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Etiology of intestinal metaplasia at the gastroesophageal junction.
Surg Endosc 2003; 17(1):43-8SE

Abstract

BACKGROUND

Intestinal metaplasia occurs in the esophagus as a consequence of gastroesophageal reflux disease and in the stomach secondary to H. pylori infection. The etiology of intestinal metaplasia limited to the gastroesophageal junction or cardia (CIM) is disputed. We hypothesized that CIM has dual etiologies: gastroesophageal reflux in some, H. pylori infection in others, and that cytokeratin immunostaining can help to differentiate between these two etiologies.

METHODS

We defined CIM as the presence of intestinal metaplasia within cardiac mucosa on biopsy from an endoscopically normal-appearing gastroesophageal junction. Thirty patients with CIM who had multiple biopsy specimens taken from the esophagus, gastroesophageal junction, and stomach were identified. Tissue blocks from biopsy specimens taken at the gastroesophageal junction were sectioned and immunostained for cytokeratins 7 and 20. The cytokeratin 7/20 staining of the CIM in each patient was determined to be either a Barrett's or non-Barrett's pattern. H. pylori infection was assessed by Giemsa staining of antral biopsy specimens.

RESULTS

H. pylori infection was present in 16 patients. A Barrett's cytokeratin 7/20 staining pattern in the CIM was present in only 46% of the H. pylori-positive patients, as compared to 86% in the 14 patients with CIM and no H. pylori (p = 0.025). Objective evidence of reflux disease was present in 71% of patients with CIM and no H. pylori, as compared to 31% of patients with H. pylori.

CONCLUSIONS

The two different patterns of cytokeratin 7/20 staining found in patients with CIM support the concept of dual etiologies for CIM. A Barrett's staining pattern was associated with objective evidence of gastroesophageal reflux and the absence of H. pylori, suggesting that cytokeratin 7/20 immunostaining is useful to determine the likely etiology of CIM.

Authors+Show Affiliations

Department of Surgery, Keck School of Medicine, University of Southern California, 1510 San Pablo Street, 514, Los Angeles, CA 90033, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12364989

Citation

Balaji, N S., et al. "Etiology of Intestinal Metaplasia at the Gastroesophageal Junction." Surgical Endoscopy, vol. 17, no. 1, 2003, pp. 43-8.
Balaji NS, DeMeester SR, Wickramasinghe KS, et al. Etiology of intestinal metaplasia at the gastroesophageal junction. Surg Endosc. 2003;17(1):43-8.
Balaji, N. S., DeMeester, S. R., Wickramasinghe, K. S., Hagen, J. A., Peters, J. H., & DeMeester, T. R. (2003). Etiology of intestinal metaplasia at the gastroesophageal junction. Surgical Endoscopy, 17(1), pp. 43-8.
Balaji NS, et al. Etiology of Intestinal Metaplasia at the Gastroesophageal Junction. Surg Endosc. 2003;17(1):43-8. PubMed PMID: 12364989.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Etiology of intestinal metaplasia at the gastroesophageal junction. AU - Balaji,N S, AU - DeMeester,S R, AU - Wickramasinghe,K S, AU - Hagen,J A, AU - Peters,J H, AU - DeMeester,T R, Y1 - 2002/10/08/ PY - 2002/03/16/received PY - 2002/06/18/accepted PY - 2002/10/5/pubmed PY - 2003/3/4/medline PY - 2002/10/5/entrez SP - 43 EP - 8 JF - Surgical endoscopy JO - Surg Endosc VL - 17 IS - 1 N2 - BACKGROUND: Intestinal metaplasia occurs in the esophagus as a consequence of gastroesophageal reflux disease and in the stomach secondary to H. pylori infection. The etiology of intestinal metaplasia limited to the gastroesophageal junction or cardia (CIM) is disputed. We hypothesized that CIM has dual etiologies: gastroesophageal reflux in some, H. pylori infection in others, and that cytokeratin immunostaining can help to differentiate between these two etiologies. METHODS: We defined CIM as the presence of intestinal metaplasia within cardiac mucosa on biopsy from an endoscopically normal-appearing gastroesophageal junction. Thirty patients with CIM who had multiple biopsy specimens taken from the esophagus, gastroesophageal junction, and stomach were identified. Tissue blocks from biopsy specimens taken at the gastroesophageal junction were sectioned and immunostained for cytokeratins 7 and 20. The cytokeratin 7/20 staining of the CIM in each patient was determined to be either a Barrett's or non-Barrett's pattern. H. pylori infection was assessed by Giemsa staining of antral biopsy specimens. RESULTS: H. pylori infection was present in 16 patients. A Barrett's cytokeratin 7/20 staining pattern in the CIM was present in only 46% of the H. pylori-positive patients, as compared to 86% in the 14 patients with CIM and no H. pylori (p = 0.025). Objective evidence of reflux disease was present in 71% of patients with CIM and no H. pylori, as compared to 31% of patients with H. pylori. CONCLUSIONS: The two different patterns of cytokeratin 7/20 staining found in patients with CIM support the concept of dual etiologies for CIM. A Barrett's staining pattern was associated with objective evidence of gastroesophageal reflux and the absence of H. pylori, suggesting that cytokeratin 7/20 immunostaining is useful to determine the likely etiology of CIM. SN - 1432-2218 UR - https://www.unboundmedicine.com/medline/citation/12364989/Etiology_of_intestinal_metaplasia_at_the_gastroesophageal_junction_ L2 - https://dx.doi.org/10.1007/s00464-002-8944-1 DB - PRIME DP - Unbound Medicine ER -