• GERD Symptom Scale
  
• Symptom-free Day Measurement
  
• Cost Measurement
  

• 24-hour pH
  
• Economic Analysis
  
• Endoscopy
  
• Esophageal manometry
  
• Health related quality of life (SF-36)
  
• Health Utility Index
  
• Respiratory function, airways hypersensitivity and inflammation and microaspiration
  

GERD encompasses a variety of symptoms and pathological findings caused by the reflux of gastric contents into the esophagus although symptoms and pathology may occur independently of each other. GERD usually presents with typical symptoms of retrosternal burning (heartburn) with or without chest pain and regurgitation of gastric contents into the back of the mouth. However, symptoms often occur in the absence of abnormalities associated with GERD, such as esophageal erosions, ulceration, stricturing or Barrett's esophagus. There is no clear correlation between symptoms and the histological features of GERD. Less prevalent manifestations of GERD include the geneses of dental erosions and respiratory disease including aspiration pneumonia, asthma, chronic laryngitis. Most often, GERD is due to excessive reflux of gastric contents into the esophagus rather than gastric acid hypersecretion. Reflux is caused by an increase in the frequency of inappropriate transient relaxations of the lower esophageal sphincter (LES). In most patients, basal resting LES pressure is normal although LES hypotonia, reduced esophageal body contractility and the presence of a hiatus hernia may exacerbate reflux or reduce esophageal clearance. Impaired esophageal mucosal resistance can increase the potential for esophageal damage. Bile acids and pancreatic enzymes have been implicated in the pathogenesis of GERD but it is generally accepted that the major causes of esophageal symptoms and injury are gastric acid and pepsin, which are active only at low ambient pH. Severity of esophagitis and of reflux symptoms correlate well with the duration of esophageal acid exposure with clear correlation between acid secretory inhibition and esophagitis healing rates for any given drug. On this basis, treatment for GERD has been directed towards:

Minimization of potential precipitating factors by lifestyle modifications such as weight loss, small meals and, avoidance of alcohol and tobacco.

Improving LES pressure, esophageal clearance and gastric emptying, using prokinetic agents.

Neutralization of acid in the stomach or esophagus, using antacids. Reduction of acid secretion, using histamine receptor antagonists(H2RAs) or PPI's.

Surgical prevention of gastro-esophageal reflux by fundoplication. In practice, the latter two approaches are the most successful for patients with more severe GERD and PPE's have proven more efficacious than H2RAs.