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Journal of Gastroenterology

, Volume 46, Issue 3, pp 332–338 | Cite as

Etiological difference between ultrashort- and short-segment Barrett’s esophagus

  • Juntaro Matsuzaki
  • Hidekazu SuzukiEmail author
  • Keiko Asakura
  • Yoshimasa Saito
  • Kenro Hirata
  • Toru Takebayashi
  • Toshifumi Hibi
Original Article—Alimentary Tract

Abstract

Background

Barrett’s esophagus has been divided into three categories based on the extent of the metaplasia: long-segment (LSBE), short-segment (SSBE), and ultrashort-segment Barrett’s esophagus (USBE). While both LSBE and SSBE are thought to be induced by gastroesophageal reflux, the etiology of USBE is still unclear.

Methods

We conducted a case–control study to identify the differences in the pathogenesis between SSBE and USBE in a hospital-based population. The endoscopic findings and clinical factors of 199 patients with short-segment endoscopically suspected esophageal metaplasia (SS-ESEM) and 317 patients with ultrashort-segment ESEM (US-ESEM) were compared with those of 199 and 317 age- and gender-matched patients without ESEM.

Results

The severity of gastric mucosal atrophy was marginally associated with the presence of US-ESEM [odds ratio (OR) 1.20, 95% confidence interval (CI) 0.98–1.46, p = 0.08], but not with that of SS-ESEM. On the other hand, the presence of gallstones and that of severe reflux esophagitis were associated with the presence of SS-ESEM (OR 2.19, 95% CI 1.21–3.98; OR 1.72, 95% CI 1.08–2.75), but not with that of US-ESEM. Presence of gastric corpus atrophy without gallstones was associated with the presence of US-ESEM, but not with that of SS-ESEM.

Conclusions

Presence of gastric corpus atrophy was associated with an increased likelihood of the presence of US-ESEM, whereas the presence of gallstones was associated with an increased likelihood of the presence of SS-ESEM, suggesting difference in etiology between US- and SS-ESEM.

Keywords

Short-segment Barrett’s esophagus Gastric corpus atrophy Gallstone 

Notes

Acknowledgments

This study was supported by the Graduate School Doctoral Student Aid Program, Keio University (to J.M.), a Grant-in-Aid for Scientific Research (B) from the Japan Society for the Promotion of Science (22300169, to H.S.), a grant from the Smoking Research Foundation (to H.S.), Keio Gijuku Academic Development Funds (to H.S.).

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Copyright information

© Springer 2010

Authors and Affiliations

  • Juntaro Matsuzaki
    • 1
  • Hidekazu Suzuki
    • 1
    Email author
  • Keiko Asakura
    • 2
  • Yoshimasa Saito
    • 1
  • Kenro Hirata
    • 1
  • Toru Takebayashi
    • 2
  • Toshifumi Hibi
    • 1
  1. 1.Division of Gastroenterology and Hepatology, Department of Internal MedicineKeio University School of MedicineTokyoJapan
  2. 2.Department of Preventive Medicine and Public HealthKeio University School of MedicineTokyoJapan

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