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. 2007 Mar;56(3):436.

Authors' reply

Robertino Mera 1,2,3,4, Elizabeth T H Fontham 1,2,3,4, Luis E Bravo 1,2,3,4, Juan C Bravo 1,2,3,4, Maria Blanca Piazuelo 1,2,3,4, Maria Constanza Camargo 1,2,3,4, Pelayo Correa 1,2,3,4
PMCID: PMC1856808  PMID: 17339250

We appreciate the interest given to our article (Gut 2005;54:1536–40) by Bhuiyan and Mencias Vera1 as well as by Gillen and McColl.2 Both letters requested individual scores for atrophy and intestinal metaplasia at baseline and at 12 years of follow‐up. Table 1 shows the scores.

Table 1 Histopathology scores at baseline and at 12 years of follow‐up in patients treated and free of Helicobacter pylori infection at 12 years.

Diagnosis at baseline Histopathology score, mean (95% CI)
Baseline 12 years
Atrophy 3.57 (3.54 to 3.60) 1.87 (1.44 to 2.29)
Intestinal metaplasia 4.46 (4.43 to 4.50) 3.83 (3.56 to 4.10)
Total 3.77 (3.68 to 3.86) 3.18 (3.10 to 3.26)

We wish to emphasise that the histopathology score (table 1, fig 1 in the original article) was based on the global diagnosis and reflects the grade of atrophy and dysplasia, and the type and extent of intestinal metaplasia. The inflammatory infiltrate was not part of this histopathology score. Therefore, the resolution of the inflammatory infiltrate does not explain the fall in the average histopathology score. Acute and chronic inflammatory scores were classified separately in the antrum and the corpus according to the updated Sydney System in an ordinal scale (0–3). Figure 2 in the original article shows the average values in the antrum over time (Gut 2005;54:1536–40).

Objective evidence of the regression of gastric atrophy was reported by our group in a previous report.3 We showed, in a subset of patients of the same cohort, that subjects cured of Helicobacter pylori infection after 6 years of follow‐up showed a major reduction of atrophy indices in the antrum, evaluated by strict morphometric techniques.

As our trial was based on precancerous end points, the size and duration in this study are insufficient to assess results on the basis of gastric cancer as an end point. Therefore, comparisons of results among studies with different end points should be made with caution.

Finally, we apologise for the error that Gillen and McColl brought to our attention, which does not affect any of our conclusions. The correct number of subjects with intestinal metaplasia at baseline who were Helicobacter pylori negative at 12 years is 37/182 or 20% (instead of 70/182).

We hope these clarifications help in the interpretation of our findings and conclusions.

Footnotes

Competing interests: None.

References

  • 1.Bhuiyan A, Mencias Vera C J. Association of preneoplastic gastric lesions and H. pylori [electronic response to Mera et al. Long term follow up of patients treated for Helicobacter Pylori infection]. Gut 2005. http://gut.bmj.com/cgi/eletters/54/11/1536#1180 (accessed 23 January 2007)
  • 2.Gillen D, McColl K E. Effect of Helicobacter pylori eradication on precancerous lesions. Gut 2006551054. [PMC free article] [PubMed] [Google Scholar]
  • 3.Ruiz B, Garay J, Correa P.et al Morphometric evaluation of gastric antral atrophy: improvement after cure of Helicobacter pylori infection. Am J Gastroenterol 2001963281–3287. [DOI] [PubMed] [Google Scholar]

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