Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
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OESO©2015
 
Volume: Barrett's Esophagus
Chapter: Short Barrett's esophagus
 

Can the prevalence of short segment Barrett's esophagus be accurately evaluated?

P. Sharma (Kansas City)

Intestinal metaplasia (IM) in the distal esophagus can occur in the form of tongues of columnar mucosa in the distal esophagus i.e. short segment Barrett's esophagus (SSBE). Barrett's esophagus was defined initially when columnar mucosa extended at least 3 cm proximal to the anatomic gastroesophageal junction (GEJ) [1]. However, recent studies have suggested that dysplasia and adenocarcinoma can also be associated with SSBE i.e. columnar mucosa < 3 cms in length [2].

Barrett's esophagus (esophageal IM) occurs secondary to reflux of gastric contents into the esophagus i.e. gastroesophageal reflux (GERD), leading to chronic inflammation of the normal squamous epithelium, which is subsequently replaced by columnar mucosa. However, for IM at the GEJ or the gastric cardia the exact relationship with Helicobacter pylori, GERD or both and other factors is currently unclear, although most of the studies suggest a link with H. pylori.

Short segment Barrett's esophagus

The diagnosis of SSBE is made when there is endoscopic evidence of columnar appearing mucosa in the distal esophagus < 3 cm in length and biopsies showing IM [2]. This relies on the recognition of the upward displacement of the squamocolumnar junction in relation to the GEJ. Identification of the GEJ is very crucial in identifying SSBE and endoscopically, the proximal margin of the gastric folds which coincide with the pinch of the end of the tubular esophagus has been reported as a reliable marker for the GEJ [3].

The prevalence of SSBE (Table I) varies from 2-12% of patients undergoing upper endoscopy. Clinical and epidemiologic features of patients with SSBE resemble those of long segment Barrett's esophagus (LSBE). SSBE patients are predominately white males with a history of gastroesophageal reflux symptoms.

Weston et al. prospectively evaluated the patient demographics and prevalence of SSBE (defined as < 2 cms.) in patients undergoing routine upper endoscopy [5]. Two hundred and thirty seven patients wereexamined and SSBE wassuspected in 42 patients but histologically confirmed in only 48%. GERD symptoms werepresent in 53% of the SSBE patients and a hiatal hernia was present in the majority. Another study by Johnston et al. studied 172 consecutive patientspresenting for upper endoscopy [6]. The prevalence of SSBE < 2 cms) was 2.4%. In this study, Caucasians with GERD symptoms were more likely to be diagnosed with SSBE.

Table I. Prevalence of intestinal metaplasia in the esophagus and the gastric cardia.

Cardia intestinal metaplasia

Biopsy specimens obtained from the GEJ or the gastric cardia (below a normally located squamo columnar junction) may reveal IM [10,11]; terminologies used include cardia IM, or esophagogastric junction specialized intestinal metaplasia (EGJ-SIM). The prevalence of cardia IM varies between 5% and 23% [4-9]. As opposed to Barrett's esophagus, cardia IM has an increased prevalence in African Americans and is frequently associated with IM in the body or the antrum of the stomach. The etiology of cardia IM is controversial. In a study by Genta et al., H. pylori was detected in the cardia of 95% of the studied subjects [12]. Goldblum et al. evaluated the relationship between cardia IM and H. pylori and found that the prevalence of cardia IM was similar in patients with and without GERD but was significantly associated with H. pylori infection [13]. In contrast, Oberg et al. have suggested that cardia IM may be related to GERD and in this study cardia IM was associated with decreased lower esophageal sphincter pressure, shorter sphincter length and increased esophageal acid exposure [14]. Moreover, there may be differences in the frequency of dysplasia in patients with SSBE versus cardia IM. In a recent study of 177 patients with SSBE, the dysplasia prevalence was 11.3% with a dysplasia incidence of 4.6% per year [15]. In contrast, 76 patients with cardia IM, the dysplasia prevalence was 1.3% with a dysplasia incidence of 1.5% per year. Cardia IM patients were significantly different from the SSBE patients with respect to age, ethnicity, dysplasia prevalence and incidence.

Conclusion

The prevalence of SSBE is approximately 8% in patients presenting for endoscopy for GERD symptoms. It is more prevalent than LSBE and appears to be distinct from cardia IM.

References

1. Skinner DB, Walther BC, Riddell RH, et al. Barrett's esophagus: comparison of benign and malignant cases. Ann Surg 1983;198:554-565.

2. 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.

3. McClave SA, Boyce HW, Gottfried MR. Early diagnosis of columnar-lined esophagus: a new endoscopic criterion. Gastrointest Endosc 1987;33:413-416.

4. Spechler SJ, Zeroogian JM, Antonioli DA, et al. Prevalence of metaplasia at the gastro-oesophageal junction. Lancet 1994;344:1533-1536.

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. Johnston MH, Hammond AS, Laskin W, et al. The prevalence and clinical characteristics of short segments of specialized intestinal metaplasia in the distal esophagus on routine endoscopy. Am J Gastroenterol 1996;91:1507-1511.

7. Morales TG, Sampliner RE, Bhattacharyya A. Intestinal metaplasia of the gastric cardia. Am J Gastroenterol 1997;92:414-418.

8. Chalasani N, Wo JM, Hunter JG, et al. Significance of intestinal metaplasia in different areas of esophagus including esophagogastric junction. Dig Dis Sci 1997;42:603-607.

9. Hirota WK, Loughney TM, Lazas DJ, et al. Specialized intestinal metaplaia;dysplasia and cancer of the esophagus and esophagogastric junction;prevalence and clinical data. Gastroenterology 1999;116:277-285.

10. Spechler SJ. The role of gastric carditis in metaplasia and neoplasia at the gastroesophageal junction. Gastroenterology 1999;117:218-228.

11. Sharma P. Recent advances in Barrett's esophagus: short-segment Barrett's esophagus and cardia intestinal metaplasia. Sem Gastrointest Dis 1999;10(3):93-102.

12. Genta RM, Huberman RM, Graham DY. The gastric cardia in Helicobacter pylori infection. Hum Pathol 1994;25:915919.

13. Goldblum JR, Vicari JJ, Falk GW, et al. Inflammation and intestinal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection. Gastroenterology 1998;114:633-639.

14. Oberg S, Peters JH, DeMeester TR, et al. Inflammation and specialized intestinal metaplasia of cardiac mucosa in a manifestation of gastroesophageal reflux disease. Ann Surg 1997;226:522-530.

15. Sharma P, Weston AP, Morales T, Topalovski M, Mayo MS, Sampliner RE. Relative risk of dysplasia for patients with intestinal metaplasia in the distal oesophagus and in the gastric cardia. Gut 2000;46:9-13.


Publication date: August 2003 OESO©2015