Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

  Browse by Author
  Browse by Movies
OESO©2011
 
Volume: Barrett's Esophagus
Chapter: Adenocarcinomas
 

Can the rate of degeneration of short segment Barrett's esophagus be evaluated?

P. Sharma (Kansas City)

The recent rapid rise in the incidence of adenocarcinoma of the distal esophagus and the gastric cardia has generated significant interest in the premalignant lesion - Barrett's esophagus [1-3]. The traditional definition of Barrett's esophagus included > 3 cm of columnar mucosa in the distal esophagus. Recent studies have suggested that dysplasia and adenocarcinoma can also be associated with short segment Barrett's esophagus (SSBE) i.e. < 3 cm of columnar mucosa [4]. Barrett's esophagus has now come to be defined by the histological presence of intestinal metaplasia (IM) within esophageal columnar mucosa.

The diagnosis of SSBE requires a combination of endoscopic and histologic criteria. At the time of upper endoscopy, there must be evidence of columnar-appearing mucosa in the distal esophagus which is < 3 cm in length and biopsies from the columnar mucosa must reveal IM [4].

Dysplasia and cancer in short segment Barrett's esophagus

The prevalence of dysplasia in patients with SSBE is approximately 8-10% [5, 6]. Three prospective series have reported the incidence of dysplasia and cancer in patients with SSBE. Sharma et al. studied 59 patients with SSBE (dysplasia prevalence 8.5%) with 32 patients followed for a mean of 36 months [6]. Dysplasia developed in 5 patients, 3 with low-grade dysplasia (LGD) and 2 with high-grade dysplasia (HGD) (dysplasia incidence 5.7% per year). One patient with HGD developed adenocarcinoma of the esophagus during follow-up. Weston et al. reported a dysplasia incidence of 6.1% per year in 26 patients followed for 10.6 + 7.8 months - no cancers developed in this group during follow-up [5]. The incidence of cancer in patients with SSBE (without HGD at index diagnosis) was 0.4% in 69 patients followed for a mean of 3.7 years. This incidence rate was lower, but not significantly different compared to cancer incidence in patients with long segment Barrett's esophagus [7].

Hamilton et al. reported the association of SSBE with esophageal cancer; 64% of adenocarcinomas of the distal esophagus and esophagogastric junction (EGJ) were associated with Barrett's and 34% of esophageal adenocarcinomas were detected in short segments of IM [8]. In one series of 31 cardia adenocarcinomas, 13 were related to Barrett's and 6 of 13 had a Barrett's length of 2.7 ± 1.8 cm [9]. In an autopsy study from the Mayo Clinic of 24 specimens of the EGJ cancers, half of the Barrett's associated tumors had a mucosa length of 1-2.5 cm [10]. Recently, investigators from the Hines VAMC reported that more than 40% of prevalence and incidence esophageal adenocarcinomas in a large population of patients with Barrett's esophagus, were associated with SSBE [11].

Given the potential of SSBE patients to develop dysplasia and cancer, it is prudent to enroll such patients in a surveillance program for the detection of cancer at an early stage. Currently available dysplasia and cancer rates are based on relatively short follow-up periods and additional data are, however, needed regarding the actual incidence of adenocarcinoma in patients with SSBE. This is important before appropriate management strategies and surveillance intervals can be developed.

References

1. Blot WJ, Devesa SS, Kneller RW, et al. Rising incidence of adenocarcinoma of the esophagus and gastric cardia. JAMA 1991;265:1287-1289.

2. Pera M, Cameron AJ, Trastek VF, et al. Increasing incidence of adenocarcinoma of the esophagus and esophagogastric junction. Gastroenterology 1993;104:510-513.

3. Blot WJ, Devesa SS, Fraumeni JF Jr. Continuing climb in rates of esophageal adenocarcinoma:An update. JAMA 1993;270:1320.

4. Sharma P, Morales TG, Sampliner RE. Short-segment Barrett's esophagus. The need for standardization of the definition and of endoscopic criteria. Am J Gastroenterol 1998;93:1033-1036.

5. Weston AP, Krmpotich P, Makdisi WF, et al. Short segment Barrett's esophagus: clinical and histological features, associated endoscopic findings, and association with gastric intestinal metaplasia. Am J Gastroenterol 1996;91:981-986.

6. Sharma P, Morales TG, Bhattacharyya A, et al. Dysplasia in short-segment Barrett's esophagus:A prospective 3-year follow-up. Am J Gastroenterol 1997;92:2012-2016.

7. Rudolph RE, Vaughan TL, Storer BE, et al. Effect of segment length on risk for neoplastic progression in patients with Barrett esophagus. Ann Intern Med 2000;132:612-620.

8. Hamilton SR, Smith R, Cameron JL. Prevalence and characteristics of Barrett esophagus in patients with adenocarcinoma of the esophagus or esophagogastric junction. Hum Pathol 1988;19:942-948.

9. Clark G, Smyrk TC, Burdiles P, et al. Is Barrett's metaplasia the source of adenocarcinomas of the cardia? Arch Surg 1994;129:609-614.

10. Cameron AJ, Lomboy CT, Pera M, et al. Adenocarcinoma of the esophagogastric junction and Barrett's esophagus. Gastroenterology 1995;109:1541-1546.

11. Schnell T, Sontag SJ, Chejfec G, et al. Does more Barrett's really mean more cancer? Comparison of incidence rates of adenocarcinoma in prospectively followed patient cohorts with short and long segments of Barrett's esophagus. Gastroenterology 1998;114:G2783.


Publication date: August 2003 OESO©2011