Duodenogastric Reflux Research Articles

Esophageal Adenocarcinoma in “Mice and Men”: Back to Basics!

Adenocarcinoma related to Barrett's esophagus (BE) is increasing in the West faster than any other cancer. There are many potential chemopreventive agents as well as predictive biomarkers of cancer progression, but what is required is a robust high-throughput model in which to test hypotheses preclinically. The pathophysiology of metaplasia and cancer has been studied in 10 animal species. Though they have considerable genetic divergence, anatomical dissimilarity, and experimental flaws, they have provided some data to test in the clinic, especially relating to activation of common genetic pathways, role of hypergastrinemia, and duodenogastric reflux in cancer progression. In this regard, the human postesophagectomy model, which has a 30% recurrence of BE within 3 yr and a 5% recurrence of adenocarcinoma over 10 yr, is now being utilized to understand how human metaplasia occurs. Furthermore, improved clinical trial designs mean that more sophisticated questions can be addressed in man.

Chemoprevention of glandular stomach carcinogenesis through duodenogastric reflux in rats by a COX‐2 inhibitor

Duodenogastric reflux (DGR) causes glandular stomach carcinogenesis in rats without carcinogens. We aimed to investigate how this carcinogenesis might be prevented by a selective COX-2 inhibitor, meloxicam. A series of 188 Fisher 344 rats underwent a surgical DGR procedure and were divided into 2 groups. One group was given commercial chow (control group), and the other an experimental chow containing meloxicam [0.3 mg/kg bw/day] (meloxicam group). The animals were sequentially sacrificed at weeks 20, 30, 40, 50 and 60 after surgery. The stomachs were removed and examined for the presence of carcinoma, incidence of reflux-induced morphologic changes, COX-2 expression and its activity. Adenocarcinoma in the glandular stomach developed in 7 of 21 animals (33%) in the control group at week 60, but none of 20 (0%) in the meloxicam group (p < 0.01). Moreover, reflux-induced gastritis was definitely alleviated in the meloxicam group compared with the control group. COX-2 immunoreactivity was predominantly detected in stromal cells such as macrophages and fibroblasts. Compared with nonsurgical rats, RNA expression of COX-2 in the mucosa increased, reaching peak at an early phase of week 20 in both groups (p < 0.005). Expression of microsomal prostaglandin E synthase-1 was lower in the meloxicam group than in the control group. PGE(2) production was significantly suppressed throughout the experiment in the meloxicam group compared with the control group (p < 0.01). Gastric carcinogenesis via duodenal reflux was mediated by the COX-2 pathway in rats. Administration of meloxicam prevented this carcinogenesis by suppressing the inflammatory process.

Barrett’s Esophagus (BE) and Carcinoma in the Esophageal Stump (ES) After Esophagectomy with Gastric Pull-Up in Achalasia Patients: A Study Based on 10 Years Follow-Up

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. To analyze late clinical, endoscopic, and pathologic findings in the esophageal stump (ES) mucosa after subtotal esophagectomy in patients treated for advanced chagasic achalasia. 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. 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. (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.

Pyloric Sphincter Dysfunction in nNOS−/− and W/Wv Mutant Mice: Animal Models of Gastroparesis and Duodenogastric Reflux

Nitrergic nerves and interstitial cells of Cajal (ICC) have been implicated in the regulation of pyloric motility. The purpose of these studies was to define their roles in pyloric function in vivo. Pyloric sphincter manometry was performed in wild-type controls, neuronal nitric oxide synthase-deficient (nNOS(-/-)) mice, and ICC-deficient W/W(v) mice, and the effect of deafferented cervical vagal stimulation was examined. Mice showed a distinct approximately 0.6-mm-wide zone of high pressure at the antroduodenal junction, representing the pyloric sphincter. In wild-type controls, the pylorus exhibited tonic active pressure of 12.4 +/- 1.6 mm Hg with superimposed phasic contractions. The motility indices, minute motility index, and total myogenic activity were reduced by vagal stimulation, and the reduction was antagonized by the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). In nNOS(-/-) mice, pyloric basal tone, minute motility index, and total myogenic activity were not significantly different from those in controls, but vagal stimulation paradoxically increased pyloric motility. In contrast, the W/W(v) mice had significantly reduced resting pyloric pressure that was suppressed by vagal stimulation in an L-NAME-sensitive manner. The stomachs of fasted nNOS(-/-) mice showed solid food residue and bezoar formation, while W/W(v) mice showed bile reflux. In nNOS(-/-) mice, loss of nitrergic pyloric inhibition leads to gastric stasis and bezoars. In contrast, basal pyloric hypotension with normal nitrergic inhibition predisposes W/W(v) mice to duodenogastric bile reflux.

Laparoscopic restoration of gastrointestinal continuity after duodenal switch

Biliopancreatic diversion (BPD) with duodenal switch (DS) for morbid obesity was first performed by Hess and Hess [ [1] Hess D.S. Hess D.W. Biliopancreatic diversion with a duodenal switch. Obes Surg. 1998; 8: 267-282 Crossref PubMed Scopus (656) Google Scholar ] in 1988. BPD-DS incorporates two distinct procedures: the BPD, which had been well established by Scopinaro et al. [ [2] Scopinaro N. Gianetta E. Civalleri D. et al. Biliopancreatic bypass for obesity: initial experience in man. Br J Surg. 1979; 66: 618-620 Crossref PubMed Scopus (417) Google Scholar ] in 1976 and the DS, established by DeMeester et al. [ [3] DeMeester T.R. Fuchs K.H. Ball C.S. Albertucci M. Smyrk T.C. Marcus J.N. Experimental and clinical results with proximal end-to-end duodeno-jejunostomy for pathologic duodenogastric reflux. Ann Surg. 1987; 206: 414-424 Crossref PubMed Scopus (173) Google Scholar ]. At 10 years, Hess et al. [ [4] Hess D.S. Hess D.W. Oakley R.S. The biliopancreatic diversion with the duodenal switch: results beyond 10 years. Obes Surg. 2005; 15: 408-416 Crossref PubMed Scopus (213) Google Scholar ] reported excellent long-term results in terms of weight loss, with a percentage of excess weight loss (%EWL) of 75% in 92% of the patients followed up, in addition to high patient satisfaction and low complication rates. Similar long-term results were also reported by Marceau et al. [ [5] Marceau P. Biron S. Hould F.S. et al. Duodenal switch: long-term results. Obes Surg. 2007; 11: 1421-1430 Crossref Scopus (162) Google Scholar ] with a %EWL of 73% ± 19% in 1356 living patients after a mean follow-up of 7.3 ± 3.7 years.

Pathogenic effects of primary duodenogastric reflux on gastric mucosa of children

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. 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. 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. 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.

Bile reflux index after therapeutic biliary procedures

BackgroundTherapeutic biliary procedures disrupt the function of the sphincter of Oddi. Patients are potential "bile refluxers". The aim of this study was to assess how these procedures affect the histology-based bile reflux index (BRI), which can be used to reflect duodenogastric reflux (DGR).MethodsGastric antrum and corpus biopsies were collected from 131 subjects (56 men, 75 women; mean age, 55.9 ± 15.6 years). Group 1 (Biliary group-BG; n = 66) had undergone endoscopic sphincterotomy, endoscopic stenting, or choledochoduodenostomy for benign pathology; Group 2 (n = 20) had undergone cholecystectomy alone; and Group 3 (n = 6) Billroth II gastroenterostomy. Group 4 (no cholecystectomy; n = 39) had upper endoscopy with normal findings and served as controls. BRI > 14 indicated DGR (BRI [+]). To eliminate confounding effects of Helicobacter pylori (Hp) infection, comparisons were made according to Hp colonization.ResultsFifty-nine subjects (45%) were Hp (+). The frequencies of BRI (+) status in antrum and corpus specimens from Hp (-) BG patients were 74.3% and 71.4%, respectively (85.7% for both antrum and corpus for choledochoduodenostomy). Corresponding results were 60% and 60% for Group 2, 100% (only corpus) for Group 3, and 57.1% and 38.1% for controls (BG, Group 2, and Group 3 vs controls – p > 0.05 antrum, p < 0.05 corpus). Fifty-four BG patients had previously undergone cholecystectomy. Excluding those, the rates of BRI (+) in Hp (-) BG patients were 75% antrum and 62.5% corpus (p > 0.05 for both vs. Group 2).ConclusionPatients who had undergone biliary procedures showed similar bile-related histological changes in both corpus and antrum biopsies, but the changes seen in controls were more prominent in the antrum than corpus. Therapeutic biliary procedures increase the rate of BRI (+) especially in the case of choledochoduodenostomy. Therapeutic biliary procedures without cholecystectomy also increase the rate of BRI (+) similar to that observed in patients with cholecystectomy.

A Report on Associations Among Gastric pH, Bleeding, Duodenogastric Reflux, and Outcomes After Trauma

The pathogenesis of multiple organ failure (MOF) in trauma patients may involve the gastrointestinal tract, but its exact origins remain elusive. In a prospective study, the gastric fluid of major torso trauma patients was examined for evidence of duodenogastric reflux and potential gastric injury, and was compared with patient outcomes regarding MOF. Patient samples were collected daily for 4 days by nasogastric tube and analyzed for pH, hemoglobin, and bile acid. Blood was collected for analysis of C-reactive protein (CRP). Outcomes were recorded for the presence or absence of MOF. The results showed that most patients exhibited alkaline gastric contents (pH >/=4.9) and elevated levels of hemoglobin immediately after the trauma. Although non-MOF patients demonstrated a decline of both mean gastric pH and bleeding by day 4, MOF patients maintained significant elevations in pH during this time period. Mean total bile acid levels were increased in all patients, signifying the presence of duodenogastric reflux. However, there were no clear differences in mean bile acid concentrations between MOF and non-MOF patients over time, although MOF patients tended to exhibit higher levels. All patients showed a progressive rise in serum CRP during the first 24 hours after trauma, which was maintained for 4 days. The initial rise in serum CRP in MOF patients was delayed compared with that in non-MOF patients. We conclude that duodenogastric reflux occurs in trauma patients in the first few days after trauma and may contribute to elevated gastric pH and bleeding. Further study is needed to verify whether monitoring the gastric juice of trauma patients during the first several days of hospitalization, for alkaline pH and excessive blood in the gastric lumen, could lead to better assessments of patient status.

Pre-anaesthetic oral lansoprazole for the prophylaxis of Mendelson′s syndrome and impact of duodenogastric reflux on pH and volume of gastric contents

Background. Lansoprazole, a proton pump inhibitor, is used in peptic ulcers and other acid dy speptic disorders. The aim of this study is to determine whether a single oral dose of lansoprazole 30 mg, administered a night before surgery , is effective on pH and volume of gastric contents after excluding those samples contaminated with duodenogastric refluxate (DGR). Patients and Methods. This clinical trial was conducted in 112 adult patients of both sex, ASA phy sical status I-II, and aged 15-70 y r. The patients in group C (control) received placebo while group L (lansoprazole 30 mg) orally at 9.00 p.m., a night before elective surgery . On the next day , gastric contents were aspirated with a large bore, multi-orifices gastric tube passed through an endotracheal tube placed blindly in esophagus after tracheal intubation and analy zed for the presence of bile salts, pH and volume. Results. Thirty three samples (30 %) out of 110 were contaminated with duodenal contents. DGR significantly affected the pH and volume in both the groups. Lansoprazole, after excluding those samples contaminated either with duodenal fluid or blood, significantly increased pH (P<0.0001), decreased volume (P=0.0326) and the proportion of the patients (10.52 % versus 30.76%) considered” at risk” compared with Placebo (P=0.0475) according to the criteria defined (pH ≤ 2.5 and volume ≥ 25 ml). Conclusions. Lansoprazole 30 mg given orally at 9.00 p.m., a night before surgery , significantly decreased the number of patients at risk of aspiration pneumonitis at the time of induction of anesthesia if the aspiration of gastric contents occurs.

Physiological duodenogastric reflux in young healthy adults

Physiological duodenogastric reflux in young healthy adults

Comments on: Effect of Roux-en-Y gastric bypass in obese patients with Barrett’s esophagus: attempts to eliminate duodenogastric reflux

This is the second study documenting complete or partial regression of long-segment Barrett’s esophagus after Roux-en-Y gastric bypass, making it a very important contribution. Controversy also continues as to whether antireflux procedures can lead to regression of Barrett’s esophagus. This study provides further credence to this hypothesis. Although several studies have been published that have shown a decrease in gastroesophageal reflux disease symptoms after bariatric surgery, none have detailed the preoperative and postoperative objective data regarding the 24-hour esophageal pH, manometry, or esophagoscopy.

Effect of Roux-en-Y gastric bypass in obese patients with Barrett’s esophagus: attempts to eliminate duodenogastric reflux

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. 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. 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. Our results suggest that RYGB might be the procedure of choice in morbidly obese patients with BE requiring surgical treatment for gastroesophageal reflux disease.

Laparoscopic Duodenal Switch for Pathologic Duodenogastric Reflux: Initial Experience

Duodenogastric reflux (DGR) is barely responsive to medications and antireflux fundoplication is not able to control the gastric symptoms. Duodenal switch (DS) preserves the physiologic food transit while creating an effective Roux-en-Y diversion to duodenal juice. However, it never enjoyed great popularity, perhaps due to the invasiveness of the open approach. The paper reports our initial experience with laparoscopic DS. Preoperative assessment, surgical technique, and outcomes are described. Normalization of DGR was demonstrated by preoperative and postoperative 24-hour bilimetry and pH-multichannel intraluminal impedance. The procedure was completed under laparoscopy in all the cases with a mean operative time of 165 minutes. Mean blood loss was 200 mL. No patient required admission to the intensive care unit. Initial experience with laparoscopic DS encourages continued use of the minimally invasive approach. A meticulous preoperative evaluation is essential to place a correct indication.

Duodenogastric Reflux in a Hiatal Hernia Seen as Retrocardiac Activity on 99mTc-Tetrofosmin Cardiac SPECT Raw-Data Images

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.

Comments on the publication “Effect of pyloric drainage procedures on gastric passage and bile reflux after esophagectomy with gastric conduit reconstruction by Palmes et al.”

I read with interest the article by Palmes et al. [1] published in this journal. The issue of whether or not to perform a pyloric drainage after esophagectomy and gastric conduit reconstruction has previously been addressed by several investigators with contradictory results. More recently, the hypothesis that omitting pyloric drainage is safe after esophagectomy has been confirmed in a meta-analysis of nine randomised control trials which showed that a pyloroplasty reduced the occurrence of early gastric outlet obstruction but had little effect on mortality, morbidity and late foregut function [2]. The retrospective study by Palmes et al. nicely adds to this controversy by showing that pyloric drainage not only does not improve gastric emptying but it may also favour bile reflux and esophagitis. The multivariate analysis performed by the authors identified pyloric drainage and an anastomosis located below the level of the arch of the azygos vein as the independent risk factors associated with postoperative reflux esophagitis. However, the authors fail to mention that the size of the gastric conduit is another factor that may significantly affect the functional outcome of an esophagectomy. Using a tubularised stomach, as opposed to the whole stomach, may contribute to a faster emptying of the conduit due to reduced gastric wall distensibility and increased endoluminal pressurisation. After the laparoscopic gastric mobilisation has become the standard approach for esophagectomy in my department, I have gradually abandoned the practice of draining the pylorus. Between 2001 and 2007, 65 patients underwent an Ivor Lewis operation through laparoscopy and right thoracotomy for a type 1 or 2 adenocarcinoma of the distal esophagus/cardia according to Siewert classification. The lesser curve was routinely resected preserving the first three to four branches of the right gastric artery, and a 4-cm-wide gastric tube was constructed; in all patients, the esophago-gastric anastomosis was placed at the apex of the right chest. The incidence of clinically significant gastric outlet obstruction was 6.1% (4/65). All these individuals were relieved by a single or multiple sessions (median 2, range 1–3) of endoscopic pneumatic dilatation of the pylorus performed within the first year after the operation. It is noteworthy that Holscher et al. [3], in a recent series of 83 patients undergoing laparoscopic conditioning of the stomach for esophageal replacement, reported a 3.6% incidence of postoperative delayed gastric emptying; all individuals were relieved with endoscopic pneumatic dilation of the pylorus, and their further course was uneventful. In conclusion, I agree that pyloric drainage is not necessary after esophagectomy, provided that a narrow gastric conduit is used to replace the esophagus and the anastomosis is performed at the apex of the right chest. This may prevent duodenogastric reflux, as demonstrated by Palmes et al., and eliminates the potential risks associated to the laparoscopic pyloromyotomy or pyloroplasty. The occasional occurrence of postoperative gastric outlet obstruction can be safely treated by endoscopic pneumatic dilatation of the pylorus. Langenbecks Arch Surg (2008) 393:117–118 DOI 10.1007/s00423-007-0242-x

Esophageal replacement in the neonatal period in infants with esophageal atresia and tracheoesophageal fistula

Aim The aim of the study was to assess the outcome after esophageal replacement using gastric pull-up performed in critically ill neonates with esophageal atresia (EA) and tracheoesophageal fistula. Methods During 1998 to 2005, gastric transposition was performed in 27 neonates (mean birth weight, 2.32 kg [1.86-3.0 kg]; mean age, 6.08 days) for post–EA and tracheoesophageal fistula leaks in 17, long gap in 6, and pure EA in 4, using transhiatal route in all. Pyloromyotomy as the drainage procedure was added for all 27 neonates. Patients were followed up at 3, 6, and 12 months for clinical evaluation, gastric clearance, duodenogastric reflux, and gastric pressure profile. Results Six neonates had ongoing serious chest infection, 3 had lung collapse, and 2 had associated congenital heart disease. Postoperative elective ventilation was provided to all neonates for 2 to 40 days (mean, 10.6 days). Nine neonates developed postoperative leaks in the neck; all healed spontaneously before discharge. Mean hospital stay was 32.6 days (range, 9-87 days). Four newborns died on postoperative days 9, 13, 15, and 29 because of existing severe sepsis in 3 and major congenital heart disease in 1. Functional evaluations were done at 3, 6, and 12 months postoperatively. Values at 6 months revealed normal gastric emptying in 16 of 23, presence of duodenal gastric reflux in 11 of 23, and mass contractions with significant rise in intragastric pressure after bolus feeds in 16 of 23 cases. Values at 12months revealed normal gastric emptying in 14 of 20, presence of duodenal gastric reflux in 8 of 20, and mass contractions with significant rise in intragastric pressure after bolus feeds in 13 (65%) of 20cases. Conclusion Gastric transposition could be a lifesaving alternative to diversion, even in the critically ill newborns after major leaks. However, it requires technical surgical expertise and an effective pain relief and neonatal intensive care.

Does troncular vagotomy modify the proliferative gastric lesions induced in rats by duodenogastric reflux&lt;A HREF="#back2"&gt;&lt;/A&gt;?&lt;A HREF="#back2"&gt;&lt;/A&gt;

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. 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. 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. 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.

IS-023 A high degree of duodenogastric reflux in chronic idiopathic intestinal pseudo-obstruction syndrome(the 44th Annual Meeting of Japanese Society of Pediatric Surgeons)

IS-023 A high degree of duodenogastric reflux in chronic idiopathic intestinal pseudo-obstruction syndrome(the 44th Annual Meeting of Japanese Society of Pediatric Surgeons)

Gastrointestinal Bleeding in Children Following Ingestion of Low‐dose Ibuprofen

Gastrointestinal Bleeding in Children Following Ingestion of Low‐dose Ibuprofen

Risk for Gastric Cancer After Cholecystectomy

It is becoming increasingly evident that chronic inflammation may predispose cancer development. In the stomach, inflammation caused by Helicobacter pylori infection is linked to gastric cancer. Cholecystectomy is regularly followed by duodenogastric bile reflux and reactive gastritis. To test whether a noninfectious long-standing inflammation impels gastric carcinogenesis as well, we assessed the risk of gastric cancer in a large, population-based cohort of cholecystectomized patients. We identified 251,672 individuals, in the Swedish National Inpatient Register, who had undergone cholecystectomy between 1970 and 1997. All incident cases of gastric cancer were identified through linkage to the Swedish Cancer Registry. Standardized incidence ratios (SIRs) were calculated for comparisons with cancer rates of the general population in Sweden. We found an 11% greater overall risk of distal gastric cancer (SIR=1.11, 95% CI 1.04-1.19). The risk increase was only observed among men (SIR=1.21, 95% CI 1.10-1.32), whereas no excess risk was evident for women. For men, the risk was elevated for up to 10 yr after surgery, but this elevation disappeared with longer follow-up time. There was no clear association between cholecystectomy and cardia cancer (SIR=0.95, 95% CI 0.76-1.16). Inconsistency over gender strata, implausibly short induction and latency time, and disappearance of the effect over time makes a causal relationship between cholecystectomy and distal gastric cancer less likely. The findings set aside concerns of harmful long-term consequences of cholecystectomy.