Abstract:Objective To investigate the pathological features of primary bile reflux gastritis (BRG) in the elderly. Methods Clinical data of 77 elderly patients with primary BRG diagnosed by endoscopy (observation group) and another 78 elderly patients suffering from chronic gastritis by Helicobacter pylori (Hp) infection but not with bile reflux (control group) admitted in our hospital from January 2013 to August 2014 were collected and retrospectively analyzed. The pathological changes in the gastric mucosa tissue were observed and compared between the 2 groups. Results The Hp infection rate was 19.5% in the primary BRG patients. The rates of mild, moderate and severe gastritis were 32.5% vs 11.5%, 58.4% vs 34.6% and 9.1% vs 53.8% in the observation group and the control groups respectively. Neutrophils infiltrating classification (no, mild, moderate and severe) were 83.1% vs 41.0%, 11.7% vs 20.5%, 5.2% vs 32.1% and 0.0% vs 6.4% respectively for the 2 groups. The detection rates of lymphoid follicles, intestinal metaplasia and gastric mucosal atrophy were 4.3% vs 26.9%, 5.2% vs 17.9% and 6.5% vs 25.6%, respectively between them. What’s more, between the Hp-positive and Hp-negative patients from the observation group, the ratios of mild, moderate and severe inflammation were 13.3% vs 37.1%, 53.3% vs 59.7% and 33.3% vs 3.2% respectively, the ratios of no, mild, moderate and severe infiltration of neutrophils were 53.3% vs 41.0%, 20.0% vs 9.7%, 20.0% vs 0.0% and 6.7% vs 0.0%, respectively, and the rates of lymphoid follicles, intestinal metaplasia and gastric grand atrophy were 53.3% vs 4.8%, 0.0% vs 6.5% and 0.0% vs 8.1%, respectively. Conclusion Primary bile reflux results in chronic inflammation in gastric mucosa, intestinal metaplasia, and gland atrophy in the elderly patients. But the incidence of BRG is lower than that of chronic gastritis due to Hp infection. Neutrophils infiltration and lymph follicles formation are mainly associated with Hp infection. However, for the patients with primary BRG, Hp infection does not increase the risks of mucosal atrophy and intestinal metaplasia.