US Gastroenterology & Hepatology Review, 2008;4(2):65-67
Erosive esophagitis is part of the spectrum of reflux disease, which includes patients with heartburn but no visible damage to the esophagus with complications such as stricture, Barrett’s, and extra-esophageal manifestations. As the degree of esophageal damage does not correlate with the severity of the symptoms,1 differentiation between erosive and non-erosive disease requires endoscopy.
To write about erosive esophagitis is to consider also a subset of patients with reflux disease who remain unidentified even in the 21st century. Patients with heartburn may take over-the-counter antacids, histamine H2-receptor antagonists (H2RAs), or proton pump inhibitors (PPIs) before they see their primary care physician, when they will most likely be prescribed a PPI. The patient may have an endoscopy only if he or she has symptoms that persist despite treatment, and by then any erosive esophagitis they had at presentation may well have healed. Nevertheless, we will examine this subset of patients.
History
Why be interested in erosive esophagitis? In part, this is historical. There have been numerous trials of duodenal and gastric ulcer healing with H2RAs where the primary end-point was healing the ulcer. Healing was important as it meant that the risk for complications, bleeding, and perforation had been eliminated. In randomized, controlled trials of omeprazole versus H2RAs, omeprazole consistently healed more duodenal and gastric ulcers and healed them faster than H2RAs.2 Early studies with H2RAs showed that they could heal mild esophagitis.3 Subsequent metaanalyses showed that H2RAs healed more patients than placebo, and omeprazole healed more patients and more severe disease than H2RAs.4 Furthermore, healing was a more objective end-point than symptoms (although endoscopic photo verification of healing was not required by any of these studies), and healing correlated with symptom relief.5,6 In addition, it was postulated that healing erosions was beneficial as it would reduce the incidence of complications. Indeed, this proved to be the case for esophageal strictures caused by reflux. Adequate treatment of acid reflux was shown to reduce the restricture rate after dilatation, first in patients with Zollinger-Ellison syndrome7 and subsequently in patients with regular reflux-induced strictures.8
Healing with Proton Pump Inhibitors versus H2-receptor Antagonists
In a large analysis of many studies where placebo, H2RAs (cimitidine, ranitidine, nizaditine, or famotidine), and omeprazole were compared, H2RAs produced healing rates of 50%, placebo 24%, and omeprazole 78%.4 In some ways it is surprising that H2RAs have such efficacy in gastroesophageal reflux disease (GERD) because of the tolerance that develops. The first dose of an H2RA decreases stimulated acid output by about 70%, but tolerance develops over the first few days of therapy, resulting in a greatly reduced acid inhibition.9
Most of these trials in patients with esophagitis allowed the use of rescue antacids; therefore, all treatment groups include antacid use. Studies on antacids alone in erosive esophagitis are limited, but such data that are available suggest that although symptom relief may be better than with placebo, healing of erosive esophagitis is not.10
The PPIs omeprazole, pantoprazole, rabeprazole, pantoprazole, and esomeprazole have all been compared with H2RAs in patients with erosive esophagitis. A meta-analysis by Chiba et al.11 showed that PPIs healed more patients and healed them faster than H2RAs. PPIs were also superior to H2RAs as maintenance therapy. Given that reflux disease is a chronic problem, it can be argued that the results of maintenance trials are more important than studies of acute relief of symptoms or healing rates. Caro et al.12 analyzed five maintenance trials that compared PPIs with H2RAs. In each case, the PPI was superior to the H2RA.
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