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Gastric acid blockade with omeprazole promotes gastric carcinogenesis induced by duodenogastric reflux

Duodenogastric reflux (DGR) in rats causes growth stimulation of the foregut mucosa that is potentiated by gastric acid blockade. It was the aim of this study to investigate if DGR with gastric acid blockade has a higher incidence of carcinomas of the foregut than DGR alone. DGR was induced in 40 Sp...

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Bibliographic Details
Published in:Digestive diseases and sciences 1999-06, Vol.44 (6), p.1132-1135
Main Authors: WETSCHER, G. J, HINDER, R. A, SMYRK, T, PERDIKIS, G, ADRIAN, T. E, PROFANTER, C
Format: Article
Language:English
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Summary:Duodenogastric reflux (DGR) in rats causes growth stimulation of the foregut mucosa that is potentiated by gastric acid blockade. It was the aim of this study to investigate if DGR with gastric acid blockade has a higher incidence of carcinomas of the foregut than DGR alone. DGR was induced in 40 Sprague-Dawley rats using a split gastroenterostomy. A cardiomyotomy was performed across the gastroesophageal junction, inducing reflux into the esophagus. Twenty of these rats received omeprazole postoperatively. After one year 18 rats (90%) with DGR + omeprazole treatment and 7 rats (35%) with DGR alone developed adenocarcinoma of the stomach (P < 0.05). None of the rats developed esophageal cancer, but esophageal mucosal hyperplasia was more pronounced in rats receiving omeprazole. Control rats, treated with omeprazole, did not develop carcinomas of the foregut. In conclusion, gastric acid blockade enhanced DGR-induced carcinogenesis of the stomach and promotes growth stimulation of the esophageal mucosa.
ISSN:0163-2116
1573-2568
DOI:10.1023/A:1026615905170