Correspondence

Atrophic Gastritis and Helicobacter pylori in Reflux Esophagitis

N Engl J Med 1996; 335:750-751September 5, 1996

Article

To the Editor:

Kuipers et al. (April 18 issue)1 describe an increased risk of atrophic gastritis, associated with an increased risk of gastric cancer,2 in patients with reflux esophagitis and Helicobacter pylori infection who are treated with omeprazole. A recent consensus statement from the National Institutes of Health (NIH) recommended using antimicrobial therapy in addition to an antisecretory agent only in H. pylori–infected patients who have peptic ulcers.3 Kuipers et al. suggest that treating H. pylori–infected patients with proton-pump inhibitors alone, whether they have ulcers or not, may increase the risk of atrophic gastritis and, consequently, of gastric cancer.

As a pediatric gastroenterologist, I see a substantial number of low-income children infected with H. pylori, the majority of whom do not have ulcers.4 Although the incidence of gastric cancer in the United States is low and H. pylori infection relatively common,5 it is crucial that the NIH consensus statement be reexamined in the light of these recent data. Broadening the indications for antimicrobial therapy not only may prove cost effective, by decreasing the need for long-term acid-suppressing therapy, but also may provide the best long-term outcome by reducing the risk of gastric cancer. Research is needed to establish whether all children and adults with H. pylori infection should receive antimicrobial therapy to eradicate this bacterium.

Anthony H. Repucci, M.D.
MetroHealth Medical Center, Cleveland, OH 44109-1998

5 References

1
Kuipers EJ, Lundell L, Klinkenberg-Knol EC, et al. Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Engl J Med 1996;334:1018-1022
Full Text | Web of Science | Medline

2
Sipponen P, Kekki M, Haapakoski J, Ihamaki T, Siurala M. Gastric cancer risk in chronic atrophic gastritis: statistical calculations of cross-sectional data. Int J Cancer 1985;35:173-177
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3
NIH Consensus Development Panel on Helicobacter pylori in Peptic Ulcer Disease. Helicobacter pylori in peptic ulcer disease. JAMA 1994;272:65-69
CrossRef | Web of Science

4
Prieto G, Polanco I, Larrauri J, Rota L, Lama R, Carrasco S. Helicobacter pylori infection in children: clinical, endoscopic, and histologic correlations. J Pediatr Gastroenterol Nutr 1992;14:420-425
CrossRef | Web of Science | Medline

5
Asaka M, Kimura T, Kato M, et al. Possible role of Helicobacter pylori infection in early gastric cancer development. Cancer 1994;73:2691-2694
CrossRef | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: We agree that a reexamination of the indications for H. pylori eradication is needed. Such eradication will probably not reduce the need for long-term acid-suppressing therapy in patients with gastroesophageal reflux disease, but it may substantially reduce their risk of atrophic gastritis. Current data support our hypothesis that the risk of H. pylori–induced atrophic gastritis depends on the acid output. We therefore favor the eradication of H. pylori in patients with gastroesophageal reflux who are treated with profound acid-suppressive maintenance therapy.

We agree with Repucci that because the World Health Organization has defined H. pylori as a carcinogen,1 there is a clear need for further research on, and discussion of, population-based programs of screening and eradication. On the basis of the very low rate of reinfection after successful eradication of H. pylori 2 and the estimate that 75 percent of gastric cancers and 90 percent of peptic ulcers are attributable to this bacterium,3 the costs and benefits of such programs can be determined. They may, for instance, be compared with the costs and benefits of screening programs for the early detection of cervical dysplasia. Nevertheless, we still lack many additional data needed to establish the validity of such calculations.

Ernst J. Kuipers, M.D., Ph.D.
Elly Klinkenberg-Knol, M.D., Ph.D.
Stephan G.M. Meuwissen, M.D., Ph.D.
Free University Hospital, Amsterdam, the Netherlands

Lars Lundell, M.D., Ph.D.
Sahlgren's Hospital, Gothenburg, Sweden

3 References

1
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Schistosomes, liver flukes and Helicobacter pylori. Vol. 61 of IARC monographs on the evaluation of carcinogenic risks to humans. Lyon, France: International Agency for Research on Cancer, 1994.

2
van der Hulst RWM, Koycu B, Keller JJ, et al. H. pylori reinfection after successful eradication analyzed by RAPD or RFLP. Gastroenterology 1996;110:Suppl:A284-A284 abstract.
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