RISK-BENEFIT ASSESSMENT OF OMEPRAZOLE IN THE TREATMENT OF GASTROINTESTINAL DISORDERS

被引:24
作者
CREUTZFELDT, W
机构
[1] Department of Medicine, Georg-August-University, Göttingen
[2] Department of Medicine, University of Göttingen, Göttingen, D-37075
关键词
D O I
10.2165/00002018-199410010-00005
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
For the treatment of duodenal and gastric ulcer and reflux oesophagitis, especially erosive oesophagitis, omeprazole has an advantage over histamine H-2-receptor antagonists because it heals significantly more patients significantly faster. Adverse effects have been observed during short term treatment with the same frequency as during treatment with H-2-antagonists. Also, maintenance treatment with omeprazole of reflux oesophagitis is significantly superior to H-2-antagonist therapy. During long term treatment for up to 8 years no further drug-related adverse effects have been observed. Moderate hypergastrinaemia occurs in some patients, especially if an omeprazole dosage of 40 mg/day is needed. A slight increase of the agyrophil (endocrine) cell volume density and an extension of micronodular hyperplasia in the oxyntic mucosa after several years of omeprazole treatment seem to be related to the severity of the corpus gastritis and not to drug-induced hypergastrinaemia, because similar changes have been observed in equal frequency in patients not receiving antisecretory drugs. Theoretical arguments against long term treatment with potent acid-suppressing drugs, such as the possible consequences of gastric bacterial overgrowth or hypergastrinaemia, are not supported by clinical observations and epidemiological data and are, therefore, speculative.
引用
收藏
页码:66 / 82
页数:17
相关论文
共 151 条
[41]  
Festen H., Klinkenberg-Knol E., Kuipers E., Lamers C., Jansen J., Et al., Cobalamin absorption during omeprazole treatment: short and long-term studies. Abstract, Gastroenterology, 104, (1993)
[42]  
Freston J.W., Clinical significance of hypergstrinaemia: relevance to gastrin monitoring during omeprazole therapy, Digestion, 51, pp. 102-114, (1992)
[43]  
Fryklund J., Falknas A.K., Heiander H.F., Omeprazole does not cause unscheduled DNA synthesis in rabbit parietal cells in vitro, Scandinavian Journal of Gastroenterology, 27, pp. 521-528, (1992)
[44]  
Furihata C., Hirose K., Matsushima T., Genotoxicity and cell proliferative activity of omeprazole in rat stomach mucosa, Mutation Research, 262, pp. 73-76, (1991)
[45]  
Goggins M.G., Os'Brion S., Kelleher B., Scott J.M., Weir D.G., Omeprazole causes malabsorption of protein-bound cobalamin. Abstract, Gastroenterology, 104, (1993)
[46]  
Graffner H., Singh G., Chaudry I., Milson J.W., Omeprazole-induced hypergastrinemia does not influence growth of colon carcinoma, Digestive Diseases and Sciences, 37, pp. 485-489, (1992)
[47]  
Gugler R., Jensen J.C., Omeprazole inhibits oxidative drug metabolism. Studies with diazepam and phenytoin in vivo and 7-ethoxycoumarin in vitro, Gastroenterology, 89, pp. 1235-1241, (1985)
[48]  
Hakanson R., Blom H., Carlsson E., Larsson H., Ryberg B., Et al., Hypergastrinaemia produces trophic effects in stomach but not in pancreas and intestines, Regulatory Peptides, 13, pp. 223-233, (1986)
[49]  
Hakanson R., Bottcher G., Sundler F., Vallgren S., Activation and hyperplasia of gastrin and enterochromaffin-like cells in the stomach, Digestion, 35, pp. 23-41, (1986)
[50]  
Hall C.N., Darkin D., Brimblecombe R., Cook A.J., Kirkham J.S., Et al., Evaluation of the nitrosamine hypothesis of gastric carcinogenesis in precancerous conditions, Gut, 27, pp. 491-498, (1986)