Lack of effect of acid suppression therapy on gastric atrophy. Nordic Gerd Study Group.

作者: Lars Lundell , Pekka Miettinen , Helge E. Myrvold , Sven A. Pedersen , Kjell Thor

DOI: 10.1053/GAST.1999.0029900319

关键词: Helicobacter pyloriGERDInternal medicineEsophagitisAtrophyBasal (phylogenetics)Intestinal metaplasiaGastroenterologyOmeprazoleRefluxMedicine

摘要: BACKGROUND & AIMS A hypothesis suggesting that profound acid inhibition therapy facilitates and hastens the development of gastric glandular atrophy in patients infected with Helicobacter pylori was investigated this randomized study comparing omeprazole antireflux surgery (ARS) for chronic gastroesophageal reflux disease (GERD). METHODS Patients esophagitis and/or GERD were enrolled; 155 to ARS long-term therapy. Baseline data obtained repeated after 3 years 131 139 omeprazole-treated patients. Histopathologic status oxyntic mucosa assessed according Sydney system. RESULTS Forty H. compared 53 group. Basal gastrin levels significantly higher pylori-infected patients, particularly No further increases serum observed during years. Despite therapy, only slight changes found prevalence inflammation corpus subjects. slow progression these irrespective no obvious difference between treatment regimens. Intestinal metaplasia (all type I) exceptionally arms. CONCLUSIONS Acid-suppressive form maintained neither nor occurrence intestinal

参考文章(30)
Regina Lamberts, Werner Creutzfeldt, Hans G. Strüber, Gorik Brunner, Enrico Solcia, Long-term omeprazole therapy in peptic ulcer disease: Gastrin, endocrine cell growth, and gastritis Gastroenterology. ,vol. 104, pp. 1356- 1370 ,(1993) , 10.1016/0016-5085(93)90344-C
Enrico Solcia, Roberto Fiocca, Ombretta Luinetti, Laura Villani, Laura Padovan, Daniele Calistri, Guglielmina N. Ranzani, Annamaria Chiaravalli, Carlo Capella, Intestinal and diffuse gastric cancers arise in a different background of Helicobacter pylori gastritis through different gene involvement. The American Journal of Surgical Pathology. ,vol. 20, pp. 8- 22 ,(1996) , 10.1097/00000478-199600001-00003
E. Solcia, C. Bordi, W. Creutzfeldt, Y. Dayal, A.D. Dayan, S. Falkmer, L. Grimelius, N. Havu, Histopathological classification of nonantral gastric endocrine growths in man. Digestion. ,vol. 41, pp. 185- 200 ,(1988) , 10.1159/000199786
K. Villako, M. Kekki, H.-I. Maaroos, P. Sipponen, R. Uibo, R. Tammur, A. Tamm, Chronic gastritis: progression of inflammation and atrophy in a six-year endoscopic follow-up of a random sample of 142 Estonian urban subjects. Scandinavian Journal of Gastroenterology. ,vol. 186, pp. 135- 141 ,(1991) , 10.3109/00365529109104000
P CORREA, A MODEL FOR GASTRIC CANCER EPIDEMIOLOGY The Lancet. ,vol. 306, pp. 58- 60 ,(1975) , 10.1016/S0140-6736(75)90498-5
H. KOOP, M. KLEIN, R. ARNOLD, Serum gastrin levels during long-term omeprazole treatment. Alimentary Pharmacology & Therapeutics. ,vol. 4, pp. 131- 138 ,(2007) , 10.1111/J.1365-2036.1990.TB00457.X
ASHLEY B PRICE, The Sydney System: histological division. Journal of Gastroenterology and Hepatology. ,vol. 6, pp. 209- 222 ,(1991) , 10.1111/J.1440-1746.1991.TB01468.X
Robert M. Genta, Recognizing atrophy: Another step toward a classification of gastritis The American Journal of Surgical Pathology. ,vol. 20, pp. 23- 30 ,(1996) , 10.1097/00000478-199600001-00004