Alkalen Reflü Gastritin İntragastrik pH ve Helicobacter Pylori Kolonizasyonu Üzerine Etkisi

Amaç: Alkalen reflü gastrit ile Helicobacter pylori ilişkisi hâlen belirsizdir. Duodenogastrik reflü sonucu mideye kaçan safra ve pankres sıvılarının mide mukozasında kimyasal irritasyon ve pH değişikliklerine yol açtığı düşünülmektedir. Ancak intragastrik pH değişikliklerinin Helicobacter pylori üzerine etkisi ve duodenum içeriğinin intragastrik pH’ya etkisi bilinmemektedir. Bu çalışmada alkalen reflü gastrit hastalarında intragastrik pH ile Helicobacter pylori varlığı arasındaki ilişki araştırılmıştır. Gereç ve Yöntemler: Çalışmaya gastroskopide alkalen reflü gastrit tespit edilen (n=30) ve kontrol grubu için antral gastrit tanısı alan hastalar (n=35) dahil edildi. Tüm hastalardan gastroskopi esnasında mide içerisinden alınan sıvı örneğinden pH çalışıldı ve antrumdan alınan örnekten üreaz testi yapıldı. Bulgular: Alkalen reflü gastrit olgularında ortalama intragastrik pH kontrol grubu ile benzerdi (Sırasıyla 3,43±1,94, 3,2±2,02, p=0,504). Hem Alkalen reflü gastrit grubunda hem de kontrol grubunda üreaz testi pozitifliği oranları benzerdi (p=0,461). Her iki grupta intragastrik pH’nın alkali veya asidik olması üreaz testi pozitifliği ile ilişkili değildi. Sonuç: Alkalen reflü gastriti hastalarında da intragastrik pH’nın asidik olduğunu ve hem duodenogastrik safra reflüsünün hem de intragastrik pH değişiklikliklerinin Helicobacter pylori kolonozisyonu üzerine etkisi olmadığını düşünüyoruz.

The Effect of Alkaline Reflux Gasritis on Intragastric pH and Helicobacter Pylori Colonization

Aim: The relationship between alkaline reflux gastritis and Helicobacter pylori remains unclear. It is thought that bile and pancreatic fluids escaping into the stomach as a result of duodenogastric reflux cause chemical irritation and pH changes in the gastric mucosa. However, the effect of intragastric pH changes on Helicobacter pylori and duodenal contents on intragastric pH are not known. The aim of this study was to investigate the relationship between intragastric pH and the presence of Helicobacter pylori in patients with alkaline reflux gastritis. Material and Methods: The patients who detected alkaline reflux gastritis (n = 30) and antral gastritis for the control group (n=35) by gastroscopy were included in the study. During gastroscopy of all patients pH was measured from the liquid sample taken from the stomach and rapid urease test was performed from the sample taken from the antrum. Results: The mean intragastric pH in cases with alkaline reflux gastritis was similar to the control group (3.43±1.94, 3.2±2.02, p=0.504, respectively). The rates of rapid urease test positivity were similar in both alkaline reflux gastritis and control groups (p=0.461). Intragastric pH was found to be alkaline or acidic was not associated with rapid urease test positivity in both groups. Conclusion: We believe that intragastric pH is acidic in patients with alkaline reflux gastritis too and both duodenogastric bile reflux and intragastric pH changes have no effect on Helicobacter pylori colonization.

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