
  • Permeability
  • Sensation Disorders / complications