Effect of Helicobacter pylorieradication on chronic gastritis during omeprazole therapy

• Published in: Gut Vol. 46; no. 5; p. 615
• Main Authors: Schenk, B E, Kuipers, E J, Nelis, G F, Bloemena, E, Thijs, J C, Snel, P, Luckers, A E G, Klinkenberg-Knol, E C, Festen, H P M, Viergever, P P, Lindeman, J, Meuwissen, S G M
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd and British Society of Gastroenterology 01.05.2000; BMJ Publishing Group LTD
• Subjects: Acids; Atrophy; atropy; Bacteria; Biopsy; Compliance; Endoscopy; gastritis; gastro-oesophageal reflux disease; Gastroesophageal reflux; Helicobacter pylori; Histology; Inflammation; omeprazole; Patients; Substance abuse treatment; Ulcers
• ISSN: 0017-5749; 1468-3288
• DOI: 10.1136/gut.46.5.615

BACKGROUND We have previously observed that profound acid suppressive therapy inHelicobacter pylori positive patients with gastro-oesophageal reflux disease is associated with increased corpus inflammation and accelerated development of atrophic gastritis. AIM To investigate ifH pylori eradication at the start of acid suppressive therapy prevents the development of these histological changes. PATIENTS/METHODS In a prospective randomised case control study, patients with reflux oesophagitis were treated with omeprazole 40 mg once daily for 12 months. H pylori positive patients were randomised to additional double blind treatment with omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg twice daily or placebo for one week. Biopsy sampling for histology, scored according to the updated Sydney classification, and culture were performed at baseline, and at three and 12 months. RESULTS In the persistently H pylori positive group (n=24), active inflammation increased in the corpus and decreased in the antrum during therapy (p=0.032 and p=0.002, respectively). In contrast, in theH pylori positive group that becameH pylori negative as a result of treatment (n=33), active and chronic inflammation in both the corpus and antrum decreased (p⩽0.0001). The decrease in active and chronic inflammation in the corpus differed significantly compared with the persistentlyH pylori positive group (both p=0.001). For atrophy scores, no significant differences were observed betweenH pylori eradicated and persistentlyH pylori positive patients within one year of follow up. No changes were observed in the H pylori negative control group (n=26). CONCLUSIONS H pylori eradication prevents the increase in corpus gastritis associated with profound acid suppressive therapy. Longer follow up is needed to determine if H pylori eradication prevents the development of atrophic gastritis.