Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

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Volume: The Esophageal Mucosa
Chapter: Endoscopy

Are control endoscopies necessary in stage II erosive esophagitis?

H. W. Boyce Jr (Tampa)

The question as posed does not indicate the system in question relative to grade II. The response to the question will be based as closely as possible on grade II of the

Savary-Miller system [1]. Grade II is defined as multiple erosive lesions, noncircum-ferential, affecting more than one longitudinal fold, with or without confluence [1].

Documented healing is defined as complete re-epithelialization of all mucosal defects determined by endoscopy with or without symptoms of gastroesophageal reflux disease (GERD). When complete resolution of all epithelial defects is evaluated as a criterion in research, healing is found to occur in a surprisingly low percentage of patients treated with standard dose H2-blocker therapy. Johansson et al. evaluated a group of patients unresponsive to phase 1 GERD therapy in a double blind crossover study comparing ranitidine and placebo [2]. None of the patients with Savary-Miller grade II or III esophagitis had complete healing of esophagitis by endoscopy. Many other studies have confirmed the overall poor healing rates for standard dose up to quadruple dose H2-blocker therapy. At least 25% of patients with grade II and III disease were unhealed at 8 weeks on ranitidine 300 mg 4 times daily [3].

In one study, improvement occurred in 88% treated with ranitidine 150 mg twice daily, but complete healing occurred in only 18%, none of whom had severe esophagitis at the beginning of the study [4].

When studies that evaluated healing by H2-blocker therapy are reviewed, one is impressed to find that complete healing occurs in only 27 to 45% of patients with primarily grade I or II disease [5]. Omeprazole was found to have an overall healing rate of 67-92%, again mainly for grades I and II. However, this ATPase inhibitor gave complete healing in 48 to 62% of patients with grade IV disease. Some patients obviously will require double or triple dose omeprazole for complete healing.

One has to be impressed with the recent findings of relatively poor overall healing rates for standard dose H2-blocker therapy that originally was thought to be the therapeutic solution for patients with erosive esophagitis. Studies to date also have shown that whether higher dose H2-blockers or standard dose ATPase inhibitors are used, there will be a number of patients who never completely heal erosive esophagitis of grade II or higher. Since the basic pathophysiology of GERD is not changed by acid suppression, the likelihood of recurrence of erosive esophagitis after complete healing will be great when the healing dose of H2-blocker or ATPase inhibitor is either stopped or reduced. Relapse of erosive esophagitis commonly occurs after stopping treatment. Only about 20% of patients remain in relapse at 6 months with about 50% suffering relapse in less than 8 weeks [5]. Long-term maintenance of healing is improved when either a double dose, higher H2-blocker therapy or an ATPase inhibitor is used [6].

Armed with this knowledge of the unimpressive healing and low remission maintenance rates for GERD treated by standard dose H2-blocker therapy, it appears obvious that control endoscopies will be necessary to assure both initial healing and maintenance of healing of esophagitis of grade II and higher. Only a therapeutic program with doses of H2-blockers and/or ATPase inhibitors that produce complete healing in at least 90% of patients will eliminate the need for control or surveillance endoscopies in patients with grade II esophagitis. Either omeprazole or another ATPase inhibitor will be capable of providing such results. Healing rates of 90-100% with omeprazole in grade I and II esophagitis at 4 weeks, compared to 53-55% with

ranitidine clearly indicate the choice of drug therapy needed to reliably assure healing of these grades, so that follow-up or control endoscopy is not needed [6].

The clinical history and pretherapy endoscopic grade of severe esophagitis provide no help in predicting which patients are more prone to relapse during maintenance therapy even with omeprazole [7]. The same situation probably exists in the majority of patients worldwide with grade II esophagitis who are being treated with the less potent acid suppression provided by standard dose H2-blocker agents.

Another factor that would be important in decisions regarding control endoscopies for grade II esophagitis would be knowledge of the natural history of this stage. Erosive esophagitis has all of the features of a chronic process that recurs in most patients when effective drug treatment is discontinued [8].

Pertinent and yet unanswered questions include:

- What is the natural history of untreated grade II esophagitis?

- Does grade II always progress to grade III?

- Does grade II esophagitis lead to complications of grade IV disease, i.e., ulcer, stricture, columnar-lined esophagus?

Answers to all of these questions could greatly simplify any decision regarding the need for control endoscopies for grade II esophagitis.

The relationship of symptoms to the endoscopic grade of reflux esophagitis is not predictable. It is a well-known fact that grade II, and less often, grade III esophagitis may be associated with very mild or even absent symptoms. Conversely, severe pyrosis may be present in the absence of epithelial injury on endoscopic examination. There is unquestionably a relationship between symptoms and reflux, especially when erosive esophagitis is present [9]. Surprisingly, as many as 85% of acid reflux episodes, as measured by an esophageal pH probe, may not produce symptoms, regardless of the severity of mucosal injury.

The answer then for today is: control endoscopy is necessary to assure healing and remission for grade II erosive esophagitis in all patients not treated by an ATPase inhibitor with maximum suppression of gastric acid secretion.


1. Savary M, Miller G. L'oesophage. Manuel et Atlas d'Endoscopie Solothurn: Verlag Gassmann, 1977.

2. Johansson KE, Boeryd B, Tibbling L. Double blind crossover study of ranitidine and placebo in gastroesophageal reflux disease. Scand J Gastroenterol 1986:21:769-778.

3. Johnson NJ, Mills JC, Wood JR Acute treatment of reflux esophagitis: a multicenter trial comparing ranitidine 150 mg b.i.d. with ranitidine 300 mg q.i.d Gastroenterology 1989;96:A242.

4. Goy JA, Maynard JH, McNauton WM, O'Shea A. Ranitidine and placebo in the treatment of reflux esophagitis. Med J Aust 1983;2:558-561.

5. Bell NJV, Hunt RH. Role of gastric acid suppression in the treatment of gastroesophageal reflux disease. Gut 1992;33: 118-124.

6. Hetzel DJ, Dent J, Reed WD et al. Healing and relapse of severe peptic esophagitis after treatment with omeprazole Gastroenterology 1988:95:903-912.

7. Klinkenberg-Knol EC, Meuwissen SGM. Medical therapy of patients with reflux oesophagitis poorly responsive to H2-receptor antagonist therapy. Digestion 1992:51:44-48.

8. Spechler SJ. Epidemiology and natural history of gastroesophageal reflux disease. Digestion 1992:51(suppl l):24-29.

9. Baldi F, Ferrarini F, Longanesi A, et al Acid gastroesophageal reflux and symptom occurrence. Dig Dis Sci 1989:34:1890-1893.

Publication date: May 1994 OESO©2015