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J Clin Pathol 2005;58:259-262 doi:10.1136/jcp.2004.022251
  • Original article

CagA in Barrett’s oesophagus in Colombia, a country with a high prevalence of gastric cancer

  1. M Kudo1,2,
  2. O Gutierrez3,
  3. H M T El-Zimaity1,
  4. H Cardona3,
  5. Z Z Nurgalieva1,
  6. J Wu1,
  7. D Y Graham1
  1. 1Michael E DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, TX 77030, USA
  2. 2Hokkaido University, Graduate School of Medicine, Department of Internal Medicine, Gastroenterology and Haematology Section, Kita 15 jo, Nishi 7 Chome, Kita-Ku, Sapporo Hokkaido, 060-8638, Japan
  3. 3National University, Department of Internal Medicine, Gastroenterology Unit, Bogotá, Colombia
  1. Correspondence to:
 Dr H M T El-Zimaity
 Rm 3A-320 (111D), Veterans Affairs Medical Center, 2002 Holcombe Blvd, Houston, Texas 77030, USA; hzimaitybcm.tmc.edu
  • Accepted 28 September 2004

Abstract

Background: In the USA, atrophic gastritis and gastric cancer are rare, whereas gastro-oesophageal reflux disease (GERD) is common. Infection with Helicobacter pylori, especially a CagA positive strain, is unusual in patients with GERD/Barrett’s oesophagus in the USA.

Aim: To examine the relation between Barrett’s oesophagus and CagA positive H pylori in Colombia, a country with a high prevalence of CagA positive H pylori associated atrophic gastritis and gastric cancer.

Methods:Helicobacter pylori and CagA status was determined among Colombian patients with long segment Barrett’s oesophagus and a control group with simple H pylori gastritis. Helicobacter pylori status was determined using a triple stain and CagA status was determined by immunohistochemistry using a specific rabbit anti-CagA serum.

Results: Gastric and oesophageal mucosal biopsies were obtained from 51 patients—39 men (mean age, 57.8 years; SD, 13.1) and 12 women (mean age, 51.8 years; SD, 14.4)—with documented long segment Barrett’s oesophagus. The results were compared with 24 Colombian patients with H pylori gastritis without oesophageal disease. Thirty two patients with Barrett’s oesophagus had active H pylori infection. CagA status was evaluated in a subset of 23 H pylori infected patients with Barrett’s oesophagus, and was positive in eight of these patients compared with 19 of 24 controls (p  =  0.01).

Conclusions: Although most Colombian patients with Barrett’s oesophagus had H pylori infection, CagA positive infections were unusual. These data illustrate how consistent corpus inflammation reduces acid secretion, which prevents Barrett’s oesophagus among those with abnormal gastro-oesophageal reflux barriers.

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