Expression of cyclooxygenases in Helicobacter pylori gastritis and residual gastritis after distal gastrectomy.

It has long been thought that duodenal reflux induces residual gastritis after distal gastrectomy. H. pylori infection appears to be another factor in residual gastritis; and H. pylori induced gastritis may exist preoperatively or may have been introduced postoperatively. Up until now, the surgical effect itself and H. pylori infection have not been well differentiated as causes of residual gastritis. Our aim in this study was to clarify the relationship between the surgical effect and H. pylori infection in residual gastritis. A residual gastritis model using the Mongolian gerbil has been established with microsurgical technique. Residual gastritis with and without H. pylori infection has been studied by histopathological examination and quantitated by Rauws' score. The expression of cyclooxygenase (both COX-1 and COX-2) has also been examined immunohistologically. Elevation of pH in gastric juice after surgery was confirmed. H. pylori infection led to deterioration after surgery. The postoperative Rauws' score with infection is higher than without infection. Levels of COX-1 were higher after surgery in both animals. COX-2 was not expressed in the animals without infection and only a little was expressed in the animals with infection. COX-2 was strongly expressed in the operated animals with infection, but the surgical effect was minute in the animals without infection. Residual gastritis consisted of both surgical gastritis and H. pylori gastritis. H. pylori gastritis is curable with eradication of the organism, but surgical gastritis is not. The COX inhibitor can be a good candidate in preventing residual gastritis after eradication of the H. pylori organism. The clinical implications of COX expression for patients with residual gastritis might deserve further study in the point of treatment of surgical and H. pylori gastritis.