Giris ve Amaç: Mideye safra asidi reflüsü ve atrofi ile intestinal metaplazi riski çesitli çalismalarda ele alinmis ve farkli sonuçlar elde edilmistir. Bu çalismanin amaci gastrit hastalarinda safra reflüsünün gastrik mukozal atrofi, intestinal metaplazi ve Helicobacter pylori arasindaki iliskiyi arastirmaktir. Gereç ve Yöntem: Çalismaya gastrit bulunan toplam 217 hasta dahil edilmis olup hastalar, intragastrik safra reflüsü bulunan (134 hasta) (n=20 patoloji ile dogrulanmis) ve safra reflüsü bulunmayan 83 hasta kontrol grubu olmak üzere iki gruba ayrilmistir. Helicobacter pylori durumu ve intestinal metaplazi ile gastrit atrofi varligi, safra reflüsü ve safra reflüsü gastriti varligi açisindan degerlendirilmistir. Bulgular: Safra reflüsü bulunan ve bulunmayan gastrit hastalari arasinda Helicobacter pylori pozitifligi (%38.8 vs %45.8), intestinal metaplazi (%32.8 vs %33.7) ve gastrik atrofi (%30.6 vs %30.1) açisindan anlamli fark saptanmamistir. Bununla birlikte safra reflüsü gastritinin patolojik dogrulama eksikligi anlamli derecede daha düsük Helicobacter pylori pozitifligi (%0.00 vs %45.6, p=0.001), intestinal metaplazi (%5.0 vs %37.7, p=0.009) ve gastrik atrofi (%0.0 vs %36.0, p=0.003) ile iliskili bulunmustur. Sonuç: Bulgularimiz safra reflüsü bulunan ve bulunmayan gastrit hastalari arasinda Helicobacter pylori poizitifligi, intestinal metaplazi ve gastrik atrofi oranlarinin benzer oldugunu ortaya çikarmistir. Ancak patolojik olarak dogrulanan safra gastriti bulunan hastalarda Helicobacter pylori, metaplazi ve atrofi sikliginin daha az oldugu saptanmistir
Background and Aims: To investigate the relation between bile reflux and gastric mucosal atrophy, intestinal metaplasia, and Helicobacter pylori status in patients with gastritis. Materials and Methods: A total of 217 patients (mean ± SD; age: 33.2±7.9 years; 51.2% males) with gastritis were divided into two groups: patients with intragastric bile reflux (n = 134; confirmed by pathology in 20 patients) and without bile reflux (control group; n = 83). The status of Helicobacter pylori and presence of intestinal metaplasia and gastric atrophy were evaluated with respect to the presence of bile reflux. Results: A positive Helicobacter pylori status, intestinal metaplasia, and gastric atrophy were observed in 85 (39.2%), 72 (33.2%), and 66 (30.4%) patients, respectively. No significant difference was noted between patients with gastritis with or without bile reflux in terms of a positive Helicobacter pylori status (38.8% vs. 45.8%), intestinal metaplasia (32.8% vs. 33.7%), and gastric atrophy (30.6% vs. 30.1%). However, the pathological confirmation of bile reflux gastritis was associated with a significantly lower rate of Helicobacter pylori positivity (0.0% vs. 45.6%; p = 0.001), intestinal metaplasia (5.0% vs. 37.7%; p = 0.009), and gastric atrophy (0.0% vs. 36.0%; p = 0.003). In patients with bile reflux (n = 134), the intestinal metaplasia and gastric mucosal atrophy rates were similar with respect to the H. pylori status. Conclusion: The rates of Helicobacter pylori positivity, intestinal metaplasia, and gastric atrophy were similar in patients with gastritis with or without bile reflux. However, the frequency of Helicobacter pylori, intestinal metaplasia, and gastric mucosal atrophy was lower in patients with pathologically confirmed biliary gastritis