Pathophysiology and pharmacological treatment of gastroesophageal reflux disease

Dig Dis. 2000;18(2):93-102. doi: 10.1159/000016970.

Abstract

Gastroesophageal reflux disease (GERD) is one of the most common diagnoses in a gastroenterologist's practice. Gastroesophageal reflux describes the retrograde movement of gastric contents through the lower esophageal sphincter (LES) to the esophagus. It is a common, normal phenomenon which may occur with or without accompanying symptoms. Symptoms associated with GERD include heartburn, acid regurgitation, noncardiac chest pain, dysphagia, globus pharyngitis, chronic cough, asthma, hoarseness, laryngitis, chronic sinusitis and dental erosions. The introduction of fiberoptic instruments and ambulatory devices for continuous monitoring of esophageal pH (24-hour pH monitoring) has led to great improvement in the ability to diagnose reflux disease and reflux-associated complications. The development of pathological reflux and GERD can be attributed to many factors. Pathophysiology of GERD includes incompetent LES because of a decreased LES pressure, transient lower esophageal sphincter relaxations (TLESRs) and deficient or delayed esophageal acid clearance. Uncomplicated GER may be treated by modification of life style and eating habits in an early stage of GERD. The various agents currently used for treatment of GERD include mucoprotective substances, antacids, H(2) blockers, prokinetics and proton pump inhibitors. Although these drugs are effective, they do not necessarily influence the underlying causes of the disease by improving the esophageal clearance, increasing the LESP or reducing the frequency of TLESRs. The following article gives an overview regarding current concepts of the pathophysiology and pharmacological treatment of GERD.

Publication types

  • Review

MeSH terms

  • Antacids / therapeutic use*
  • Circadian Rhythm
  • Enzyme Inhibitors / therapeutic use*
  • Esophagus / physiopathology
  • Gastroesophageal Reflux / drug therapy*
  • Gastroesophageal Reflux / physiopathology*
  • Histamine H2 Antagonists / therapeutic use*
  • Humans
  • Hydrogen-Ion Concentration
  • Manometry
  • Neurotransmitter Agents / therapeutic use*
  • Pressure
  • Proton Pump Inhibitors

Substances

  • Antacids
  • Enzyme Inhibitors
  • Histamine H2 Antagonists
  • Neurotransmitter Agents
  • Proton Pump Inhibitors