Effect of Helicobacter pyloriinfection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis. Issue 6 (1st June 1999)

• Record Type: Journal Article
• Authors: Nardone, G; Staibano, S; Rocco, A; Mezza, E; D'Armiento, F P; Insabato, L; Coppola, A; Salvatore, G; Lucariello, A; Figura, N; De Rosa, G; Budillon, G
• Is Part Of: Gut. Volume 44:Issue 6(1999)
• Page Start: 789
• Page End: 799
• Publication Date: 1999-06-01
• Subjects: H pylori infection -- atrophic gastritis -- genomic instability -- eradication therapy; Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gut.44.6.789
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : BACKGROUND: Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability. AIM: To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression. METHODS/SUBJECTS: Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer. RESULTS: All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged. CONCLUSIONS: Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.