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Background: Most studies of the relationship between duodenogastric reflux (DGR) and Helicobacter pylori have reported that the presence of DGR decreases H. pylori colonization, while H. pylori infection increases the frequency of DGR by impairing antroduodenal motility. The present study aimed to investigate the relationship between primary DGR and the prevalence of H. pylori in children, as well as the degree of colonization and the presence and severity of gastritis., Methods: Included in the study were 410 patients between the ages of 2 and 18 years, referred to the pediatric gastroenterology clinic with complaints of dyspepsia, abdominal pain, and nausea/vomiting, who underwent upper gastrointestinal system endoscopic examination and stomach biopsy. The study group included 60 patients with DGR, while 350 non-DGR patients formed the control group., Results: The mean age of patients with DGR was 15.7 ± 2.1 years, while the mean age of the control group was 14.2 ± 3.8 years (p = 0.02). Of those with DGR, 50 (83.3%) were girls, while in the control group, 215 (61.4%) were girls (p = 0.001). Of patients with DGR, 16 were H. pylori (+) (26.7%), while in the control group, 168 were H. pylori (+) (48%) (p = 0.002). There was no significant difference between the 2 groups with respect to H. pylori degree of colonization (p = 0.08). Gastritis was present in 56 (93.3%) patients in the DGR group and 322 (92%) patients in the control group (p = 0.72). A significant difference was found between the 2 groups in terms of gastritis severity (p = 0.01)., Conclusions: The mean age of patients with DGR was significantly higher than that of patients without DGR, and DGR was found to be more common in girls. In patients with DGR, H. pylori prevalence was significantly lower than in those without DGR; however, no significant difference was found between the 2 groups with respect to the colonization degree., (© 2021 S. Karger AG, Basel.)

Aims: Rat models of duodenogastric reflux have been used to study gastric stump cancer (GSC), but the underlying molecular mechanisms are poorly understood. Unlike rats, mice can be genetically modified, providing a superior model for studying the molecular mechanisms underlying GSC development, which is associated with duodenogastric reflux. This study aimed at developing a mouse model of duodenogastric reflux., Main Method: C57BL/6 mice were randomly assigned to the control (n = 6), sham operation (n = 9), or gastrojejunostomy group (n = 12). Mice were sacrificed at 1, 3, and 6 months after surgery. Stomach tissue was stained with hematoxylin and eosin. Lesions were classified as chronic inflammation, intestinal metaplasia, or atypical hyperplasia., Key Findings: Nine mice underwent gastrojejunostomy without mortality. The animals in the gastrojejunostomy group exhibited chronic inflammation at 1, 3, and 6 months after surgery, showing intestinal metaplasia (n = 2) and atypical hyperplasia (n = 1) at 3 months and intestinal metaplasia (n = 2) and atypical hyperplasia (n = 2) at 6 months. The mice in the control group did not exhibit chronic inflammation or intestinal metaplasia, whereas those in the sham operation group exhibited chronic inflammation at 1, 3, and 6 months after surgery, without intestinal metaplasia or atypical hyperplasia. Intestinal metaplasia or atypical hyperplasia were more common in the gastrojejunostomy group than in the sham operation group (p = 0.012)., Significance: A duodenogastric reflux mouse model can be created using gastrojejunostomy without gastrectomy., (Copyright © 2020. Published by Elsevier Inc.)

Background and Objectives: Although there are many studies that investigate the relationship between duodenogastric reflux (DGR) and Helicobacter pylori in adult patients, the reported data are contradictory. In addition, there are very few studies in the literature investigating the relationship between DGR and H.pylori in the pediatric age group. In the present study, we investigated the effect of primary DGR on H.pylori and gastritis. Materials and Methods: A total of 361 patients who were referred to the clinic of our hospital with dyspeptic complaints who had an upper gastrointestinal system endoscopy and a gastric biopsy were included in the study. Results: DGR was detected in 45 cases, and 316 cases that did not have DGR were considered as the control group. Comparisons were made between the DGR cases and the control group in terms of risk factors (age, gender), the presence and density of H.pylori , and the presence and severity of gastritis. The average age of the patients who were included in the study was 11.6 ± 4.6 years. A total of 128 (36%) of the cases were male and 233 (64%) were female. DGR was present in 45 (13%) of the cases. The average age of the patients with DGR was 13.9 ± 3.1 years, the average age of the control group was 11.3 ± 4.7, and there were statistically significant differences ( p < 0.001). No significant differences were detected in terms of gender between DGR and the control group ( p > 0.05). H.pylori (+) was detected in 29 (64%) of patients with DGR, and in 202 (64%) of the control group. No significant differences were detected between H.pylori prevalence ( p = 0.947). Gastritis was detected in 37 (82%) of the patients with DGR, and in 245 (77%) of the control group ( p = 0.476). No significant differences were detected between the presence and density of H.pylori , gastritis presence, severity and DGR ( p > 0.05). Conclusions: The ages of patients with DGR were significantly higher than in the control group, and advanced age was shown to be a risk factor for primary DGR. It was found that the presence of DGR has no effect on the presence and severity of H.pylori . Given this situation, we consider it is important to eradicate H.pylori infection, especially in the case where H.pylori is present together with DGR.

Hyperinsulinemia could have a role in the growing incidence of esophageal adenocarcinoma (EAC) and its pre-cancerous lesion, Barrett's Esophagus, a possible consequence of Gastro-Esophageal Reflux Disease. Obesity is known to mediate esophageal carcinogenesis through different mechanisms including insulin-resistance leading to hyperinsulinemia, which may mediate cancer progression via the insulin/insulin-like growth factor axis. We used the hyperinsulinemic non-obese FVB/N (Friend leukemia virus B strain) MKR (muscle (M)-IGF1R-lysine (K)-arginine (R) mouse model to evaluate the exclusive role of hyperinsulinemia in the pathogenesis of EAC related to duodeno-esophageal reflux. FVB/N wild-type (WT) and MKR mice underwent jejunum-esophageal anastomosis side-to end with the exclusion of the stomach. Thirty weeks after surgery, the esophagus was processed for histological, immunological and insulin/Insulin-like growth factor 1 (IGF1) signal transduction analyses. Most of the WT mice (63.1%) developed dysplasia, whereas most of the MKR mice (74.3%) developed squamous cell and adenosquamous carcinomas, both expressing Human Epidermal growth factor receptor 2 (HER2). Hyperinsulinemia significantly increased esophageal cancer incidence in the presence of duodenal-reflux. Insulin receptor (IR) and IGF1 receptor (IGF1R) were overexpressed in the hyperinsulinemic condition. IGF1R, through ERK1/2 mitogenic pattern activation, seems to be involved in cancer onset. Hyperinsulinemia-induced IGF1R and HER2 up-regulation could also increase the possibility of forming of IGF1R/HER2 heterodimers to support cell growth/proliferation/progression in esophageal carcinogenesis., Competing Interests: The Authors declare no conflict of interest.

Background: Cholecystectomy alters bile release dynamics from pulsatile meal-stimulated to continuous, and results in retrograde duodeno-gastric bile reflux (DGR). Bile is implicated in mucosal injury after gastric surgery, but whether cholecystectomy causes esophagogastric mucosal inflammation, therefore increasing the risk of metaplasia, is unclear., Study Design: This study examined whether cholecystectomy-induced DGR promotes chronic inflammatory mucosal changes of the stomach and/or the esophagogastric junction (EGJ). Four groups of patients were studied and compared with controls. A group of patients was studied before and 1 year after cholecystectomy; 2 further groups were studied long-term post-cholecystectomy (LTPC) at 5 to 10 years and 10 to 20 years. All underwent abdominal ultrasound and upper gastrointestinal endoscopy with gastric antral and EGJ biopsies, noting the presence of gastric bile pooling. Biopsy specimens were stained for Ki67 and p53 overexpression, and the bile reflux index (BRI) was calculated., Results: At endoscopy, bile pooling was observed in 9 of 26 (34.6%) controls, in 8 of 25 (32%) patients pre-cholecystectomy, in 15 of 25 (60%) 1 year post-cholecystectomy patients (p = 0.047), and 23 of 29 (79.3%) LTPC patients (p = 0.001). Bile reflux index positivity at the EGJ increased from 19% of controls through 41% of LTPC patients (p = 0.032). Ki67 was overexpressed at the EGJ in 19% of controls, but in 62% of LTPC patients (p = 0.044); p53 was overexpressed at the EGJ in 19% of controls compared with 66% of LTPC patients (p = 0.001)., Conclusions: Duodeno-gastric bile reflux was more common in patients with gallstones than in controls, and its incidence doubled after cholecystectomy. This was associated with inflammatory changes in the gastric antrum and the EGJ, evident in most LTPC patients. Ki67 and p53 overexpression at the EGJ suggests cellular damage attributable to chronic bile exposure post-cholecystectomy, increasing the likelihood of dysplasia. Further studies are required to determine whether DGR-mediated esophageal mucosal injury is reversible or avoidable, and whether surveillance endoscopy is indicated after cholecystectomy., (Copyright © 2016 American College of Surgeons. Published by Elsevier Inc. All rights reserved.)

Unlabelled: Gastroduodenal refluxate found in the upper aerodigestive tract is not clinically uncommon. We recently demonstrated the neoplastic potential of gastroduodenal fluids (GDF) on hypopharyngeal mucosa, via NF-κB, using in vitro and in vivo models. Here we will explore the in vivo effect of GDF on laryngeal mucosa (LM) to induce early preneoplastic lesions related to NF-κB activation, along with deregulation of specific microRNA (miRNA) markers previously linked to laryngeal cancer. We used histological, immunohistochemical, automated quantitative analysis and quantitative polymerase chain reaction to examine LM from 35 C57Bl/6J mice previously treated with topical GDF against corresponding controls (4 experimental and 3 control groups; 5 mice/group). Our analysis showed that GDF produced early preneoplastic lesions in treated LM related to NF-κB activation. LM treated by acid and bile combination demonstrated significantly higher expression of the analyzed cell proliferation markers (Ki67, CK14, ∆Np63), oncogenic p-STAT3, and changes of cell adhesion molecules (E-cadherin, ϐ-catenin) versus untreated LM or LM exposed to acid alone (P < .0005). Furthermore, acidic bile but not neutral bile appeared to accelerate the expression of "oncomirs" miR-21, miR-155, and miR-192 (acidic bile versus neutral bile, P < .0001), while reducing tumor suppressor miR-375 (acidic bile versus neutral bile, P = .0137), previously linked to NF-κB and laryngeal cancer. Finally, acidic bile induced reduction of miR-34a, miR-375, and miR-451a, exhibiting an inverse correlation with NF-κB activation., Significance: Bile in combination with acid has a selective tumorigenic effect on LM, inducing deregulation of "oncomirs" and tumor suppressor miRNAs, produced by NF-κB activation with molecular and early histopathological alterations linked to neoplastic transformation. Systematic acid suppression may in part convey a protective role., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

Comparative analysis of dissemination by H. pylori of the bile portions in patients of a control group, suffering an acute calculous cholecystitis (ACCH), was performed. Dissemination of H. pylori in a control group was significantly less, than in a bile portions of patients, suffering ACCH. While analyzing the rate and degree of dissemination by H. pylori of the gastic and gallbladder mucosa biopsies of patients, suffering chronic non-calculous cholecystitis, associated with duodenogastric reflux and gastroduodenitis, bacteria were revealed trustworthy more often and in more number, than in a gallbladder mucosa in patients, suffering ACCH.

The Purpose of the Study: Determine the pathogenetic significance of express molecules PCNA, Bcl-2, NF-Kb and tachykinins (substance P, neurokinin A) in patients with gastroesophageal reflux disease (GERD), receiving polychemotherapy (PCT)., Materials and Methods: In total 60 patients were examined with GERD time-divided into 2 equal groups on the receiving PCT Leukemia over standard dose for at least one year. The first group consisted of 30 subjects with non-erosive GERD (NEGERD) endoscopically positive form receiving PCT. The second group consisted of 30 subjects with erosive form of GERD (EFGERD) receiving PCT. Patients underwent endoscopy, morphological and immunohistochemical examination of the esophageal mucosa to the definition expression of molecules PCNA, Bcl-2, neurokinin A, substance P and factor Nf-Kb. In patients with refractory form of GERD to proton pump inhibitors therapy (PPIs), additionally imposed ursodeoxycholic acid., The Results: Patients with NEGERD receiving PCT in 33.3% of cases formed refractory to PPIs form of the disease, when EFGERD refractoriness occurs in 46.7% of patients, which is associated with slowing the proliferation of epithelial cells of the esophagus due to decreased expression of PCNA. Reduced expression of neurokinin A in patients receiving PCT is associated with less activity and intensity of inflammation of esophageal mucosa. Against the background of a high degree of PCT expression of Bcl-2 and factor Nf-Kb, which may explain the frequent detection of atrophic and meta- plastic changes in the esophageal mucosa. Appointment of ursodeoxycholic acid in the complex therapy of GERD can overcome resistance to PPIs and improve the performance of cell renewal., Conclusion: Due to the frequent development of GERD refractory to PPIs in patients suffering from diseases requiring the appointment of long-term courses of PCT requires the appointment of cytoprotective therapy, as that can be used ursodeoxycholic acid.

Aim: To investigate the phenotypic and visceral signs of connective tissue dysplasia (CTD) and comorbid diseases of the digestive system in gastroesophageal reflux disease (GERD) patients with different types of esophageal reflux as the predictors of its variants., Material and Methods: In 124 patients with GERD the clinical features, phenotypic and visceral signs of undifferentiated CTD were studied in details., Results: In 82.0% of patients with GERD associated with gastroesophageal type of reflux (GER) phenotypic and especially visceral signs of STD were detected, mainly in the form of cardiochalasia and hiatal hernia. In patients with duodenogastroesophageal reflux symptoms (DGER) the signs of STD were marked in 42.0% of cases, mostly in the form of biliary tract structure abnormalities. The risk of GERD associated with prevalence of GER, was 11.9 times higher in the presence of diagnostically meaningful combination of 6 or more signs of STD than in patients with DGER. Realization of predictor options in GER occurs in the preference of sharp, acidic foods, spices, taking medications that reduce lower esophageal sphincter tone. GERD, associated with DGER, is formed in patients with family history of diseases of the biliary tract and in the preference of food rich of calories., Conclusion: Study of STD symptoms as predictors of structural development of GERD and its variants is prospective to predict disease, choice of profession and eating behavior, primarily in young adults.

Background: Our goal was to verify surgical factors that affect duodenogastric reflux (DGR) after esophagectomy through the use of a flow visualization model that would mimic an intrathoracic gastric tube., Methods: Transparent gastric tube models for different routes (retrosternal space [RS] and posterior mediastinum [PM]) were fabricated. Various distal pressures were applied to the experimental model filled with water, and the flow was recorded with a high-speed camera. The volume and maximum height of the refluxate through the pylori of two different sizes (7.5 mm, 15 mm) in two different postures (upright, semi-Fowler) was measured by analyzing the video clips., Results: For the large pylorus setting, when the pressures of 20, 30, and 40 mmHg were applied in the upright position, the volumes of the refluxate in the RS/PM tubes were 87.7 ± 1.1/96.4 ± 1.7 mL, 150.8 ± 1.1/158.0 ± 3.2 mL, and 156.8 ± 3.3/198.0 ± 4.7 mL (p < 0.05), and the maximum heights were 101.6 ± 4.8/113.4 ± 2.9 mm, 151.4 ± 2.2/165.4 ± 1.5 mm, and 166.1 ± 1.7/193.7 ± 6.6 mm (p < 0.05). The data for the small pylorus setting or in the semi-Fowler position showed similar tendencies. For any given route, posture or pressure setting, DGR in the large pylorus model was definitively higher than that for small one., Conclusions: This fluid mechanics study demonstrates posterior mediastinal gastric interposition or pyloric drainage procedure, or both, is associated with high reflux of duodenal contents.

Introduction: Duodenogastric reflux, commonly encountered as an aftermath of gastroenteroanastomosis, with or without gastric resection (Billroth I, Billroth II), vagotomy and pyloroplastic surgery, is known to cause inflammatory-dystrophic-metaplastic lesions of gastric mucosa. Our objective was to determine the effects of surgery-induced duodenogastric reflux on the development of precarcinogenic lesions or carcinoma in correlation with the reflux duration., Material and Methods: The experiment was performed on three groups of Wistar rats with 1) Billroth II-induced reflux surgery, 2) resection of the Rouxr-en-Y type reconstruction, and 3) control group with no resection. The aim of the experiment was to study the effects ofduodenogastric reflux on the rat gastric mucosa in correlation with two different types of gastroenteroanastomosis 8, 16 and 24 weeks after the surgery., Results: In Billroth II group, hyperplastic changes were observed as early as in week 16. Statistically significant results were recorded in week 24, with 6.7% of metaplastic alterations, including dysplasia of all three degrees, dominantly severe dysplasia in 66.67%, early carcinoma in 20% and gastric carcinoma in 6.67%. In the Roux-en-Y group, gastric mucosa remained predominantly normal (60%), with somewhat increased frequency ofgastritis and dysplasia in week 24. In the control group, the finding of normal gastric mucosa was constant., Conclusion: The experiment confirms that direct contact of duodenal juice with gastric mucosa associated with Billroth II resection causes precarcinogenic lesions. Development of adenocarcinoma caused solely by duodenogastric reflux, excluding a carcinogenic agent is possible 20 weeks after the experiment--earlier than suggested by previous researchers.

The definition of early carcinoma of the esophagus has changed with time on the basis of new data. As from 2007 an early carcinoma is defined as an intramucosal carcinoma with or without metastasis. In the subclassification based on invasion depth, m1 and m2 squamous cell carcinomas have no metastasis and are considered curable by endoscopic resection alone, whereas less than 10% of m3 carcinomas and some 20% of sm1 squamous cell carcinomas have lymph node metastasis. In this article the relationship between various histopathological findings and the incidence of lymph node metastasis is reviewed. The m3 and sm1 superficial squamous cell carcinomas showing 0-I and 0-III types, large tumors over 50 mm in size or those showing vessel permeation have higher incidences of lymph node metastasis. In the field of gastrointestinal surgical pathology pathologists are now expected to not only diagnose the presence or absence of malignancy but also to investigate in detail many of the histological factors related to the prevalence of lymph node metastasis.

Background/aims: Esophagitis after total gastrectomy has been associated with biliary and pancreatic reflux into the esophagus. The aim is to clarify the effect of PPI (rabeparazole) on these factors in esophagitis., Methodology: Sixteen 8-week old male Wistar rats underwent total gastrectomy and esophagoduodenostomy to induce esophageal reflux of duodenal juice. In 5 rats, the sham operation induced a midline laparotomy alone. One week following surgery, they were treated with control (saline) or PPI (rabeprazole) (30mg/kg) ip. Three weeks after operation, all rats were euthanized and the esophagus was evaluated histologically. Esophageal injury was evaluated by macroscopic and microscopic findings, and expression of COX2 and PGE2. Esophageal washing was aspirated for the evaluation of bile acid activity., Results: At 3 weeks after surgery, duodenal reflux induced esophageal erosions and ulcer formation as well as marked thickening of esophageal wall. The macroscopic ulcer score and histological ulcer length were significantly reduced by treatment with rabeprazole. The enhanced expression of COX2 and PGE2 in the control group was also markedly inhibited in the rabeprazole treated group. The bile acid activity in the esophageal lumen was significantly increased in the control group and this increase was significantly inhibited in the rabeprazole treated group., Conclusions: Rabeprazole significantly reduces inflammation and hyperplasia in esophageal mucosa. These results indicate that bile acid, inhibited by rabeprazole, plays an important role in mucosal damage induced by duodenal reflux.

A detailed analysis of clinico-endoscopic peculiarities of gastric ulcer type I and II was presented. The peculiarities of a clinical course and the complications character of differently localized gastric ulcers were determined. There was shown the connection between concomitant disorders of esophagogastroduodenal motor-evacuation function and gastric ulcer localization and type. While tactics of treatment and operative procedure choosing it is mandatory to take into account the clinical course peculiarities and the results of endoscopic investigation.

Aim: To determine the chronic cholangitis risk factors and to provide a practically significant diagnostic criteria of chronic cholangitis in patients after cholecystectomy., Materials and Methods: Were examined the clinical, anamnestic data, clinical laboratory and instrumental studies of the condition of the hepatobiliary system in 127 patients with chronic cholangitis after cholecystectomy. The determination of microbial contamination of bile was performed during the duodenal intubation., Results: In the bile microbial landscape study were noted the violation of biliary system microbiota in 92.1% of cases. Herewith identified a combination of bacterial factors with parasitic invasion (mixed infection) in 28 (22.0%) patients. Cholangitis develops in the presence of duodeno biliary reflux, duodenal motility disorders and hypotonia of Oddi's sphincter in the early postoperative period. In the late periods after cholecystectomy, cholangitis chronization defines outflow obstruction and cholestasis due to functional or organic causes in most patients., Conclusions: Risk factors for chronic cholangitis should be referred to long history of gallstone disease, performance of cholecystectomy in the emergency order against the inflammatory process of thehepatobiliary system, absence of adequate correction of postoperative hypertension of bile duct, destruction of sphincter apparatus major duodenal papilla during surgery.

The article presents research data of duodenogastral reflux (DGR) role in patients with gastroesophageal reflux disease. It is shown that in the presence DGR, the reflux esophagitis is detected at a higher frequency and outside of esophageal manifestations of the disease. The comorbidities of hepatobiliary zone and pancreas contributes to the DGR development, as well as the syndrome of bacterial overgrowth in the small intestine.

Endoscopical and histological features of oesophagogastroduodenal zone, parameters of pH-metry and electrogastroenterography, qualitative and quantitative characteristics of microbiocenosis were studied in 80 female persons with postcholecystectomy syndrome more then a year after cholecystectomy. In the presence of duodenogastral reflux the most natural is the combination of distal oesophagitis, antral atrophic gastritis and duodenitis, accompanied with low level of gastric acidity, gastric hypokinesis and duodenal dyskinesis, dysbacteriosis of mucosal microflora with its quantitative increase and appearance of bacteria with expressed pathogenicity non-typical for this biotope. These data should be taken into consideration for determination of pre- and postoperative treatment tactics for patients with gallstones.

Background: Selective serotonin reuptake inhibitors (SSRIs) are the most widely used antidepressants in the world. Recent studies, however, have raised the concern that SSRIs increase the risk of gastrointestinal dysfunction. Therefore, we conducted a case-control study on gastrointestinal symptoms and endoscopic findings in patients who were taking SSRIs in Japan., Methods: Forty-one patients who were taking SSRIs (SSRI-treated group) and 82 age- and sex-matched patients who were not taking antidepressants (control group) were selected from the population of patients who underwent endoscopic examination from January 1, 2005 to March 31, 2010 in our institution, and their subjective symptoms and endoscopic findings were analyzed. Patients who were taking proton pump inhibitors (PPIs) and/or histamine H(2)-receptor antagonists (H2RAs) were excluded from this study., Results: The chief complaints at the endoscopic examination were classified into the following 4 categories: reflux symptoms, dysmotility symptoms, ulcer-like symptoms, and no upper abdominal symptoms. No significant difference was found in the complaint rate of each category between the SSRI-treated and the control groups. No significant differences were found between the groups in endoscopic findings, the LANZA score and the rate of chief complaints in patient classes stratified by the endoscopic finding., Conclusion: It was not evident that SSRIs induced mucosal damage of the upper gastrointestinal tract. And, it is considered that SSRIs do not increase the risk of upper gastrointestinal symptoms in patients treated with SSRIs for 1 month or longer. The present study suggests that SSRI medication does not have a bad influence on gastrointestinal symptoms and gastrointestinal organic diseases.

To study the impact of Opisthorchis infestation on the upper digestive tract and small bowel in chronic inflammatory bowel diseases, the authors examined 164 patients with inflammatory bowel diseases, including 71 patients with ulcerative colitis and 45 with Crohn's disease without parasitosis and 48 with chronic opisthorchiasis (31 with ulcerative colitis and 17 with Crohn's disease). A control group consisted of 20 healthy individuals and 20 patients with chronic opisthorchiasis. A diagnosis was established by colonofibroscopy and a morphological study of colonic biopsy specimens. Gastric mucosal atrophic changes and motor evacuatory disorders as duodenogastric reflux were significantly more frequently encountered in inflammatory bowel diseases concurrent with chronic opisthorchiasis. The presence of Opisthorchis infestation significantly worsened fat and carbohydrate malabsorption in the small bowel in inflammatory bowel diseases.

Objective: To determine the frequency of duodenogastric reflux (DGR), and to assess the changes in the gastric mucosa in the presence of bile reflux., Materials and Methods: Our study includes the results of 1371 gastroduodenoscopies carried out in 2008, for patients between 65 and 92 years old, the study includes both kind of patients who were admitted to hospital and those who were investigated on an outpatient basis. The main group includes 695 patients with various level of DGR severity, and the control group consists of 676 patients without DGR., Results: DGR was diagnosed in 14.8% more in women. In case of the presence of DGR we have found changes in the antrum mucosa as congestion, and minor erosion, hyperplasia, metaplasia of gastric and esophageal mucosa, and stomach polyps. And we have not noticed such changes when DGR was absent. We have found that the high frequency of antral hyperplasia is correlated to the DGR severity., Conclusion: DGR is diagnosed in more than 10% of patients who undergo gastroduodenoscopy. DGR is an indicator of conditions often associated with various morphological changes in gastric mucosa; therefore this finding has to be taken in consideration in the further investigations and management of such patients.

The article examines the state of the antral mucosa of the stomach in 43 young patients with duodeno-gastric reflux without any clinical manifestations. In 69.9% of investigated revealed changes in the gastric mucosa, characteristic of reflux gastritis. The comparative characteristic of stereometric indicators of cellular elements, infiltrated own plate of a mucous membrane of a stomach is spent at a reflux-gastritis and the mixed gastritis (at presence Helicobacter pylori). Article is illustrated by 2 tables.

Background: The initial response of esophageal mucosa to gastroduodenal reflux is inflammation and hyperplasia. Secretory phospholipase A(2) (sPLA(2)) is a known mediator of gut inflammation, and its levels are increased in Barrett's esophagus. We hypothesized that the sPLA(2) gene is required to produce esophageal mucosal hyperplasia in response to gastroduodenal reflux., Methods: C57BL/6 (n = 5) sPLA(2) (-/-) mice and C57BL/6( Cg-Tg(PLA2G2A)703N16 ) mice (n = 4) sPLA(2) (-/+) underwent a side-to-side surgical anastomosis between the duodenum and gastroesophageal junction (DGEA). Control animals [sPLA(2) (-/-) (n = 5), sPLA(2) (-/+) (n = 4)] underwent laparotomy with incision and repair of the esophagus. Tissue was harvested after 4 weeks, and H&E staining was performed to quantify esophageal mucosal thickness. Ki67 and sPLA(2) immunostaining were performed to quantitate differences in cell division and sPLA(2) expression., Results: Mice expressing human sPLA(2) had a 2.5-fold increase in thickness of the esophageal mucosa as compared to controls (p = 0.01). A 6.5-fold increase in proliferation (p = 0.02) and a twofold increase in sPLA(2) expression (p = 0.04) were demonstrated in animals exposed to gastroduodenal reflux., Conclusions: The presence of sPLA(2) is necessary for early mucosal hyperplasia produced by exposure of the esophagus to gastroduodenal contents. sPLA(2) expression is upregulated by gastroduodenal reflux, strengthening its role as a critical mediator of early mucosal hyperplasia.

Purpose: To investigate the combined effects of reflux of duodenal contents through the pylorus and treatment with N-methyl-N'-nitro-nitrosoguanidine (MNNG) on the development of lesions in the glandular stomach, at the gastrojejunal anastomosis and in the forestomach of rats., Methods: Eighty Male Wistar rats were divided into 4 groups: G1: MNNG + Reflux, G2: Reflux, G3: MNNG and G4: Gastrostomy. MNNG was given in the drinking water (100 mg/ml) for 12 weeks and then two groups (G1 and G2) were submitted to a gastrojejunal anastomosis followed by section of the afferent loop and suture of both stumps to allow reflux of duodenal contents through the pylorus. The animals were sacrificed 18 and 36 weeks after surgery. The lesions obtained in the antral mucosa, at the gastrojejunal anastomosis and in the forestomach were analysed histologically., Results: Duodenal reflux induced proliferative lesions at both glandular and squamous mucosa of the stomach. In the antrum, adenomatous hyperplasia (AH) was observed in 20% and 50% of the animals at the 18th and 36th weeks respectively. Aditionally 85% of the animals presented AH at the gastrojejunal anastomosis and 60% developed squamous hyperplasia at the squamous portion of the stomach. MNNG treatment plus duodenal reflux enhanced the development of malignant tumors at both glandular and squamous mucosa, since there were 30% of antral adenocarcinomas and 45% of squamous carcinomas at the 18th week and the frequency of these malignant tumors rose to 50% in the antrum and 65% in the squamous mucosa at the 36th week., Conclusion: The reflux of duodenal contents through the pylorus enhanced the development of proliferative lesions, benign and malignant, in the glandular stomach and in the forestomach of rats.

Experimental gastroduodenal ulcer was simulated after pre-injection of serotonin; gastroesophageal reflux disease and duodenogastral reflux were induced. Activation of the serotoninergic system promoted the development of alteration processes in gastroduodenal ulcer.

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., (Copyright (c) 2009 American Cancer Society.)

Background: Subtotal esophagectomy and gastric pull-up with cervical anastomosis is the main treatment for advanced achalasia. This surgical technique has been associated to esophagitis and also Barrett's epithelium following esophagectomy., Aim: To analyze late clinical, endoscopic, and pathologic findings in the esophageal stump (ES) mucosa after subtotal esophagectomy in patients treated for advanced chagasic achalasia., Methods: 101 patients submitted to esophagectomy and cervical gastroplasty were followed-up prospectively for a mean of 10.5 +/- 8.8 years. All patients underwent clinical, endoscopic and histopathological evaluation every 2 years. Gastric acid secretion was also assessed., Results: The incidence of esophagitis in the esophageal stump (45.9% at 1 year; 71.9% at 5 years, and 70.0% at 10 years follow-up); gastritis in the transposed stomach (20.4% at 1 year, 31.0% at 5 years, and 40.0% at 10 or more years follow-up), and the occurrence of ectopic columnar metaplasia and Barrett's Esophagus in the ES (none until 1 year; 10.9% between 1 and 5 years; 29.5% between 5 and 10 years; and 57.5% at 10 or more years follow-up), all rose over time. Gastric acid secretion returns to its preoperative values 4 years postoperatively. Esophageal stump cancer was detected in the setting of chronic esophagitis in five patients: three squamous cell carcinomas and two adenocarcinomas., Conclusion: (1) Esophagitis and Barrett's esophagus in the esophageal stump rose over time. (2) These mucosal alterations and the development of squamous cell carcinoma and adenocarcinoma are probably due to exposure to duodenogastric reflux, and progressively higher acid output in the transposed stomach.

We conducted a literature review to identify elements of duodenogastroesophageal reflux (DGER)--namely pancreatic fluids, hydrochloric acid, pepsin, and bile--as to the effects each has when refluxed to the extraesophageal structures. Further, we wished to acquaint clinicians with the possibilities that, in addition to hydrochloric acid, the other components of DGER are likewise contributing to disease in the extraesophageal areas. Our review included studies that have indicated reflux of the above mentioned components of DGER to the pharynx, larynx, tracheobronchial tree, oral cavity, nasopharynx, nose and sinuses, eustachian tube, and middle ear. Findings demonstrate that injury to the upper aerodigestive tract can occur from a variety of substances secreted from the stomach and duodenum. Treatment for DGER is nonspecific. We conclude that patients with an incomplete response to acid suppression may have significant involvement of pepsin, bile, or both. Future studies are needed to clarify the importance of these elements and to suggest more precise treatments.

Objective: Duodenogastric reflux (DGR) is a reverse flow of duodenal juice into stomach through pylorus composed of bile acid, pancreatic secretion, and intestinal secretion. The increased entero-gastric reflux results in mucosal injury that may relate not only to reflux gastritis but also esophagitis, gastric ulcers, carcinoma of stomach and esophagus. However, the exact mechanisms of gastric mucosal damage caused by DGR are still unknown. 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, Hp infection and intragastric acidity., Method: Totally 81 patients with upper gastrointestinal manifestations were enrolled and they were graded according to the symptom scores and underwent endoscopic, histological examinations and 24-hour intra-gastric bilirubin was monitored with Bilitec 2000. Of the 81 cases, 51 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, Hp infection, intragastric acidity were analyzed respectively., Result: The total fraction time of bile reflux in the patients with hyperemia and yellow stain gastric antral mucosa under endoscopy was significantly higher than that without those changes [17.1% (0.5% approximately 53.2%) vs. 6.5% (0 approximately 58.6%), Z = -1.980, P < 0.05; 19.8% (0.5% approximately 58.6%) vs. 8.8% (0 approximately 38.0%), Z = -2.956, P < 0.01 respectively]. Histologically, the cases with intestinal metaplasia had significantly higher total fraction time of bile reflux than in the cases without intestinal metaplasia [29.0% (1.9% approximately 58.6%) vs. 14.3% (0 approximately 53.7%), Z = -2.026, P < 0.05], but no significant difference was found either between the cases with and without chronic inflammation (P > 0.05) or between the cases with and without active inflammation (P > 0.05). The severity of bile reflux was positively correlated with the score of abdominal distention (r = 0.258, P < 0.05), but no correlation with either the severity of intragastric acid (r = -0.124, P > 0.05), or Hp infection (r = 0.016, P > 0.05) was found., Conclusion: Primary DGR could cause gastric mucosal lesions manifested mainly as hyperemia and bile-stained gastric antral mucosa under endoscopy and the gastric antral intestinal metaplasia histologically in children. There was no significant correlation between DGR and gastric mucosal inflammatory infiltration. DGR had no relevance to Hp infection and intragastric acidity. We conclude that DGR is probably an independent etiological factor and might play a synergistic role in the pathogenesis of gastric mucosal lesions along with gastric acid and Hp infection.

Background: To assess the effect of Roux-en-Y gastric bypass (RYGB) at a tertiary referral Center of Excellence for bariatric surgery on the length and presence of dysplasia in morbidly obese patients with Barrett's esophagus (BE). Esophageal reflux of gastroduodenal contents (acid, bile) contributes to the development of BE and progression in the dysplasia-carcinoma sequence. Obese patients have a high prevalence of gastroesophageal reflux and might be at an increased risk of developing BE and esophageal adenocarcinoma. The effect of eliminating duodenogastroesophageal reflux on BE is not known., Methods: We performed a retrospective review of all patients with pre-existing, biopsy-proven, long-segment (>3 cm) BE undergoing RYGB at our institution. Only patients with >1 year of endoscopic, biopsy-controlled follow-up (mean 34 mo) were included., Results: Five patients (3 men and 2 women) were identified. The mean +/- standard error of the mean preoperative length of BE was 6 +/- 2 cm; 2 patients had low-grade dysplasia and 1 indeterminate dysplasia. At the postoperative follow-up (>1 yr) examinations, the length of BE had decreased in 4 patients; the overall length was 2 +/- 1 cm; and only 1 patient had dysplasia. All patients experienced a decrease in the length of BE (n = 4), complete disappearance of BE (n = 2), or improvement in the degree of dysplasia (n = 3). The body mass index had decreased from 43 +/- 4 kg/m(2) to 33 +/- 3 kg/m(2), and all experienced subjective improvement in reflux symptoms postoperatively. RYGB resulted in complete or partial regression of BE in 4 of 5 patients and improvement in reflux symptoms in all., Conclusion: Our results suggest that RYGB might be the procedure of choice in morbidly obese patients with BE requiring surgical treatment for gastroesophageal reflux disease.

We present a patient with a large hiatal hernia resulting in duodenogastric reflux that was seen as abnormal activity below and behind the heart (retrocardiac) on SPECT images and on (99m)Tc-tetrofosmin cardiac SPECT raw-data projection images. Incidental findings such as extra- and retrocardiac activity in the thorax and abdomen should be included on all comprehensive cardiac SPECT reports.

The dietary components responsible for the development of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) remain unclear. Wistar rats were divided into four groups based on their diet: a low soybean-oil diet, a low cow-fat diet, a high soybean-oil diet, and a high cow-fat diet. First, we evaluated the bile acid composition of the bile juice in each group without operation, using high-performance liquid chromatography. Because only high cow-fat intake induced changes in the composition of bile acids in bile juice, we then selected animals fed with a low soybean-oil diet and those with a high cow-fat diet to carry out esophago-jejunostomy for reflux of the duodenal contents, and compared sequential morphological changes between these groups up to 30 weeks after surgery. At 30 weeks after surgery, the reflux animals in the high cow-fat group showed a significantly higher incidence of BE and Barrett's dysplasia than those in the low soybean-oil group, and the incidence of EAC in the high cow-fat group was also slightly higher than that in the low soybean-oil group. High dietary animal fat changed the bile-acid composition and increased the concentration of taurine conjugates in the bile juice. These increased bile acids promoted the development of BE and Barrett's dysplasia leading to EAC.

The aim of this study is to investigate the cyclooxygenase (COX)-2 expression in esophageal epithelium of rat duodenoesophageal reflux model and the effect of a selective COX-2 inhibitor on esophageal adenocarcinogenesis in rats. A series of rats underwent a duodenoesophageal reflux procedure and were divided into 2 groups. One group was given commercial chow (control group), and the other group was given experimental chow containing nimesulide, a selective COX-2 inhibitor (nimesulide group). The animals were sacrificed sequentially after surgery and esophageal examinations were performed. In the control group, esophagitis, Barrett's esophagus (BE) and adenocarcinoma (EAC) were observed, and the frequency of these conditions increased with time. COX-2 expression, PGE(2) level and proliferative activity were up-regulated, predominantly in the inflamed esophageal epithelia, from the 10(th) week. In the nimesulide group, the esophagitis was mild and the frequency of BE was significantly lower than the control group, while EAC was not observed throughout the experiment. PGE(2) level and proliferative activity were lower in the nimesulide group than in the control group. COX-2 may play an important role in esophageal carcinogenesis through the activation of the inflammation-metaplasia-adenocarcinoma sequence. Nimesulide is effective in preventing BE and EAC by suppressing COX-2 activity.

Purpose: to investigate if combining VT to DGR through the pylorus can modulate the biological behavior of PL induced by DGR and to verify if TV alone can induce morphologic lesions in the gastric mucosa., Methods: 62 male Wistar rats were assigned to four groups: 1 - Control (CT) gastrotomy; 2 - Troncular Vagotomy (TV) plus gastrotomy; 3 - Duodenogastric reflux through the pylorus (R) and 4 - Troncular vagotomy plus DGR (RTV). The animals were killed at the 54 week of the experiment. DGR was obtained by anastomosing a proximal jejunal loop to the anterior gastric wall. TV was performed through isolation and division of the vagal trunks. Gastrotomy consisted of 1 cm incision at the anterior gastric wall. PL were analyzed gross and histologically in the antral mucosa, at the gastrojejunal stoma and at the squamous portion of the gastric mucosa., Results: Groups R and RTV developed exophytic lesions in the antral mucosa (R=90.9%; RTV=100%) and at the gastrojejunal stoma (R=54.54%; RTV=63.63%). Histologically they consisted of proliferative benign lesions, without cellular atypias, diagnosed as adenomatous hyperplasia. Both groups exposed to DGR presented squamous hyperplasia at the squamous portion of the gastric mucosa (R= 54.5%; RTV= 45.4%). TV, alone, did not induce gross or histological alterations in the gastric mucosa. TV did note change the morphologic pattern of the proliferative lesions induced by DGR., Conclusions: DGR induces the development of PL in the pyloric mucosa and at the gastrojejunal stoma. TV does not change the morphologic pattern of the proliferative lesions induced by DGR. TV alone is not able to induce morphologic lesions in the gastric mucosa.

Objective: To assess the long-term results of the duodenal switch operation made for pathologic transpyloric duodenogastric reflux (DGR)., Summary Background Data: DGR symptoms and lesions are poorly responsive to medical treatment., Methods: A duodenal switch operation was made on 48 patients suffering from pathologic transpyloric DGR either unrelated (n = 28) or secondary (n = 20) to previous upper gastrointestinal (GI) surgery, including cholecystectomy or vagotomy. The diagnosis was based on the combination of several objective arguments: a long history of gastric symptoms (ie, nausea, epigastric pain, and/or bilious vomiting) poorly responsive to medical treatment (48 of 48), gastroesophageal reflux symptoms unresponsive to proton-pump inhibitors (PPI) (23 of 29), gastritis on upper GI endoscopy (37 of 48) and/or at histology (28 of 41), presence of a bilious gastric lake at >1 upper GI endoscopy (30 of 48), DGR at diisopropyl iminodiacetic acid (DISIDA) scintigraphy scanning (7 of 13), pathologic 24-hour intragastric bile monitoring with the Bilitec device (40 of 41), and absence of Helicobacter pylori antral infection (39 of 41)., Results: At follow-up (median, 81 months), gastric symptoms were nil, had improved, and remained unchanged in 29 (60.4%), 16 (33.3%), and 2(4.2%) patients, respectively, and 1 patient experienced symptomatic recurrence after a 92-month symptom-free period (2.1%). Among the 44 patients who had postoperative upper GI endoscopy, 42 (95.5%) had no gastritis whereas 5 (11.3%) had an ulcer at the duodenojejunostomy. Gastric exposure to bile at postoperative 24-hour intragastric Bilitec test in 36 patients was nil, within the normal range, and still slightly pathologic in 15 (41.7%), 19 (52.8%), and 2 (5.5%), respectively., Conclusions: The duodenal switch operation made on patients in whom diagnosis of pathologic transpyloric DGR is supported by several objective arguments provides most of them with symptomatic and endoscopic improvement parallel to abolishment or normalization of gastric exposure to bile. Postoperative PPI therapy during a 2-month period is to be recommended to prevent the development of an anastomotic ulcer.

Purpose: To analyze mucosal proliferation and its characteristics, through specific models of duodenogastric reflux, in the stomach of Wistar rats., Methods: Seventy-five healthy and adult male rats were divided into three groups: group I--control (n = 25 animals), submitted to gastrotomy of the posterior wall of the glandular stomach; group II--DGR (n = 25 animals), submitted to duodenogastric reflux through latero-lateral gastrojejunal anastomosis in the posterior wall of the glandular stomach and group III--DGR-P (n = 25 animals), submitted to duodenogastric reflux through the pylorus following the same procedure of group II, sectioning and closing the afferent loop. The animals were observed during 36 weeks and subsequently the mucosal lesions were analyzed, with macroscopic and microscopic examination of the prepyloric, the gastrojejunostomy and the squamous area of the stomach., Results: Group I did not present any kind of lesion. Macroscopic lesions of the prepyloric area in groups II and III were 0% and 20%, respectively. Macroscopic lesions of the gastrojejunal stoma in groups II and III were 36% and 88%, respectively, and 12% and 28%, respectively, in the squamous area. Microscopically, adenomatous hyperplasia (AH), squamous hyperplasia (SH) and adenocarcinoma (AC) were diagnosed. The occurrence of AH at the prepyloric area in groups II and III was 0% and 40%, respectively, and in the gastrojejunal stoma, 40% and 72%, respectively. The occurrence of SH in the squamous area in groups II and III was 12% and 20%, respectively, without statistical differences between the groups. AC was found only in three animals of groups III (12%)., Conclusions: The duodenogastric reflux in this experimental model caused high frequency of proliferative lesions of the gastrojejunal stoma and in the prepyloric area, while adenocarcinoma was a rare occurrence.

Background: Reflux of the duodenal contents with gastric acid has been reported to contribute to the development of esophageal mucosal damage and inflammation. Recent studies show that pancreatic trypsin can stimulate the production of inflammatory mediators, including chemokines and prostaglandins from human esophageal epithelial cells in vitro. The aim of the present study was to investigate the role of pancreatic trypsin in the pathogenesis of chronic esophageal inflammation induced by gastroduodenal reflux in rats., Methods: Esophagogastroduodenal anastomosis was carried out in male Wistar rats by anastomosing the jejunum to the gastroesophageal junction under diethyl ether inhalation anesthesia. The animals undergoing surgery were treated with the control diet, rabeprazole sodium, nizatidine, ecabet sodium, camostat mesilate (CMM), ONO-1714, a specific inducible nitric oxide synthase (iNOS) inhibitor, or meloxicam, a selective cyclooxygenase-2 (COX-2) inhibitor. Esophageal injury was evaluated by macroscopic and microscopic findings, and mRNA expression for CINC-1, COX-2, and iNOS was determined by real-time polymerase chain reaction (PCR). Trypsin activity within the esophageal lumen was measured 2 weeks after surgery, and the expression of protease-activated receptor (PAR)-1 and -2 was confirmed by reverse transcription (RT)-PCR., Results: At 8 weeks after surgery, gastroduodenal reflux induced esophageal erosions and ulcer formation as well as marked thickening of the esophageal wall. Histological study showed an increase of thickness of the esophageal mucosa, hyperplasia of the epidermis and basal cells, ulcer formation, and marked infiltration of inflammatory cells. The macroscopic ulcer score and histological ulcer length were significantly reduced by treatment with rabeprazole or CMM but not by nizatidine or ecabet sodium, compared with each control. Rabeprazole, nizatidine, or ecabet sodium did not affect the severity of mucosal hyperplastic scores or histological parameters in esophagitis. In contrast, the CMM group showed a significant decrease in the mucosal hyperplastic and inflammatory scores. The enhanced expression of CINC-1, COX-2, and iNOS mRNA in the control group was also markedly inhibited in the CMM-treated group. ONO-1714 or meloxicam treatment significantly reduced the macroscopic scores of ulcer and hyperplasia. The trypsin activity in the esophageal lumen was significantly increased in the control diet group, and this increase was significantly inhibited in the CMM-treated group. The expression of PAR-1 and -2 mRNA was confirmed in rat esophageal epithelium., Conclusions: With this model, we have demonstrated that CMM significantly reduces inflammation and hyperplasia in the esophageal mucosa. These results indicate that trypsin, which is primarily inhibited by CMM, plays an important role in the mucosal damage induced by gastroduodenal reflux and that it can be a therapeutic target in patients with gastroduodenal reflux esophagitis.

Gastroesophageal reflux (GER), through the occurrence of gastroesophagopharyngeal reflux (GEPR), is an established cause of several otorhinolaryngological (ORL) manifestations. It has been suggested that unexplained excessive throat phlegm might also be a manifestation of GER, but formal evidence is lacking. The aim of the present study was to investigate the prevalence of GER as well as duodenogastroesophageal reflux (DGER) in consecutive patients with chronic complaints of excessive throat phlegm. Fifty-nine consecutive patients with chronic unexplained excessive throat phlegm, transparent in 33 patients (TTP) and yellow in 26 patients (YTP), underwent gastrointestinal endoscopy, 24-hr dual esophageal pH monitoring, and fiberoptic DGER monitoring. Proximal esophageal DGER monitoring was performed in seven YTP patients and analysis of bile acids in throat phlegm was performed on 16 samples. The effect of high-dose acid suppressive therapy was evaluated at 2-week intervals. Endoscopy and pH monitoring established a diagnosis of pathological GER in 75% of the patients. Pathological DGER was present in 56% of the patients and this was associated with YTP. Proximal DGER exposure was high in all investigated subjects and chemical analysis revealed a median bile acid concentration of 0.184 microM in nine YTP samples and no detectable bile acids in seven TTP samples. After a median of 4 weeks of acid suppressive therapy, most patients improved and 61% became asymptomatic. YTP patients were more likely to require maintenance acid suppressive therapy than TTP patients. Unexplained excessive throat phlegm is a sign suggestive of GER and GEPR, and unexplained yellow throat phlegm a sign suggestive of duodenogastroesophagopharyngeal reflux (DGEPR).

This study investigated the assessment of visceral perception and gastric tone using insufflation during endoscopy. The intragastric pressure was measured during insufflation in 16 patients with gastro-oesophageal reflux disease, 25 patients with functional dyspepsia and 24 normal controls, using a pressure transducer inserted through the forceps aperture until gastric symptoms appeared. The intragastric pressure at the visceral perception threshold, the time to threshold and the time-pressure curve gradient were measured. The visceral perception threshold was significantly reduced in the functional dyspepsia group compared with the normal controls. Balloons were also inserted into the duodenal bulbs of 10 normal controls to investigate the effect of efflux of air into the duodenum; the measured parameters were not influenced by inflation and deflation. These results suggest that it is possible to assess visceral perception and gastric tone by measuring changes in intragastric pressure, using gastric stimulation by insufflation during endoscopy.

Introduction: It is widely accepted that long segments of Barrett's esophagus are caused by end-stage gastroesophageal reflux disease (GERD), but little is known about the correlation of severity of GERD and extent of metaplasia., Methods: Twenty normal volunteers and 142 patients with different extent of intestinal metaplasia (39 with intestinal metaplasia limited to the esophagogastric junction, 48 with short segments of Barrett's esophagus, and 55 with long segments) underwent manometry and combined pH-bilirubin monitoring., Results: The extent of intestinal metaplasia correlated to the exposition of gastric and duodenal juice in the esophagus and inversely with a competent lower esophageal sphincter., Conclusions: The extent of intestinal metaplasia is related to the severity of GERD.

Duodenogastric reflux (DGR) was assessed in patients surgically treated for choledochal cyst, with emphasis on two different biliary reconstruction methods: Roux-en-Y hepaticojejunostomy (HJ) and hepaticoduodenostomy (HD). Gastric bile monitoring with the Bilitec device revealed excessive DGR in patients in the HD group. Endoscopic findings demonstrated mild to moderate gastric mucosal erosion in patients after HD. In contrast, neither DGR nor gastritis was found in patients after HJ. This preliminary study suggests that HJ, rather than HD, should be recommended as a method of biliary reconstruction for pediatric patients with choledochal cyst. Careful observation of DGR should be continued in patients who have undergone HD.

We reviewed our experience of Roux-en-Y hepaticojejunostomy (RYHJ) and hepaticoduodenostomy (HD) performed for the surgical repair of choledochal cyst (CC), with special emphasis on postoperative complications related to the type of biliary reconstruction performed. Eighty-six patients underwent primary cyst excision for CC from 1986 to 2002 at our institution. Forty-six cases with concurrent intrahepatic bile duct dilatation (IHBD) were excluded because HD was not used for biliary reconstruction if IHBD was present. Thus, 28 cases had RYHJ, and 12 had HD. Differences between the RYHJ and HD groups with respect to type of CC, age at cyst excision, and length of follow-up were not statistically significant. However, the incidences of postoperative complications related to biliary reconstruction, such as endoscopy-proven bilious gastritis due to duodenogastric bile reflux [4/12 (33.3%) of the HD group], and adhesive bowel obstruction/cholangitis [2/28 (7.1%) of the RYHJ group] were significantly different (p<.05). Our experience suggests that HD is not ideal for biliary reconstruction in CC because of a high incidence (33.3%) of complications due to duodenogastric bile reflux. Currently, RYHJ is our exclusive technique of choice for biliary reconstruction during the surgical repair of CC.

Summary Background Data: Duodenogastric-esophageal reflux disease is directly linked to Barrett's esophagus and to the development of esophageal adenocarcinoma. Despite this link, little is known about the mutagenic potential of refluxed material on the esophageal mucosa. We hypothesize that the reflux of gastric and duodenal content causes mutations in esophageal mucosa in vivo., Methods: Seven Sprague Dawley/Big Blue F1 lacI transgenic rats underwent esophagoduodenostomy (ED) to surgically create duodeno-gastric-esophageal reflux. Fourteen nonoperated rats served as negative (n = 7) and as positive (n = 7/methyl-N-amyl-nitrosamine [MNAN] intraperitoneally) controls. The animals were killed 16 weeks after operation or injection, the entire esophageal mucosa was harvested, and mutation frequency was determined through standard Big Blue Mutagenesis Assay., Results: Gross esophagitis was evident in all operated animals. The frequency of lacI mutations in esophageal mucosal cells of animals with ED was significantly higher, nearly 1.5-fold, than that of nonoperated animals. Nitrosamine administration resulted in a nearly 20-fold increase of lacI mutation frequency. Thirteen mutations were successfully sequenced, 46% occurred at CpG dinucleotide sites and 61% were either C to T or G to A transitions., Conclusions: The data provide preliminary evidence of the mutagenic potential of bile reflux on esophageal epithelium. The specific mutations are markedly higher than would be expected by chance and are similar to that found in p53 mutations of human esophageal adenocarcinoma, providing a link to human esophageal cancer.

Background/aims: Patients who undergo distal gastrectomy often develop duodenogastric reflux and preoperative H. pylori infection is eradicated spontaneously after distal gastrectomy in some patients. However, whether a causal relationship exists has not yet been studied. This report examines the correlation between H. pylori eradication and the amount of duodenogastric reflux following distal gastrectomy., Methodology: Among 72 consecutive patients who underwent curative distal gastrectomy with radical lymphadenectomy for gastric cancer, 37 patients had H. pylori infection preoperatively and were included in this study. The period of bile reflux (percent time) into the gastric remnant was measured with the Bilitec 2000 under standardized conditions on the 14th day after the surgery. Endoscopic examination was performed to determine the presence of H. pylori infection on week 12 after surgery., Results: The percent time was higher in patients whose H. pylori infection had been eradicated after distal gastrectomy (58.1+/-9.2%) than in patients who had H. pylori infection after distal gastrectomy (33.8+/-5.7%)., Conclusions: Duodenogastric reflux correlates with spontaneous eradication of H. pylori infection following distal gastrectomy.

Duodenogastric reflux (DGR) has been found to give rise to a hypochlorhydria secondary to alkaline reflux. We investigated whether there is a link between DGR and the gastrin, somatostatin, and serotonin cell numbers and the granular content of gastrin, somatostatin, and serotonin in endocrine cells in human antral mucosa. We investigated 38 selected Helicobacter pylori-negative patients with visual primary excessive DGR in upper endoscopy and symptoms of epigastric pain and bile vomiting. Ten control patients were included in this study. None of the patients had peptic ulcer or had received any medication. Antrum (10 biopsies from five different zones: the lesser and major curvature, the anterior and posterior wall, and the pylorus) and corpus (two biopsies from major curvature about 10 cm below the cardia) biopsy specimens were collected for routine histology, as well as for light and electron immunohistochemistry. In patients without atrophy or intestinal metaplasia and in patients with mild atrophy or mild intestinal metaplasia, the number of gastrin and somatostatin cells was not different from that in controls. In moderate atrophy or moderate intestinal metaplasia, however, the number of gastrin and somatostatin cells decreased. Serotonin cell number was significantly higher in all patients with DGR as compared with controls. The mean somatostatin granular content was increased (3.6+/-0.2 vs. 3.2+/-0.1). In addition, lysosomes with engulfed somatostatin granules were found. The mean serotonin granular content was decreased (2.3+/-0.3 vs. 2.9+/-0.3), while the mean gastrin granular content remained unchanged (2.5+/-0.3 vs. 2.4+/-0.2). Ultrastructurally, the granules in serotonin-positive cells corresponded to the gastric variant or to the intestinal variant of serotonin cells. The endocrine cells were found to have few granules positive for serotonin. It is concluded that DGR inhibits somatostatin granular release, but stimulates both serotonin granular release and serotonin cell growth.

Purpose: It's well known that Helicobacter pylori (H.p.) infection plays a leading role in gastric cancer in 70% of patients. A role of bile acids reflux in the stomach as a potentially cancerogenic factor is disputable. As the influence of both factors for malignancy, is still unknown, it was the aim of our investigations in peptic ulcer (PU) patients complicated with duodenogastric reflux (DGR)., Material and Methods: 79 PU patients (49 men, 27 women, aged 18 to 61, middle age--41.8 yrs) were observed; DGR was found in 40 of them. For all patients endoscopic examination with antral and fundal parts of the stomach mucosa biopsy were performed. The morphological picture was estimated by Dixon's scale., Results: The similar H.p. colonization level of the stomach mucosa independently of DGR presence was shown. A bile reflux co-exists with diminished acute and chronic inflammation activity and atrophy level. The quantity of the patients with complete intestinal metaplasia did not depend of DGR (32.5% vs. 33.3%), but in the patients with DGR it developed 16 years earlier (42.8 and 58.7 yrs, p < 0.05)., Conclusions: The combination of bile reflux and H.p. infection may cause progression to gastric cancer not by traditional stepwise: inflammation-atrophy-metaplasia.

Background/aims: In this study, we investigated the presence of Helicobacter pylori infection and gastric histological changes in unoperated patients with and without duodenogastric reflux., Methods: Twenty-two women and 15 men, mean age of 51.17 years, who had duodenogastric reflux during endoscopy were included. Thirty-seven age-and gender-matched patients without duodenogastric reflux served as controls. The Helicobacter pylori infection was detected by histology. The Helicobacter pylori density and gastric histology according to the modified Sydney system were evaluated with specimens from antrum, corpus and fundus., Results: The presence of Helicobacter pylori, Helicobacter pylori density, chronic inflammation score, lymphoid follicles, atrophy, and intestinal metaplasia were similar in patients with and without duodenogastric reflux (p>0.05). Acute inflammation was found to be lower in the antrum (p<0.05) in the duodenogastric reflux-positive group., Conclusion: Duodenogastric reflux does not affect the presence of Helicobacter pylori and gastric histopathologic changes.

Primary chronic gastroduodenitis (PCGD) accounts for 60-85% of the diseases of the gastroduodenal zone. In our study 90 patients with PCGD were divided into three groups getting one of the following therapies: electric sleep, hofitol, electric sleep plus hofitol. The effects of the treatments were assessed with updated techniques including computed pH-metry. Hofitol showed a good effect on dyspepsia, enhanced the alkalizing ability of the duodenal bulb. Electric sleep relieved pain and asthenoneurotic syndromes, decreased high acidity of the gastric juice in the body of the stomach. Electric sleep in combination with hofitol normalized macroscopic picture of the upper gastrointestinal tract and corrected imbalanced immunity.

To investigate the relationship between duodenogastric reflux and ulceration, gastric fluid was collected from the 1st (n = 26) and 3rd (n = 45) gastric compartments of llamas and alpacas during postmortem examination. Gastric fluids were analyzed for the presence of bile acids. Additionally, the 3rd compartment was examined grossly for the presence of erosions or ulcers, and the intestines were examined for evidence of fluid distention. Detectable bile acids were found in the 3rd compartment fluid of 1 of 28 camelids without ulcers, 7 of 14 camelids with ulcers, and 3 of 3 camelids with intestinal distention. Third compartment bile content was significantly higher in camelids with ulcers (median = 2.9 micromol/L) or intestinal distention (median = 371.5 micromol/L) than those with neither (median = 0 micromol/L). Bile acids were detected in the 1st gastric compartment in only 2 camelids. These findings suggest a reflux of duodenal contents, including bile acids, into the 3rd compartment in camelids with ulcers, similar to what is seen in camelids with poor intestinal emptying. Whether bile reflux was the cause of the ulcers or occurred after or concurrent to their development remains unknown.

Background: To elucidate the histogenesis of Barrett's esophagus and esophageal adenocarcinoma, we designed a duodeno-gastric reflux model in which normal stomach function and normal nutritional status are retained., Methods: Male Wistar rats were used in the experiment. The esophago-gastric junction was side-to-side anastomosed to a loop of jejunum about 3 cm distal to Treitz's ligament. The animals were not exposed to any known carcinogens during the experiment. Sequential morphological changes were studied for up to 50 weeks after surgery. Serial sections were made and stained with hematoxylin and eosin (H&E). In addition, immunohistochemical staining for bromodeoxyuridine (BrdU) was performed along with histochemical staining for mucins using paradoxical concanavalin A (ConA), galactose oxidase Schiff (GOS), and high-iron diamine-alcian blue (HID-AB)., Results: Severe esophagitis with squamous cell hyperplasia was noted in all animals after surgery. At week 20 after surgery, glandular metaplastic cells positive for ConA first appeared within the basal cell layer of esophageal squamous cell epithelium, and then GOS-positive cells and HID-AB goblet cells appeared. This is a characteristic of the specialized columnar epithelium of Barrett's esophagus. We detected esophageal adenocarcinomas in 1 out of 8 subjects at week 40 and in 3 out of 8 subjects at week 50 after surgery., Conclusions: Reflux of duodenal contents causes specialized columnar epithelium of Barrett's esophagus and esophageal adenocarcinoma. As part of the sequence of events leading to the development of Barrett's esophagus, pyloric-foveolar metaplasia was observed followed by the appearance of intestinal goblet cells. The pyloric-foveolar metaplasia appears to be associated with chronic mucosal damage and regeneration. This multiplastic cell lineage is referred to as 'gut-regenerative cell lineage' (GRCL).

Objective: Our objective was to determine the relationship between reflux of duodenogastric contents with different degrees of esophagitis, and its levels and activity, with regard to the severity of esophagitis-induced duodenogastroesophageal reflux disease (DGERD)., Material and Methods: Our study design was prospective, transversal, descriptive, observational, and open. We took samples of gastric and esophageal juices from patients with a diagnosis of gastroesophageal reflux disease (GERD) and esophagitis during the period from March to August 2002. Sample material was placed in black rubber-covered assay tubes to prevent bilirubin degradation. In our Unit's central laboratory, these samples were centrifuged for 30 min, the dissolved material separated, and a reactive strip was introduced to measure the amount of bile pigment. Endoscopic study reports were provided by this Department on terminating the procedure. Univariate analysis was used to obtain results., Results: In 60% of cases, the esophageal liquid was positive for total bilirubin; 40% presented stage II esophagitis, 27% chronic esophagitis, and 27%, stage I esophagitis. Specific quantifications of total bilirubin at different stages of esophagitis demonstrated in stage II 50% with levels of 0.1-1, 33% with a level of 2-3, in cases of chronic esophagitis 75% with levels of 0.1-1, and with stage I esophagitis, 25% with levels of 2-3 mg/dl. Measurement of gastric pH showed 18 (69%) <3 and esophageal pH of 20 (67%) > 4, with 10 (33%) referring occasional or asymptomatic dyspepsia. We determined presence of duodenal elements in esophagus by means of quantification of total bilirubin in 60% of patients, observing greatest frequency of stage II esophagitis. Low but continuous levels of duodenal, principally biliary, elements continued in patients with DGERD, producing greatest damage in esophageal mucosa.