The Pathogenic Effects Of Primary Duodenogastric Reflux On Gastric Mucosa Of Children

Background Duodenogastric reflux (DGR) is a reverse flow of duodenal juice into stomach through pylorus composed of bile acid, pancreatic secretion, and intestinal secretion. DGR is often physiological, which occurs at the early morning and/or postprandial time. It could be pathological when it went excessively .The increased entero-gastric reflux provides mucosa injury that may relate not only to reflux gastritis but also esophagitis , gastric ulcers, carcinoma of stomach and esophagus. DGR can be classified to two types, primary DGR or secondary DGR . Secondary DGR is always due to the operations on stomach, duodenum and cholecyst. In the contrast, primary DGR caused by non-operation factors and the pathogenisis is not totally be understood, which probably be correlate with the disorders of gastric or duodenal motility, the gallbladder sphincter function and the gut hormone secretion. The duodenal juice mainly consists of the bile acid, which is a sort of lipophilic steroid and may result in direct injuries of mucosal epithelial cells and their tight junctions. Some researches have showed that the bile acid directly damaged the chemical environment of mucosa surface and played a synergistical role in gastric mucosal lesions along with gastric acid and H. pylori infection. Regurgitated bile could affect the wholegastric mucosa to some extent. However, the exact mechanisms of gastric mucosal damage caused by DGR are still unknown. There was a few reports on the correlation of the degree of the gastric mucosa lesions with the severity of DGR and relations of DGR to H. pylori infection or intragastric acidity. In pediatrics, the relevant reports are even rare. The objective of the present study is to investigate the pathogenic effect of primary DGR on gastric mucosa in children, and to explore the correlation of DGR with clinical symptoms, H. pylori infection and intragastric acidity.Method 81 patients with upper gastrointestinal manifestation were graded the symptom score and underwent endoscopic, histological examination and 24-hour intra-gastric bilirubin monitoring with Bilitec 2000 . Of which, 51 were underwent the 24-hour intra-gastric pH monitoring by ambulatory pH recorder simultaneously. The total fraction time of bile reflux was considered as a marker to evaluate the severity of DGR. The total fraction time of bile reflux was compared between the patients with positive and negative results under endoscopy and histologically respectively. The correlations of the total fraction time of bile reflux with clinical symptom score, H.pylori infection, intragastric acidity were analyzed respectively.Result The total fraction time of bile reflux in the patients with hyperemia or yellow stain gastric antral mucosa under endoscopy had significantly higher than without those changes (p<0.05, p<0.01 respectively). Histologically, there was significantly higher total fraction time of bile reflux in the cases with intestinal metaplasia than in the cases without intestinal metaplasia (p<0.05), but neither significantly difference between with the chronic inflammation and without the chronic inflammation (p>0.05) nor between with the active inflammation and with the non-active inflammation (p>0.05). The severity of bile reflux was positive correlated with the score of abdominal distention (r=0.258, p<0.05), but no relevant to the severity of intragastric acid (r= -0.124, p>0.05), nor H. pylori infection(r=0.016,p>0.05).Conclusion Primary DGR could cause astric mucosa lesions showed mainly hyperemia and bile-stained gastric antral mucosa under endoscopy and the gastric antral intestinal metaplasia histologically in children. There was no significantly correlation of DGR with gastric mucosa inflammatory infiltration. DGR had no relevance to H. pylori infection and intragastric acidity. We concluded that DGR was probably an independent etiological factor and might play a synergistical role in the pathogenesis of gastric mucosal lesions along with gastric acid and H. pylori infection.