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Gut 2003;52:194-198 doi:10.1136/gut.52.2.194
  • Stomach

Inflammation and intestinal metaplasia at the squamocolumnar junction in young patients with or without Helicobacter pylori infection

  1. A Oksanen1,
  2. P Sipponen2,
  3. R Karttunen3,
  4. H Rautelin4
  1. 1Herttoniemi Municipal Hospital, FIN-00099 Helsinki, Finland, and Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki and Helsinki University Central Hospital Laboratory Diagnostics, FIN-00014 Helsinki, Finland
  2. 2Department of Pathology, Jorvi Hospital, FIN-02740 Espoo, Finland
  3. 3Department of Medical Microbiology, University of Oulu, FIN-90220 Oulu, Finland
  4. 4Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki and Helsinki University Central Hospital Laboratory Diagnostics, FIN-00014 Helsinki, Finland
  1. Correspondence to:
    Dr A Oksanen, Herttoniemi Hospital, PL 6300, FIN-00099 Helsinki, Finland;
    aino.oksanen{at}hel.fi
  • Accepted 3 September 2002

Abstract

Background: Intestinal metaplasia (IM) in the oesophagus is a known risk factor for adenocarcinoma of the oesophagus. The incidence of adenocarcinoma of the cardia and oesophagus has increased in Western countries simultaneously with a decrease in Helicobacter pylori prevalence.

Aims: To determine the association of H pylori infection with inflammation and IM at the squamocolumnar junction (SCJ) in young individuals.

Patients: A total of 168 (121 women; 72%) consecutive outpatients, ≤45 years, undergoing gastroscopy, and with no prior H pylori eradication treatment.

Methods: Biopsy specimens taken from the antrum, corpus, SCJ, and oesophagus were assessed according to the updated Sydney system, and type of IM (complete or incomplete) was determined. Serum samples from H pylori positive patients were studied for CagA antibodies.

Results: In 86% of 37 patients with gastritis in the antrum and/or corpus (24 histologically H pylori positive) and in 23% of 125 patients with a healthy stomach, inflammation was present in the glandular mucosa at the SCJ. In the latter, cardiac mucosa more often than fundic mucosa at the SCJ was inflamed (p<0.001), the inflammation was usually milder in nature, and was associated with signs of reflux disease. IM (incomplete or complete) at the SCJ was evident in nine of those 24 with a healthy stomach and inflamed cardiac mucosa at the SCJ but in none of those with H pylori gastritis.

Conclusions: IM at the SCJ can also appear in young individuals in whom it seems to be associated with reflux related isolated inflammation in cardiac mucosa at the SCJ but not with H pylori gastritis.

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