BACKGROUND: Atrophic gastritis, involving the gastric body mucosa, predisposes to gastric neoplastic lesions (GNL). However, regular gastroscopic-histological follow-up for GNL is not recommended for patients with atrophic gastritis. AIM: To evaluate risk factors for the progression to GNL in a cohort of patients with atrophic gastritis. METHODS: A total of 300 patients with atrophic gastritis [205 women, aged 54 (18-78) years] underwent gastroscopy with six gastric antrum and body biopsies. All patients had at least one follow-up gastroscopy/histology at an interval of at least 1 year after the atrophic gastritis diagnosis. Baseline clinical and histological features were analysed as risk factors for the development of GNL by Cox-regression. RESULTS: During a median follow-up of 4.3 (1-16.5) years, 15 GNL were detected in 14 of the 300 patients with atrophic gastritis: three were gastric cancer, whereas 12 were non-invasive neoplasia. The annual incidence for GNL was 1%. Cox-regression analysis identified the following risk factors: age over 50 years (HR 8.8, 95%CI 1.2-68.4), atrophic pangastritis (HR 4.5, 95% CI 1.5-14.1) and severe intestinal metaplasia in the gastric body (HR 4.0, 95% CI 1.3-11.8). CONCLUSIONS: Atrophic pangastritis, severe body intestinal metaplasia and/or age over 50 years increase the risk for developing GNL in patients with atrophic gastritis. In this subset of patients, an endoscopic-histological follow-up for GNL surveillance may be worthwhile.
BACKGROUND:Atrophic gastritis, involving the gastric body mucosa, predisposes to gastric neoplastic lesions (GNL). However, regular gastroscopic-histological follow-up for GNL is not recommended for patients with atrophic gastritis. AIM: To evaluate risk factors for the progression to GNL in a cohort of patients with atrophic gastritis. METHODS: A total of 300 patients with atrophic gastritis [205 women, aged 54 (18-78) years] underwent gastroscopy with six gastric antrum and body biopsies. All patients had at least one follow-up gastroscopy/histology at an interval of at least 1 year after the atrophic gastritis diagnosis. Baseline clinical and histological features were analysed as risk factors for the development of GNL by Cox-regression. RESULTS: During a median follow-up of 4.3 (1-16.5) years, 15 GNL were detected in 14 of the 300 patients with atrophic gastritis: three were gastric cancer, whereas 12 were non-invasive neoplasia. The annual incidence for GNL was 1%. Cox-regression analysis identified the following risk factors: age over 50 years (HR 8.8, 95%CI 1.2-68.4), atrophic pangastritis (HR 4.5, 95% CI 1.5-14.1) and severe intestinal metaplasia in the gastric body (HR 4.0, 95% CI 1.3-11.8). CONCLUSIONS:Atrophic pangastritis, severe body intestinal metaplasia and/or age over 50 years increase the risk for developing GNL in patients with atrophic gastritis. In this subset of patients, an endoscopic-histological follow-up for GNL surveillance may be worthwhile.
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