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. 2007 Sep;41(8):751-5.
doi: 10.1097/MCG.0b013e31802c347d.

Detection rate of Helicobacter pylori against a background of atrophic gastritis and/or intestinal metaplasia

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Detection rate of Helicobacter pylori against a background of atrophic gastritis and/or intestinal metaplasia

Ji Youn Yoo et al. J Clin Gastroenterol. 2007 Sep.

Abstract

Background: To evaluate the detection rate of the CLOtest, Giemsa stain, and culture for the diagnosis of Helicobacter pylori organisms in patients with or without atrophic gastritis (AG) and/or intestinal metaplasia (IM).

Methods: We used either the CLOtest, Giemsa staining, or culture to determine the presence of H. pylori in 430 participants who were documented to be infected with H. pylori from September 2003 to June 2006. The detection rates of the methods were evaluated according to the presence of AG and IM in antrum and body, which were classified using the updated Sydney system classification.

Results: Positivity by the CLOtest markedly reduced depending on the degree of AG and IM in both antrum and body (P<0.05), and the positivity of Giemsa staining was markedly reduced as the degree of IM increased (P<0.01), but was not affected by the degree of AG (P=0.08) in antrum or body. When the results of these tests were evaluated in terms of combinations of AG and IM, the positivity of CLOtest was found to be lower in AG with IM than in AG without IM, (50.0% vs. 80.0% in antrum, 47.5% vs. 78.0% in body, respectively, P<0.01). In addition, the positivity of Giemsa stain was less frequent in AG with IM than in AG without IM in antrum (65.1% vs. 100%, respectively, P<0.01). However, the positivity of Giemsa stain in the body showed no statistical difference between AG without IM and AG with IM (97.6% vs. 91.7%, respectively).

Conclusions: Invasive H. pylori tests, especially the CLOtest, had a lower detection rate for H. pylori in the presence of mucosal atrophy and IM, and this became more prominent in the presence of higher levels of IM and AG.

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Comment in

  • Where have all the Helicobacters gone?
    Genta RM. Genta RM. J Clin Gastroenterol. 2007 Sep;41(8):727-8. doi: 10.1097/MCG.0b013e3180684265. J Clin Gastroenterol. 2007. PMID: 17700419 No abstract available.

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