DGR is physiological in humans (Ritchie 1984). Thus, reflux gastritis is found to be associated with the amount of bile refluxate. Antral biopsies revealed decreased and even no gastritis in patients with post-cholecystectomy DGR (Farsakh et al. 1995). In contrast, Wilson et al. have concluded that excessive DGR after cholecystectomy is found to be associated with persistent dyspeptic symptoms which correlated with high levels of bile refluxate and chronic gastritis on endoscopy (Wilson et al. 1995). Larusso et al. have also mentioned in a long term prospective study with ten patients that fasting bile reflux of total bile acids and DGR related gastritis increase progressively following the cholecystectomy procedure during the postoperative period (Lorusso et al. 1992). However, early onset of post-cholecystectomy DGR has presented comparable results with long-term reflux gastritis. Elhak et al. have found an increase in inactive form of chronic superficial gastritis and reflux gastritis on postoperative first year (Gad Elhak et al. 2004). Aprea et al. have evaluated elderly cholecystectomized patients with control endoscopy on postoperative 6 months and have concluded cholecystectomy is a significant risk factor for biliary gastritis (Aprea et al. 2012).
Post-cholecystectomy DGR related early chronic atrophic changes of gastric mucosa have not been clearly identified. DGR and mechanisms of gastric mucosal injury was shown in several in vitro and in vivo animal studies (Eastwood 1975; Stein et al. 1999; Nogi et al. 2001). The destructive effect of duodenal content over the gastric mucosa is defined as reactive gastritis (Sobala et al. 1993). Foveolar hyperplasia, oedema and congestion of lamina propria, acute and chronic inflammatory cells are the distinctive histopathological findings linked to reflux gastritis. Dixon et al. concluded that, prolonged exposure to the bilious duodenal content worsens mucosal injury and initiates endoscopic and histopathological sequence of gastric mucosal changes as atrophy, intestinal metaplasia and dysplasia (Dixon et al. 1986). H. pylori has been strongly accepted as a pathogen and a precursor of gastric mucosal transformation in each of these stages. Although bile reflux into the stomach is a potential inducer of intestinal metaplasia (Houghton et al. 1986), synergistic effect of the underlying H. pylori gastritis is stated as an essential factor in development of gastric mucosal changes (Sobala et al. 1991, 1993). The role of H. pylori infection in gallstones has been clearly demonstrated in several studies (Takahashi et al. 2014; Zhang et al. 2015). However, there is an ongoing debate about H. pylori colonization and its effects over the gastric mucosa in patients with DGR following the cholecystectomy procedure. Many studies mentioned that post-cholecystectomy DGR initiates gastric mucosal injury and reduces H. pylori colonization (Farsakh et al. 1995; Gad Elhak et al. 2004; Sobala et al. 1993; Atak et al. 2012). In contrast to these studies there are such reports demonstrated that patients with DGR after cholecystectomy have been presented with higher H. pylori colonization rates (Zullo et al. 1998).
In present study, early postoperative endoscopy revealed significantly higher rates of DGR and DGR related superficial chronic gastritis. Postoperative histological interpretations displayed increased H. pylori density, neutrophil activity, mucosal inflammation and atrophy degree. Although the Updated Sydney scores did not show significant difference between mild, moderate and severe groups, increased postoperative mean values were correlated with clinical outcomes. In this group of patients without H. pylori eradication therapy, postoperative pathological DGR and presence of H. pylori infection were found to be independent risk factors in development of early atrophic changes. These data suggested that early gastric mucosal atrophy following cholecystectomy procedure is possibly related to not only early onset of pathological DGR and excessive amount of bile refluxate but also presence of active H. pylori gastritis. Underlying H. pylori infection and DGR were thought to be the accompanying factors which potentiate the efficacy of each other’s detrimental effects over the gastric mucosa.
Limitations to our study depend on the challenges in determining the postoperative development of gastritis process and exact timing of histological sampling. Most of the adult population requiring cholecystectomy procedure have concomitant gastrointestinal disorders including H. pylori gastritis and DGR. Therefore, it is difficult to identify cholecystectomy as a sole risk factor for early mucosal atrophy. As indicated in our study, defining the exclusion criteria and evaluating the cumulative effects of DGR, underlying H. pylori gastritis and cholecystectomy procedure over the gastric mucosa should be more effective to specify the significant postoperative outcomes. Although gastric mucosal injury advances stepwise in a long time interval, postoperative early sampling of gastric mucosa should also reveal additional information about progression of preoperative existing lesions.
In conclusion, our study demonstrated cholecystectomy as a cause of severe DGR. Early onset of pathological DGR was also strongly associated with early gastric mucosal changes. Underlying H. pylori infection may be the most effective factor in development of early mucosal atrophy. These independent factors influence the predisposition to DGR related chronic atrophic changes. In regard to these findings, preoperative endoscopy should be performed to reduce the additive adverse effects of H. pylori gastritis and DGR over the gastric mucosa by managing the appropriate medical therapy during the preoperative course.
