[Gastric mucosa lesions in gastric ulcer disease. Initial study and 1-year follow-up after Helicobacter pylori eradication]

F Bermejo, D Boixeda, J P Gisbert, J M Sanz, V Defarges, G Alvarez Calatayud, C Martín de Argila
Gastroenterología y Hepatología 2000, 23 (6): 269-74

OBJECTIVE: To study histologic gastric mucosa lesions in patients with gastric ulcer disease and to assess their evolution in the year after Helicobacter pylori eradication.

METHODS: Seventy-three patients with gastric ulcer were prospectively studied. On endoscopy, biopsy specimens were taken from the antrum and gastric body for hematoxylin and eosin staining and urease testing. Serology and 13C-urea breath test were carried out. Fifty-six patients treated for H. pylori infection were monitored with histologic study at months 1, 6 and 12 after therapy to eradicate H. pylori infection.

RESULTS: In patients with gastric ulcer, the prevalence of H. pylori was 86.3% (95% CI: 76-92%). Similar percentages in patients with chronic gastritis (CG) and in those with active chronic gastritis (ACG) were noted in the antrum and gastric body. However, severe active chronic gastritis was more prevalent in the antrum (p < 0.01). In patients with H. pylori infection who were not treated with non-steroidal anti-inflammatory drugs (NSAIDs), the percentages of both CG and ACG were higher than those observed in patients with both risk factors (p < 0.01) and in those treated with NSAIDs and with no infection (p < 0.0001). The prevalence of glandular atrophy (17.8%; 11-28%) and of intestinal metaplasia (68.5%; 57-78%) was higher in the antrum than in the gastric body (4.1%; 1-11% and 16.4%; 10-26%, respectively) (p < 0.01). In the antrum of patients with successful treatment, the percentages of CG:ACG before treatment and 1, 6, and 12 months after treatment completion were: 100%:97%, 74%:14%, 44%:11% and 11%:2%, respectively. In the gastric body these rates were: 88%:86%, 51%:14%, 23%:4% and 4%:0%. Improvement of CG was observed at month 1 after treatment completion, which was then confirmed at months 6 and 12 (p < 0.01) whereas improvement of ACG was most often achieved at month 1 after treatment completion (p > 0.001). No changes in atrophy and intestinal metaplasia were observed after H. pylori eradication.

CONCLUSIONS: Histologic gastritis associated with gastric ulcer disease involves both the antrum and gastric body, although prevalence of severe ACG, atrophy and intestinal metaplasia were higher in the antrum. Histologic gastritis were closely related to H. pylori infection but is unrelated to NSAIDs. H. pylori eradication results in progressive CG improvement over the first year, as well as in early ACG improvement (as soon as 1 month after treatment completion); however, atrophy and intestinal metaplasia remain unchanged.

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