Long-term sequelae of Helicobacter pylori gastritis

EJ Kuipers, AS Peña, HPM Festen, SGM Meuwissen… - The Lancet, 1995 - thelancet.com
EJ Kuipers, AS Peña, HPM Festen, SGM Meuwissen, AM Uyterlinde, R Roosendaal, G Pals
The Lancet, 1995thelancet.com
Chronic Helicobacter pylori gastritis has been put forward as a risk factor for development of
gastric mucosal atrophy and gastric cancer. The purpose of our study was to investigate the
long-term effects of H pylori gastritis on the gastric mucosa. We prospectively studied 49
subjects negative for H pylori and 58 positive subjects for a mean follow-up of 11· 5 years
(range 10-13 years). Serum samples were obtained at the initial and follow-up visits for
determination of H pylori IgG antibodies. Gastroscopies with biopsy sampling were done in …
Abstract
Chronic Helicobacter pylori gastritis has been put forward as a risk factor for development of gastric mucosal atrophy and gastric cancer. The purpose of our study was to investigate the long-term effects of H pylori gastritis on the gastric mucosa. We prospectively studied 49 subjects negative for H pylori and 58 positive subjects for a mean follow-up of 11·5 years (range 10-13 years). Serum samples were obtained at the initial and follow-up visits for determination of H pylori IgG antibodies. Gastroscopies with biopsy sampling were done in all patients at both visits. Biopsy specimens were used for assessment of H pylori infection and histology. Development of atrophic gastritis and intestinal metaplasia occurred in 2 (4%) uninfected and 16 (28%) infected subjects. Regression of atrophy was noted in 4 (7%) infected subjects. Development of atrophic gastritis and intestinal metaplasia was significantly associated with H pylori infection (p=0·0014; odds ratio 9·0, 95% Cl 1·9-41·3). The proportion of atrophic gastritis in the study population showed an annual increase of 1·15% (0·5-1·8%). We conclude that H pylori infection is a significant risk factor for development of atrophic gastritis and intestinal metaplasia. Our findings support strongly the causative role of this infection in gastric carcinogenesis.
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