Gastro-oesophageal reflux disease
06 March,13

Gastro-oesophageal reflux disease results from the reflux of gastric or duodenal contents into the oesophagus. Symptoms include heartburn, acid regurgitation, and dysphagia (difficulty in swallowing); oesophageal inflammation and ulceration (reflux oesophagitis), and stricture formation may occur. Protracted reflux over several years can lead to the development of Barrett\'s oesophagus (columnar epithelial metaplasia), which is a risk factor for oesophageal cancer.

Lifestyle measures for management of the disease include avoidance of alcohol and aggravating foods such as chocolate and coffee. Raising the head of the bed for patients with nocturnal symptoms, and avoiding lying down within 2 to 3 hours of a meal may be useful. Weight loss may be helpful in overweight patients, as the risk of symptomatic disease and its consequences increases with body-mass index. Cessation of smoking does not appear to alter reflux symptoms. Withdrawing drugs that reduce gastro-oesophageal sphincter tone and hence exacerbate reflux may be considered: such drugs include theophylline and antimuscarinics.

Antacids are used for mild disease and as adjuncts to other therapies. Alginate-containing antacids are said to form an alkaline \'raft\' that floats on the surface of the stomach contents to impede reflux and protect the oesophageal mucosa; they are more effective than simple antacids for symptomatic relief.

Should more vigorous therapy be needed suppression of gastric acid secretion is a likely next step. In the first instance, particularly in patients with mild oesophagitis, this may be with a histamine H2-antagonist such as cimetidine or ranitidine. Although H2-antagonists have been found to relieve symptoms and reduce antacid consumption, rates of oesophageal healing depend on the severity of the disease and duration of therapy. Doubling the standard dose of H2-antagonists does not increase the effect much, but giving divided doses may possibly be of additional benefit.

Alternatively, a prokinetic drug such as metoclopramide may improve gastro-oesophageal sphincter function and accelerate gastric emptying. These appear to be as effective as H2-antagonists. An H2-antagonist used with cisapride may be more effective than either drug alone. However, concern over the risk of cardiotoxicity and potential for serious interactions with cisapride has led to severe restrictions on its use.

A better alternative for resistant disease, or for initial therapy in patients with moderate or severe disease, may be treatment with a proton pump inhibitor such as omeprazole or lansoprazole. Proton pump inhibitors are more effective than H2-antagonists in terms of both rate and extent of reduction in symptoms and healing of oesophagitis. Consequently, some advocate the use of proton pump inhibitors as first-line drugs even in mild disease, using a step-down approach after successful therapy. In refractory cases, giving a proton pump inhibitor with an H2-antagonist may be more effective than just increasing the dose of the former.

In patients with mild disease, a trial of withdrawal of drug therapy is appropriate after successful initial drug therapy. Short courses of therapy as and when symptoms demand (intermittent treatment) may be effective in uncomplicated disease. However, in patients with severe oesophagitis, long-term maintenance therapy is likely to be required. Maintenance with H2-antagonists has generally been disappointing although some patients respond. A proton pump inhibitor is more effective. Another approach is to use a combination for maintenance and in one study omeprazole with cisapride provided more effective maintenance than ranitidine or cisapride alone or in combination. Again, however, cisapride is now unlikely to be used in practice because of the risks.

Helicobacter pylori eradication does not heal or prevent relapse of gastro-oesophageal reflux disease. However, eradication has been suggested on the basis that treatment with proton pump inhibitors is associated with worsening of gastritis in H. pylori-infected patients. Conversely, epidemiological evidence suggests that H.

In infants, gastro-oesophageal reflux is common but usually resolves spontaneously with increasing age and requires no treatment. Occasionally, it may be associated with complications such as failure to thrive, oesophagitis, and pulmonary symptoms of acid regurgitation, but can be managed by upright positioning and the use of thickened foods; drug therapy is controversial.

It has been suggested that where drug therapy is needed, an alginate-antacid combination may be appropriate initially; cisapride, alone or with an antisecretory drug, has been given but the risk of cardiotoxicity makes the use of cisapride in infants extremely problematic. Metoclopramide may have some benefit but again this must be weighed against the risk of adverse effects. Evidence of benefit with domperidone is poor.

Gastro-oesophageal reflux is commonly encountered during normal pregnancy, and is generally managed by lifestyle and dietary modifications. If drug therapy is required, nonsystemically absorbed antacids or sucralfate should be tried first. If these are ineffective, ranitidine may be tried. Proton pump inhibitors are not licensed for use during pregnancy although the relative risk associated with exposure seems to be quite low

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