Aim. A study of atrophic gastritis severity and rate in patients with gastric polyps (GP).Materials and methods. The study enrolled 61 patients with hyperplastic (HGP) and 41 — with adenomatous GP (AGP). All patients had 24-h gastric pH-metry, control of the pepsinogen I, II and gastrin-17 levels, in addition to a general clinical, endoscopic, histological examination and testing for Helicobacter pylori.Results. GP patients had benign manifestations prevailed with epigastric heaviness and

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... ow, and a scarce history of H. pylori testing at no control of rendered eradication therapy. A symptomatic proton pump inhibitor treatment in GP was either prescribed or voluntary. Focal atrophic gastritis in endoscopy was revealed in 12 (19.7 %) HGP and 16 (39.0 %) AGP patients, diffused atrophic gastritis — in 49 (80.3 %) HGP and 25 (60.9 %) AGP patients. Low-grade chronic gastritis in histology prevailed in HGP, moderate — in AGP, and severe — in 21.9 % cases. Moderate (27.9 %) to severe (65.6 %) atrophy of gastric mucosa was registered in HGP, with 53.7 and 39.0 % respective AGP cases. Polyp dysplasia was detected in 20 % HGP and 75.6 % AGP cases. Pepsinogen I <25 µg/L at a pepsinogen I/II ratio ><3 was observed in 38 (62.3 %) HGP and 18 (43.9 %) AGP patients. Hypo- and anacidic were 65.6 % HGP and 31.7 % AGP patients. >H. pylori-positive were 52.5 % HGP and 70.7 % AGP cases.Conclusion. A largely similar aetiopathogenesis of gastric polyps and chronic atrophic gastritis warrants the H. pylori diagnosis and a more detailed patient control for chronic gastritis grading and staging, functional insufficiency of gastric mucosa and the severity of hyperplastic and dysplastic change. The H. pylori eradication, in contrast to anti-secretory therapy, allows the containment of chronic gastritis and is a critical measure in gastric cancer prevention.