Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

  Browse by Author
  Browse by Movies
Volume: Barrett's Esophagus
Chapter: Diagnosis

What is the prevalence of intestinal metaplasia at the cardioesophageal junction when there is no columnar epithelium lining the distal esophagus?

D.A. Antonioli (Boston)

Adenocarcinomas arising in Barrett's esophagus and in the gastric cardia have both demonstrated a dramatic increase in prevalence in Western countries over the past three decades [1]. The demographic features of both neoplasms are similar, but the precursor histologic lesion of cardia neoplasms is not clearly defined. However, the evidence suggests that carcinoma of the cardia arises in a background of carditis with intestinal metaplasia (IM) [2]. The genesis of chronic carditis has been a subject of controversy, but it most likely has a multifactorial origin involving H. pylori infection in some patients and gastroesophageal reflux disease in others [3].

Detecting carditis with IM in mucosal biopsy specimens may be useful in defining a subset of patients with carditis requiring more intense surveillance. However, foci of carditis with IM cannot be distinguished from normal or inflamed cardiac mucosa by gross inspection using routine endoscopic techniques. Thus, the reported prevalence of carditis with IM in patients without Barrett's esophagus has varied in recent endoscopic investigations from 6% to 25% [4-10]. There are several reasons for this wide range in prevalence. Since carditis with IM cannot be recognized grossly using routine endoscopy, biopsy sampling has, of necessity, been random. Thus, the greater the number of mucosal samples taken, the more likely that foci of carditis with IM will be detected; the yield of carditis with IM from taking 4 or 5 specimens may be 3 to 4 times greater than from taking only 2 or 3 specimens [4, 5]. The location of the specimens is also important: carditis with IM is more prevalent immediately distal to the gastroesophageal junction than it is 1 to 5 mm below this landmark [4-10]. Finally, the demographics of the population being studied influence the detection rate: carditis with IM is more common in men than women, and in both sexes it increases in prevalence with increasing age [4-10]. Thus, the composition and age of the patient cohort must be considered when evaluating reports on the prevalence of carditis with IM.

Given the limitations of routine endoscopy in detecting carditis with IM, attempts are underway to identify this condition more accurately. One approach is to apply methylene blue to the mucosal surface to highlight areas of intestinalized epithelium [11, 12]. Another technique is the use of enhanced magnification endoscopy in combination with the application of acetic acid to the mucosa to detect architectural patterns of metaplastic (i.e., intestinalized) mucosa [13, 14]. If these techniques can successfully determine the true prevalence of carditis with IM in various populations, they will not only avoid the contradictory results of earlier studies but also provide a framework for evaluating the natural history of carditis with IM and its association with clinical, endoscopic, and other histologic features of carditis.


1. Devesa SS, Blot WJ, Fraumeni JF Jr. Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer 1998;83:2049-2053.

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

3. Chen YY, Antonioli DA, Spechler SJ, et al. Gastroesophageal reflux versus Helicobacter pylori infection as the cause of gastric carditis. Mod Pathol 1998;11:950-956.

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

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

6. Hackelsberger A, Gunther T, Schultze V, et al. Intestinal metaplasia at the gastro-oesophageal junction: Helicobacter pylori gastritis or gastro-oesophageal reflux disease? Gut 1998;43:17-21.

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

8. Pereira AD, Suspiro A, Chaves P, et al. Short segments of Barrett's epithelium and intestinal metaplasia in normalappearing oesophagogastric junction: the same or two different entities? Gut 1998;42:659-662.

9. 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.

10. El-Serag HB, Sonnenberg A, Jamal MM, et al. Characteristics of intestinal metaplasia in the gastric cardia. Am J Gastroenterol 1999;94:622-627.

11. Canto MI, Setrakian S, Petras RE, et al. Methylene blue selectively stains intestinal metaplasia in Barrett's esophagus. Gastrointest Endosc 1996;44:1-7.

12. Morales TG, Bhattacharyya A, Carmargo E, et al. Methylene blue staining for intestinal metaplasia of the gastric cardia with follow-up for dysplasia. Gastrointest Endosc 1998;48:26-31.

13. Guelrud M, Herrera I, Essenfeld H, Castro J. Enhanced magnification endoscopy: a new technique to identify specialized intestinal metaplasia in Barrett's esophagus. Gastrointest Endosc 2000:51:AB91.

14. Guelrud M, Herrera I. Acetic acid improves identification of remnant islands of Barrett's epithelium after endoscopic therapy. Gastrointest Endosc 1998;47:512-515

Publication date: August 2003 OESO©2011