Acid suppression in the long-term treatment of peptic stricture and Barrett's oesophagus.Digestion. 1992; 51 Suppl 1:49-58.D
Peptic stricture and Barrett's oesophagus are not only the major, but also the most common, complications of gastro-oesophageal reflux disease. The clinical problems that these manifestations present are highly significant, and in patients with peptic stricture the resultant dysphagia can be a major disability that causes nutritional problems. Dilation of a stricture exposes the patient to a small, but significant, risk of oesophageal perforation. Barrett's oesophagus per se rarely causes morbidity, but carries a significant risk of developing oesophageal carcinoma, with its attendant morbidity and mortality. Successful anti-reflux surgery for peptic stricture and Barrett's oesophagus effectively abolishes pathological oesophageal acid exposure and provides the best indicator of the potential benefits that may be obtained from treatment with acid-inhibitory drugs. The reported experience clearly indicates that successful anti-reflux surgery results in resolution of peptic stricture following initial dilation, concomitant with persistent control of oesophageal acid exposure. In patients with Barrett's oesophagus, healing of oesophagitis is well documented after successful surgery, but it is unclear whether the Barrett's epithelium progresses or regresses significantly in all but a minority of patients. It is now established that acid pump inhibition can reduce pathological oesophageal acid exposure as effectively as successful anti-reflux surgery. In a minority of patients, however, omeprazole, 40 or 60 mg daily, divided into two doses, is necessary to achieve this effect. This is particularly true for patients with the more severe forms of disease, in whom peptic stricture and Barrett's oesophagus are most prevalent. Results indicate that peptic stricture can resolve during effective gastric acid inhibition with omeprazole, and results from controlled trials on the management of these patients with omeprazole are awaited. Similarly, there are reports of regression of Barrett's oesophagus during omeprazole therapy, but the completeness and predictability of any such effect have not yet been adequately evaluated. There is sufficient experience from long-term omeprazole treatment of gastro-oesophageal reflux disease to indicate that maintenance of a satisfactory response of peptic stricture or Barrett's oesophagus depends upon continued effective gastric acid inhibition.