Gastro-oesophageal reflux disease (
GERD) is primarily due to incompetence of the lower oesophageal sphincter (LOS) and crural diaphragm, with transient LOS relaxation frequently accounting for daytime reflux. In the absence of drugs that adequately correct the motility defects of
GERD, treatment is directed towards decreasing gastric acidity. Oesophageal healing is related to control of 24-h intragastric acidity, the degree of
acid suppression and
duration of treatment. H2-receptor antagonists are generally less effective in
GERD than in
peptic ulcer disease. While providing symptomatic relief in
non-erosive GERD, they are often ineffective in healing erosive oesophagitis.
Proton pump inhibitors provide more rapid and complete healing and symptom resolution. They are superior to H2-receptor antagonists in the long-term management of erosive oesophagitis and in reducing recurrence of oesophageal
stricture following mechanical dilatation. In Barrett's oesophagus, high-dose
proton pump inhibitors in combination with
laser/photodynamic ablation
therapy can produce metaplastic regression, although this does not preclude future emergence of
adenocarcinoma. Surgical morbidity and mortality rates in
GERD generally remain higher than those associated with long-term
pharmacotherapy. However, direct comparisons between laparascopic anti-reflux surgery and
proton pump inhibitor maintenance
therapy remain to be performed. Although there is no evidence that H. pylori
infection worsens the severity of oesophagitis or that H. pylori is carcinogenic in the metaplastic oesophageal mucosa. It has been suggested that H. pylori-positive patients requiring long-term
proton pump inhibitor therapy receive bacterial eradication
therapy to reduce the risk of developing
atrophic gastritis.