Impact of the Biliary Diversion Procedure on Carcinogenesis in Barrett??s Esophagus Surgically Induced by Duodenoesophageal Reflux in Rats

Nishijima, Koji; Miwa, Koichi; Miyashita, Tomoharu; Kinami, Shinichi; Ninomiya, Itasu; Fushida, Sachio; Fujimura, Takashi; Hattori, Takanori

doi:10.1097/01.sla.0000130850.31178.8c

Cited by 81 publications

(78 citation statements)

References 46 publications

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“…Esophagitis occurs in patients who have undergone total gastrectomy without biliary diversion and in patients with achlorhydria (Helsingen, 1961;Orlando and Bozymski, 1973;Palmer, 2002;Yumiba et al, 2002;Sandvik and Halvorsen, 1988). Barrett's esophagus has been described after total gastrectomy with esophagojejunostomy (Nishijima et al, 2004). This supports the view that NAR, represented by the reflux of duodenal contents alone, has a role in esophageal mucosal injury.…”

Section: Pathological Refluxsupporting

confidence: 64%

“…DGER was more harmful than GOR with higher percentage of adenocarcinoma. Nishijima et al (2004) created three different models for reflux: gastrectomy plus esophago-jejunostomy, gastrectomy plus esophago-duodenostomy and gastrectomy plus Roux-en-Y anastomosis. They concluded that esophago-jejunostomy procedure does not cause regression of Barrett's esophagus but prevents the development of adenocarcinoma.…”

Section: What We Have Learned From Animal Reflux Modelsmentioning

confidence: 99%

“…AMJ the metaplasia-dysplasia-carcinoma sequence (Gillen et al, 1988a;Attwood et al, 1992;Miwa et al, 1995;Nishijima et al, 2004;Kivilaakso et al, 1980;Fujimura, 1991;Clark et al, 1994;DeMeester et al, 1987;DeMeester and Ireland, 1997;Di Marco et al, 1990;Fein et al, 2000a;2000b;Fujikawa et al, 1994;Gerlach et al, 1997;Harmon et al, 1978;Hofmann et al, 1969;Hofmann and Mysels, 1992;Hossain et al, 1988;Isozaki et al, 1995;Kauer and Stein, 2002;Kauer, 2005;Kivilaakso et al, 1981;Segalin et al, 1994;Lillemoe et al, 1983;Miwa et al, 1992b;Smallwood and Hoffman, 1976;Theisen et al, 2003;Ireland et al, 1996). Manifold et al (2000a) studied the role of omeprazole in gastric carcinogenesis induced by duodeno-gastric reflux.…”

Section: Science Publicationsmentioning

confidence: 99%

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Review Article; Duodeno-Gastro-Esophageal Reflux Combined and Isolated

Nasr¹

2013

American Medical Journal

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Barrett's esophagus is the chief risk factor for esophageal adenocarcinoma. Reflux of gastric acid has long been related to the development of esophagitis and Barrett's esophagus, but the role of duodenal contents is controversial. We review the literature on the role of duodenal contents in the development of esophagitis, Barrett's esophagus and adenocarcinoma in addition to the role of acid suppressant therapy in the development or prevention of these changes. A computer-based search of the literature using the terms "Bilirubin, Barrett, Bile Reflux, duodeno-gastric reflux and oesophagus/esophagus" was performed. The role of bile and other constituents of duodenal refluxate were examined. Techniques for identifying nonacid reflux were also reviewed, as were the role of pH, medication and surgery in modulating disease severity. Complicated Barrett's esophagus is associated with increased exposure to gastric and duodenal refluxate. Biological effect of bile acids depends on the conjugation status, the pH of the milieu and the pKa of bile acids. While Proton Pump Inhibitors reduce the levels of DGER, they also produce changes in gastric and lower esophageal pH that activate different bile acids at different pH levels resulting in unexpected injury. Conjugated bile acids are harmful in acidic environment while unconjugated bile acids are harmful at neutral pH environment. An overlap of toxicity among conjugated and unconjugated bile acids occurs between strongly acidic and neutral pH levels. Normalisation of gastric and duodenal refluxate should ideally be the goal of treatment.

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Section: Pathological Refluxsupporting

confidence: 64%

Section: What We Have Learned From Animal Reflux Modelsmentioning

confidence: 99%

Section: Science Publicationsmentioning

confidence: 99%

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Review Article; Duodeno-Gastro-Esophageal Reflux Combined and Isolated

Nasr¹

2013

American Medical Journal

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“…36,37 The operation was, therefore, modified to include the Roux-en-Y anastomotic technique, 38 which has the added advantage of decreasing biliary reflux and preventing subsequent gastric cancer risk. 39,40 The vast majority of procedures are performed laparoscopically 41 and demonstrate low postoperative adverse outcomes. A recent multicenter, prospective, observational study 42 revealed an overall operative 30-day mortality to be 0.3%.…”

mentioning

confidence: 99%

Metabolic surgery and cancer

Ashrafian

Ahmed

Rowland

et al. 2010

Cancer

136

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The worldwide epidemic of obesity and the global incidence of cancer are both increasing. There is now epidemiological evidence to support a correlation between obesity, weight gain, and some cancers. Metabolic or bariatric surgery can provide sustained weight loss and reduced obesity-related mortality. These procedures can also improve the metabolic profile to decrease cardiovascular risk and resolve diabetes in morbidly obese patients. The operations offer several physiological steps, the so-called BRAVE effects: 1) bile flow alteration, 2) reduction of gastric size, 3) anatomical gut rearrangement and altered flow of nutrients, 4) vagal manipulation and 5) enteric gut hormone modulation. Metabolic operations are also associated with a significant reduction of cancer incidence and mortality. The cancer-protective role of metabolic surgery is strongest for female obesity-related tumors; however, the underlying mechanisms may involve both weight-dependent and weight-independent effects. These include the improvement of insulin resistance with attenuation of the metabolic syndrome as well as decreased oxidative stress and inflammation in addition to the beneficial modulation of sex steroids, gut hormones, cellular energetics, immune system, and adipokines. Elucidating the precise metabolic mechanisms of cancer prevention by metabolic surgery can increase our understanding of how obesity, diabetes, and metabolic syndrome are associated with cancer. It may also offer novel treatment strategies in the management of tumor generation and growth. Cancer 2011;117:1788-99. V C 2010 American Cancer Society.KEYWORDS: metabolic surgery, bariatric surgery, cancer, oncology.The worldwide epidemic of obesity and the global incidence of cancer are both increasing. According to the World Health Organization (WHO), obesity is rising by 30 million cases per year, 1 whereas the overall number of new cancer cases will increase by 300,000 cases per year.2 Both obesity and cancer contribute to increased worldwide mortality and healthcare costs. They are now both recognized as global healthcare concerns and have been the subject of worldwide calls to action. 3,4Several treatment strategies have been developed to decrease obesity; these include prevention, lifestyle, behavioral modification, and pharmacotherapy. The weight-loss effects of these strategies have only been marginally successful, 5 and, therefore, a surgical solution has been developed to provide consistent weight loss in severely obese patients. The operations initially titled ''bariatric procedures'' have demonstrated long-term weight loss at more than 15 years after surgery 6,7 ; however in addition, they achieve pronounced metabolic effects including diabetes resolution in the majority of morbidly obese patients. [8][9][10] As a result, these procedures are now considered as ''metabolic'' operations. 10-14The epidemiological association between obesity rates and cancer rates has come under increased scrutiny as there is now evidence to establish obesity as a significant...

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“…37 The formation of DYS or CLE is regarded as an early stage in carcinogenesis and is an irreversible change. 31,38 The persistent inflammation because of duodenal reflux may promote the process from DYS to SCC or CLE to ADC. Therefore, earlier administration of a selective COX-2 inhibitor could be more effective in preventing this carcinogenesis.…”

mentioning

confidence: 99%

A selective cyclooxygenase‐2 inhibitor prevents inflammation‐related squamous cell carcinogenesis of the forestomach via duodenogastric reflux in rats

Oba

Miwa

Fujimura

et al. 2009

Cancer

Self Cite

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BACKGROUND:Duodenal reflux causes inflammation‐related squamous cell carcinogenesis in the forestomach of rats without any carcinogens. The aim of this study was to investigate the efficacy of a selective cyclooxygenase (COX)‐2 inhibitor, meloxicam, in preventing this carcinogenesis.METHODS:A series of 188 rats underwent a surgical duodenogastric reflux procedure and were divided into 2 groups. One group was given commercial chow (control group), and the other was given experimental chow containing meloxicam (0.3 mg/kg body weight/day) (meloxicam group). The animals were sequentially sacrificed at Weeks 20, 30, 40, 50, and 60 after surgery. The forestomach was examined for the presence of carcinoma, the incidence of reflux‐related morphological changes, COX‐2 expression, and its activity.RESULTS:At Week 60, squamous cell carcinoma developed in 8 of 21 animals (38%) in the control group, but none of 20 (0%) in the meloxicam group (P < .05). In addition, basal cell dysplasia developed in 19 of 21 (90%) animals in the control group, but only 4 of 20 (20%) in the meloxicam group (P < .01). COX‐2 immunoreactivity was predominantly detected in macrophages in the epithelial stroma. Compared with nonsurgical rats, RNA expression of COX‐2 in the epithelium was up‐regulated, reaching peak at an early stage of Week 20 in both groups (P < .005). The expression of microsomal prostaglandin E synthase‐1 was lower in the meloxicam group than in the control group. PGE2 production was significantly suppressed throughout the experiment in the meloxicam group compared with the control group (P < .005).CONCLUSIONS:Meloxicam was effective in preventing reflux‐induced squamous cell carcinogenesis via an inflamed squamous epithelium. Cancer 2009. © 2009 American Cancer Society.

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Impact of the Biliary Diversion Procedure on Carcinogenesis in Barrett??s Esophagus Surgically Induced by Duodenoesophageal Reflux in Rats

Abstract: It is likely that the converting procedure from the esophagojejunostomy to induce DER to biliary diversion does not lead to regression of BE but prevents the development of esophageal adenocarcinoma in the rats.

Cited by 81 publications

References 46 publications

Review Article; Duodeno-Gastro-Esophageal Reflux Combined and Isolated

Review Article; Duodeno-Gastro-Esophageal Reflux Combined and Isolated

Metabolic surgery and cancer

A selective cyclooxygenase‐2 inhibitor prevents inflammation‐related squamous cell carcinogenesis of the forestomach via duodenogastric reflux in rats

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