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

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OESO©2015
 
Volume: Barrett's Esophagus
Chapter: Pathophysiology
 

Helicobacter pylori and intestinal metaplasia at the esophagogastric junction: the US experience

R.K.H. Wong (Washington)

The US experience concerning esophagogastric junction-specialized intestinal metaplasia (EGJ-SIM) is varied. First, there is a problem with nomenclature. There are several terms used to describe specialized intestinal metaplasia (IM) 0-3 cm below the esophagogastric junction (EGJ): EGJSIM, cardia-specialized IM, intestinal metaplasia at the gastroesophageal junction (IMAGE) and ultra short segment Barrett's esophagus (SSBE). Investigators also use the term cardia and fundus to mean arbitrarily 0-3 cm below the EGJ, however, the term "cardia" to a histologist means mucous secreting glands just below and adjacent to the squamocolumnar junction. Recent studies by Kilgore et al. [1], indicate that it is a real entity measuring X = 1.8 mm (range: 1-4 mm).

Table I. Cardia intestinal metaplasia: the USA experiences.

In the US experience, there are 11 articles concerning EGJ-SIM (Table I). Prior to 1997, most of these articles dealt with the prevalence of EGJ-SIM. From 1998-2000, 4 articles suggested that H. pylori was the etiology of this entity while 2 implicated gastroesophageal reflux disease (GERD) and 1 suggested that both GERD and H. pylori caused EGJ-SIM.

Studies for H. pylori as a cause of esophagogastric junctionspecialized intestinal metaplasia

Goldblum et al. [2] studied a GERD and non-GERD population (n = 87). In both groups, the prevalence of H. pylori infection was similar: 41-48%. In the patients with carditis, H. pylori infection was similar: 40-41% for both the control and GERD population. EGJSIM was noted in 23% of controls and 3% of GERD subjects but 100% of control and GERD patients were infected with H. pylori. This study strongly suggested that H. pylori was the cause of EGJ-SIM.

Chen et al. [3], showed that as the degree of carditis increased, the infectivity rate of H. pylori increased suggesting that carditis was closely associated with H. pylori infection.

Studies for gastroesophageal reflux disease being the cause of esophagogastric junction-specialized intestinal metaplasia

Lembo et al. [4] in a study of GERD patients only (n = 30), noted that EGJ-SIM was present at the squamocolumnar junction (biopsies that had squamous and columnar tissue) in 33% of patients studied. Carditis and EGJ-SIM was significantly more prevalent at the squamocolumnar junction (Z-line) as compared to locations 1-3 cm below the squamocolumnar junction. Only 13% of patients in this study were H. pylori positive. This study showed that the discrepancy between EGJ-SIM prevalence may relate to the location of the biopsy. If the biopsy is closer or adjacent to the squamocolumnar junction, a higher prevalence will be noted. The authors also felt that EGJ-SIM was related to GERD rather than H. pylori.

Oberg et al. [5] noted similar findings with 96% of patients having carditis when both squamous and columnar tissue was noted on biopsy.

Study in favor of both H. pylori and gastroesophageal reflux disease as a cause of esophagogastric junction-specialized intestinal metaplasia

Goldstein et al. [6] studied cardia biopsies in 150 patients undergoing esophagogastric disease for upper gastrointestinal symptoms. He noted that carditis was significantly associated with esophageal inflammation in patients who were H. pylori negative. In H. pylori positive patients, carditis was most closely associated with antral inflammation. He concluded that carditis and EGJ-SIM was multifactorial being caused by either H. pylori or GERD.

Overall, the US studies suggest that biopsing the squamocolumnar junction and incorporating both the esophageal and columnar tissue in the biopsy may result in a higher yield of both carditis and EGJ-SIM. Both H. pylori and GERD are causes of EGJ-SIM.

References

1. Kilgore SP, Ormsby AH, Gramlich TL, Rice TW, Richter JE, Falk GW, Goldblum JR. The gastric cardia, fact or fiction. Am J Gastroenterol 2000;95(4):921-924.

2. Goldblum JR, Vicari JJ, Falk GW, Rice TW, Peek RM, Easley K, Richter JE. Inflammation and intestinal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection. Gastroenterology 1998;114(4):633-639.

3. Chen YY, Antonioli DA, Spechler SJ, Zeroogian JM, Goyal RK, Wang HH. Gastroesophageal reflux disease versus Helicobacter pylori infection as the cause of gastric carditis. Mod Pathol 1998;11(10):950-956.

4. Lembo T, Ippoliti AF, Ramers C, Weinstein WM. Inflammation of the gastro-oesophageal junction (carditis) in patients with symptomatic gastro-oesophageal reflux disease: a prospective study. Gut 1999;45(4):484-488.

5. Oberg S, Peters JH, DeMeester TR, Chandrasoma P, Hagen JA, Ireland AP, Ritter MP, Mason RJ, Crookes P, Bremner CG. Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg 1997;226(4):522-532.

6. Goldstein NS, Karim R. Gastric cardia inflammation and intestinal metaplasia: associations with reflux esophagitis and Helicobacter pylori. Mod Pathol 1999;12(11):1017-1024.

7. Morales TG, Bhattacharyya A, Johnson C, Sampliner RE. Is Barrett's esophagus associated with intestinal metaplasia of the gastric cardia? Am J Gastroenterol 1997;92(10):1818-1822.

8. El Serag HB, Sonnenberg A, Mazen MSc, Jamal MM, Kunkel D, Crooks L, Feddersen RM. Characteristics of intestinal metaplasia in the gastric cardia. Am J Gastroenterol 1999;94(3):622-627.

9. Weston AP, Krmpotich PT, Cherian R, Dixon A, Topalovski M. Prospective evaluation of intestinal metaplasia and dysplasia within the cardia of patients with Barrett's esophagus. Dig Dis Sci 1997;42(3):597-602.

10. Chalasani N, Wo JM, Hunter, JG, Waring JP. Significance of intestinal metaplasia in different areas of esophagus including esophagogastric junction. Dig Dis Sci 1997;42(3):603-607.

11. Spechler SJ, Zeroogian JM, Antonioli DA, Wang HH, Goyal RK. Prevalence of metaplasia at the gastro-oesophageal junction. Lancet 1994;344:1533-1536.

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


Publication date: August 2003 OESO©2015