Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

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Volume: The Esophageal Mucosa
Chapter: Epidemiology

Is it possible to specify the prevalence of CLE in esophagitis?

AJ. Cameron (Rochester)

A review of work relevant to this question is complicated by the lack of uniform definition of terms. The length of esophageal columnar mucosa required to diagnose CLE varies from 2 to 5 cm. The presence of intestinal metaplasia may or may not be a criterion. Reflux esophagitis may be defined by either endoscopic findings or histologic changes. Some series were collected retrospectively, and their data base may be less than ideal. Despite these problems, a reasonable answer to the question can be given.

CLE may occur with or without esophagitis. In CLE patients, esophagitis takes the form of inflammation in the squamous mucosa proximal to the CLE. Table 1 shows the proportion of patients with reflux-related esophageal mucosal abnormality that had CLE in six series. CLE was found in 7 to 33% (mean: 12%) of patients with endoscopic evidence of gastroesophageal reflux disease.

The difficulty in specifying the prevalence of CLE in esophagitis is that esophagitis often resolves when treated, but CLE does not. Although antacids alone are not very effective, clinical trials have shown that treatment of reflux esophagitis with H2 receptor antagonist drugs for 8 to 12 weeks results in healing of esophagitis in about 50% of cases. Treatment with proton pump inhibitor drugs (such as omeprazole) for a similar period can heal esophagitis in about 90% of cases. By contrast, we have shown that the length of CLE usually remains unchanged over years in patients given antacids and H2 blockers [1], and treatment with omeprazole

Table 1..

Year of publication


Patients with esophagitis or CLE

Patients with CLE


Naef et al. [2]




Burbige and Radigan [3]


8 (20%


Starnes et al. [4]


40 (9%)


Schnell et al. [5]


54 (33%)


Rothery et al. [6]


58 (7%)


Winters et al. [7]



or lansoprazole for 1 or 2 years causes little [8] or no regression of CLE [9]. Therefore, the relative numbers of patients with esophagitis and CLE in different series may depend on whether previous treatment has been given.

From the epidemiologic standpoint, more useful information is obtained by prospective studies of consecutive patients with gastroesophageal reflux symptoms. The following series were found:

Schnell et al. [5] performed endoscopy in 428 patients with frequent heartburn and regurgitation. Fifty-four (13%) had CLE and 109 (25%) had erosions or ulcer without CLE. Thus, 33% of patients with mucosal changes had CLE.

Winters et al. [7] endoscoped 97 patients with reflux symptoms (heartburn, regurgitation, dysphagia) occurring every week. Twelve patients had CLE (12%) and 44 (45%) had esophagitis without CLE. Thus, 21% of patients with mucosal changes had CLE.

Mann et al. [10] endoscoped 180 male patients with symptoms of reflux esophagitis. CLE was found in 20 (11%). Of interest, the severity of esophagitis was the same in patients with and without CLE. After 6 months of treatment with antacids, cimetidine, and metoclopramide, esophagitis resolved or was much improved, but no regression of CLE was seen.

In summary, the prevalence of CLE in three series of patients endoscoped for symptoms of gastroesophageal reflux was very similar, 11, 12 and 13%. The prevalence of esophagitis without CLE was higher, 25 to 45%. However, the prevalence of CLE is likely to remain stable, whereas the prevalence of esophagitis depends on whether treatment for reflux has been given.


1 Cameron AJ, Lomboy CT. Barrett's esophagus: age, prevalence, and extent of columnar epithelium. Gastroenterology 1992;103:1241-1245.

2. Naef AP, Savary M. Columnar-lined esophagus: an acquired lesion with malignant predisposition. J Thor Cardiovasc Surg 1975;70:826-834.

3. Burbige EJ, Radigan JJ. Characteristics of the columnar-cell lined (Barrett's) esophagus. Gastrointest Endosc 1979;25:133-136.

4. Starnes VA, Adkins RB, Ballinger JF et al. Barrett's esophagus A surgical entity. Arch Surg 1984;119:563-566.

5. Schnell TO, Sontag SJ, Wannier J et al. Endoscopic screening for Barrett's esophagus, esophageal adenocarcinoma and other mucosal changes in ambulatory subjects with symptomatic gastroesophageal reflux. Gastroenterology 1985:88:1576 (Abstract).

6. Rothery CA, Patterson JE, Stoddard CJ et al. Histological and histochemical changes in the columnar-lined (Barrett's) oesophagus. Gut 1986;27:1062-1068.

7. Winters C, Spurling TJ, Chobanian SJ et al. Barrett's esophagus. A prevalent, occult complication of gastroesophageal reflux disease. Gastroenterology 1987;92:118-124.

8. Gore S, Healey CJ, Sutton R et al. Regression of columnar-lined (Barrett's) oesophagus with continuous omeprazole therapy. Gut 1992;33(suppl):S32 (Abstract).

9. Sampliner RE, Mackel C, Jennings D et al. Effect of 12 months of a proton pump inhibitor (lansoprazole) on Barrett's esophagus - a randomized trial. Gastroenterology 1992;102:A157 (Abstract).

10. Mann NS, Tsai MF, Nair PK. Barrett's esophagus in patients with symptomatic reflux esophagitis. Am J Gastroenterol 1989;84:1494-1496.

Publication date: May 1994 OESO©2015