Ten‐year prospective follow‐up study on the relationship between Helicobacter pylori infection and progression of atrophic gastritis, particularly assessed by endoscopic findings

• Published in: Alimentary pharmacology & therapeutics 2002-04, Vol.16 (s2), p.198-203
• Main Authors: Sakaki, N., Kozawa, H., Egawa, N., Tu, Y., Sanaka, M.
• Format: Article
• Language: English
• Subjects: Adult; Aged; Biopsy; Endoscopy, Gastrointestinal; Female; Follow-Up Studies; Gastric Mucosa - pathology; Gastritis, Atrophic - diagnosis; Gastritis, Atrophic - etiology; Gastritis, Atrophic - pathology; Helicobacter Infections - complications; Helicobacter Infections - microbiology; Helicobacter pylori - isolation & purification; Humans; Male; Middle Aged; Prospective Studies
• ISSN: 0269-2813; 1365-2036
• DOI: 10.1046/j.1365-2036.16.s2.13.x

Aim: To ascertain the progression of atrophic gastritis due to Helicobacter pylori infection, we conducted a 10‐year prospective follow‐up study with annual endoscopy of the stomach. Methods: Prospective endoscopic observation was started in 53 subjects in 1989 and 1990 after informed consent was obtained. The progression of atrophic gastritis was evaluated mainly by the endoscopic pattern of atrophy. Histological assessment was performed on biopsy specimens taken from the lesser curvature of the lower corpus. By 2000, 43 patients (20 males, 23 females, mean age 56.7 years at entry) had completed at least 10 years of endoscopic follow‐up. Results: Eight H. pylori‐negative patients with normal fundic mucosa showed no change endoscopically or histologically. In 35 H. pylori‐positive patients, the progression of histological atrophy was observed in 46% and intestinal metaplasia was observed in 49%. Fifteen of 35 H. pylori‐positive cases exhibited a cephaloid shift of the endoscopic atrophic border. The cephaloid shift of the atrophic area occured suddenly. The cumulative progression rate of atrophic patterns was 6% after 2 years, 22% after 4 years, 34% after 6 years and 43% after 10 years. These atrophic changes were related to neutrophil infiltration. Conclusion: The progression of atrophic gastritis is a result of chronic active gastritis caused by H. pylori infection.