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Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa.
SpringerPlus 2016
AIMS: To evaluate association between duodenogastric reflux and early gastric mucosal changes before and after the cholecystectomy procedure.
MATERIALS AND METHODS: Patients were evaluated with preoperative and postoperative endoscopy and endoscopic biopsy. Demographic and clinical characteristics, histological parameters, presence of duodenogastric reflux, and Updated Sydney scores were noted.
RESULTS: A total of fifty patients who obeyed the follow-up were enrolled into the study. Median age of the patients was 43 years (range 25-84). Male-female ratio was 0.51 (17/33). Duodenogastric reflux % and Updated Sydney scores before and after cholecystectomy were 24 (48%) versus 39 (78%) and 2.38 ± 2.21 versus 3.46 ± 3.05, respectively (p = 0.001, p < 0.000). Mucosal inflammation degree showed significant increase in 15 (30%) patients, decrease in 7 (14%) patients and equality in 28 (56%) patients (p = 0.037). Neutrophil activation degree was significantly higher in 21 (42%) patients, lower in 5 (10%) patients after the surgery (p = 0.005). Postoperative glandular atrophy degree was also higher in 13 (26%) patients and equal in 37 (74%) patients (p = 0.001). Pre- and postoperative degree of intestinal metaplasia and H. pylori density did not any show significant difference (p = 0.157, p = 0.248, respectively).There were significant positive correlation between postoperative H. pylori infection and mucosal activity, inflammation, atrophy and intestinal metaplasia.
CONCLUSION: Cholecystectomy is a potent inducer of pathologic duodenogastric reflux. Early onset of duodenogastric reflux and underlying H. pylori gastritis cause early gastric mucosal injury following cholecystectomy procedure by interacting collectively.
MATERIALS AND METHODS: Patients were evaluated with preoperative and postoperative endoscopy and endoscopic biopsy. Demographic and clinical characteristics, histological parameters, presence of duodenogastric reflux, and Updated Sydney scores were noted.
RESULTS: A total of fifty patients who obeyed the follow-up were enrolled into the study. Median age of the patients was 43 years (range 25-84). Male-female ratio was 0.51 (17/33). Duodenogastric reflux % and Updated Sydney scores before and after cholecystectomy were 24 (48%) versus 39 (78%) and 2.38 ± 2.21 versus 3.46 ± 3.05, respectively (p = 0.001, p < 0.000). Mucosal inflammation degree showed significant increase in 15 (30%) patients, decrease in 7 (14%) patients and equality in 28 (56%) patients (p = 0.037). Neutrophil activation degree was significantly higher in 21 (42%) patients, lower in 5 (10%) patients after the surgery (p = 0.005). Postoperative glandular atrophy degree was also higher in 13 (26%) patients and equal in 37 (74%) patients (p = 0.001). Pre- and postoperative degree of intestinal metaplasia and H. pylori density did not any show significant difference (p = 0.157, p = 0.248, respectively).There were significant positive correlation between postoperative H. pylori infection and mucosal activity, inflammation, atrophy and intestinal metaplasia.
CONCLUSION: Cholecystectomy is a potent inducer of pathologic duodenogastric reflux. Early onset of duodenogastric reflux and underlying H. pylori gastritis cause early gastric mucosal injury following cholecystectomy procedure by interacting collectively.
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