Explore chapters and articles related to this topic
The gastrointestinal system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Sharon J. White, Francis A. Carey
This pattern of mucosal response is often termed ‘bile reflux gastritis’. Indeed, reflux of bile and alkaline small intestinal material is a common cause of gastric epithelial cell injury in patients with gastroduodenal motility disturbances, which may be an isolated (primary) phenomenon or may follow surgery to the pyloric region. Similar patterns of mucosal change may be seen after other chemical injuries, particularly long-term NSAID ingestion, and the term ‘chemical gastritis’ is therefore preferred. Histologically, there is marked hyperplasia in the proliferative compartment of the gastric pits (the neck cells) with oedema of the mucosa (Figure 10.24). A cellular inflammatory infiltrate is often remarkably absent or scant. H. pylori is not usually seen.
Palliative Gastrojejunostomy and the Impact on Nutrition in Cancer
Published in Victor R. Preedy, Handbook of Nutrition and Diet in Palliative Care, 2019
Dorotea Mutabdzic, Poornima B. Rao, Jeffrey M. Farma
As with any surgical procedure, there are risks of bleeding, infection and anastomotic leak. More specific to the gastrojejunostomy procedure are rates of delayed gastric emptying varying with technique and ranging from 2% to 31% (Doberneck and Berndt, 1987). There is frequent biliopancreatic drainage into the stomach leading to the possibility of bile reflux–induced gastritis. In addition, because of the direct transit of acidic gastric contents into the more distal and less buffered small bowel, anastomotic ulceration (a marginal ulcer) and bleeding within the efferent jejunal limb can occur (Lillemoe, 1998).
Oesophageal Diseases
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Shajahan Wahed, S. Michael Griffin
Barrett’s oesophagus develops when the normal oesophageal lining changes from stratified squamous to columnar epithelium (Figure 53.4). It is common in the Western world and has an increasing incidence. It occurs as a result of chronic inflammation secondary to acid, alkaline and bile reflux.14–16 Genetic factors might also increase an individual’s predisposition to this condition and its progression.17 This metaplastic epithelium increases the risk of developing adenocarcinoma of the oesophagus.18–20 A formal diagnosis of Barrett’s requires the reporting of two separate specimens from a specialist gastrointestinal pathologist. Dysplastic changes within the Barrett’s epithelium can occur, subclassified as either low-grade or high-grade. Confirmed low-grade dysplasia increases the risk of progression on to high-grade dysplasia or adenocarcinoma although some will not progress.21, 22 High-grade dysplasia poses a significant risk of developing adenocarcinoma and, given the subjectivity of biopsies, might indicate that there is adenocarcinoma already present. Patients with a diagnosis of low- or high-grade dysplasia within Barrett’s oesophagus should be referred to specialist centres for management.
Esophageal chemical clearance and mucosa integrity values in refractory gastroesophageal reflux disease patients with different esophageal dynamics
Published in Scandinavian Journal of Gastroenterology, 2023
Yanqiu Li, Lixia Wang, Dong Yang, Zhifeng Zhang, Xiaoyu Sun, Xiaoling Geng, Jiarong Lin, Zhijun Duan
The risk factors that are associated with PSPWI and MNBI have not been clearly studied. PSPWI was related to acid reflux, mixed reflux, proximal reflux episodes, large volume burden and long volume clearance time [21,22]. Meanwhile, MNBI was low in pathologic and borderline AET and correlated with symptoms response to anti-reflux therapy [23]. For MNBI subgroups, distal MNBI was calculated as the average of MNBI values in the channels located at 3, 5, 7 and 9 cm above the LES and proximal MNBI was calculated as the average of MNBI values in the channels located at 15 and 17 cm above the LES [49]. Same as MNBI, distal MNBI, but not proximal MNBI, was negatively related to AET and independently predicted symptomatic improvement after anti-reflux therapy [49]. Moreover, distal MNBI and PSPWI were negatively correlated with AET, BET and reflux events [19]. Except for conventional metrics, abnormal PSPWI and MNBI were also associated with the presence of refractory symptoms in patients with extra-esophageal symptoms [67]. Our data suggested that PSPWI and MNBI were positively correlated with DCI while negatively correlated with age, ineffective swallows, acid exposure and reflux events. Except for acid reflux events, bile reflux also presented a negative correlation with PSPWI and MNBI [68]. More interestingly, we found that PSPWI and MNBI had a significantly positive correlation. Because impaired esophageal chemical clearance contributed to esophageal mucosa injury. And PSPWI cut-off value of 53% was the best level for distinguishing normal MNBI from pathologic MNBI [69].
Deoxycholic acid induces gastric intestinal metaplasia by activating STAT3 signaling and disturbing gastric bile acids metabolism and microbiota
Published in Gut Microbes, 2022
Duochen Jin, Keting Huang, Miao Xu, Hongjin Hua, Feng Ye, Jin Yan, Guoxin Zhang, Yun Wang
A total of 161 volunteers without Hp infection or cholecystectomy history were recruited to undergo upper endoscopic examination and provide corpus biopsy samples for histological analysis, immunohistochemical staining and RNA extraction in an epidemiological screening program for GC in rural areas of Yangzhou, China. Hp infection status was examined by the rapid urease test. Those with bile reflux into the gastric cavity due to nausea and vomiting caused by the invasive endoscopic procedure were excluded. Finally, obvious primary bile reflux and bile-stained gastric mucosa were observed in 10 subjects under endoscopic views. Among them, 4 subjects were found to have IM based on mucosal specimens, while the remaining subjects were reviewed as histologically normal based on the Updated Sydney System.63 Six volunteers without bile reflux or histopathological IM were randomly selected as the control group for further analysis. General information about the age, sex, bile reflux status and histological assessment of the 16 enrolled subjects is listed in Table S2. This study was approved by the ethics review board of Nanjing Medical University (number 2018-SR-285).
Negative correlations between bile reflux gastritis and Helicobacter pylori infection
Published in Scandinavian Journal of Gastroenterology, 2022
Xian-hua Zhuo, Jia-chen Sun, Wei-jie Zhong, Yi Lu
Current studies on BRG and H. pylori infection are contradictory. Some studies suggested that the relationship between HP infection and BRG was positive [26–28]. Li et al. argued that a high grade of bile reflux would promote gastric diseases, including HP infection [19]. Other studies did not agree on this is the case. More studies tended to consider they were a negative correlation [29–32]. This was also demonstrated in our study. Melike et al. also supported this argument [33]. However, No relationship had been identified during the course of the study focused on children by Mehmet et al. [34]. Mukaisho et al. argued that patients with BRG had a smaller probability of getting H. pylori infection because the function of bile acids was as an inhibitor which was related to chemorepulsive action [35]. Miyashita et al. found that H. pylori infection could clear spontaneously, especially, in some patients with gastric surgery [36]. This argument had been expressed by Suh et al. [37].