Review article: current practice and future perspectives in the management of gastro-oesophageal reflux disease.
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.
Lambert
R
R
Department of Medicine, Hôpital Edouard Herriot, Lyon, France.
D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D001471:Barrett Esophagus / Q000209:etiology; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D004940:Esophageal Stenosis / Q000209:etiology; D005764:Gastroesophageal Reflux / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D006635:Histamine H2 Antagonists / Q000627:therapeutic use*; D006801:Humans; D054328:Proton Pump Inhibitors
D000897:Anti-Ulcer Agents; D004791:Enzyme Inhibitors; D006635:Histamine H2 Antagonists; D054328:Proton Pump Inhibitors