N Sakaki1, H Kozawa, N Egawa, Y Tu, M Sanaka. 1. Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital, Bunkyo-ku, Tokyo, Japan. sakaki-k@komagome-hospital.bunkyo.tokyo.jp
Abstract
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.
AIM: To ascertain the progression of atrophic gastritis due to Helicobacter pyloriinfection, 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. pyloriinfection.
Authors: Tan Han Loong; Ngiu Chai Soon; Nik Ritza Kosai Nik Mahmud; Jeevinesh Naidu; Rafiz Abdul Rani; Nazefah Abdul Hamid; Marjanu Hikmah Elias; Isa Mohamed Rose; Azmi Tamil; Norfilza M Mokhtar; Raja Affendi Raja Ali Journal: Biomed Rep Date: 2017-09-20
Authors: Harry Hua-Xinag Xia; Shiu Kum Lam; Wai Man Wong; Wayne Hsing-Cheng Hu; Kam Chuen Lai; Sau Hing Wong; Suet Yi Leung; Siu Tsan Yuen; Nicholas A Wright; Benjamin Chun-Yu Wong Journal: World J Gastroenterol Date: 2003-06 Impact factor: 5.742