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1. Mabrut JY, Collard JM, Baulieux J: [Duodenogastric and gastroesophageal bile reflux]. J Chir (Paris); 2006 Nov-Dec;143(6):355-65
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  • This study reviews current data regarding duodenogastric and gastroesophageal bile reflux-pathophysiology, clinical presentation, methods of diagnosis (namely, 24-hour intraluminal bile monitoring) and therapeutic management.
  • In patients with concomitant gastroesophageal reflux, the backwash of duodenal content into the lower esophagus can cause mixed (alkaline and acid) reflux esophagitis, and lead, in turn, to esophageal mucosal damage such as Barrett's metaplasia and adenocarcinoma.
  • Proton pump inhibitors decrease the upstream effects of DGR on the esophagus by decreasing the volume of secretions; promotility agents diminish gastric exposure to duodenal secretions by improving gastric emptying.
  • [MeSH-minor] Anion Exchange Resins / therapeutic use. Anti-Ulcer Agents / therapeutic use. Barrett Esophagus / etiology. Barrett Esophagus / physiopathology. Bile Acids and Salts / analysis. Cholecystectomy / adverse effects. Cholestyramine Resin / therapeutic use. Chromatography, High Pressure Liquid. Cisapride / therapeutic use. Duodenum / surgery. Esophagitis, Peptic / etiology. Esophagitis, Peptic / physiopathology. Gastric Acidity Determination. Gastrointestinal Agents / therapeutic use. Gastroplasty. Helicobacter Infections / complications. Helicobacter pylori. Humans. Hydrogen-Ion Concentration. Proton Pump Inhibitors. Risk Factors. Stomach Neoplasms / etiology. Sucralfate / therapeutic use

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  • (PMID = 17285081.001).
  • [ISSN] 0021-7697
  • [Journal-full-title] Journal de chirurgie
  • [ISO-abbreviation] J Chir (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anion Exchange Resins; 0 / Anti-Ulcer Agents; 0 / Bile Acids and Salts; 0 / Gastrointestinal Agents; 0 / Proton Pump Inhibitors; 11041-12-6 / Cholestyramine Resin; 54182-58-0 / Sucralfate; UVL329170W / Cisapride
  • [Number-of-references] 182
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2. Murphy JO, Ravi N, Byrne PJ, McDonald GS, Reynolds JV: Neither antioxidants nor COX-2 inhibition protect against esophageal inflammation in an experimental model of severe reflux. J Surg Res; 2008 Mar;145(1):33-40
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  • BACKGROUND: Reflux-induced injury and oxidative stress result in esophageal inflammation and the potential for progression to intestinal metaplasia and adenocarcinoma.
  • RESULTS: Esophagitis was present in all 63 animals completing the study and was severe in 27 (43%).
  • No animal developed metaplasia or tumor.
  • [MeSH-minor] Animals. Ascorbic Acid / therapeutic use. Disease Models, Animal. Dose-Response Relationship, Drug. Esophagus / pathology. Esophagus / surgery. Female. Jejunum / surgery. Lactones / therapeutic use. Random Allocation. Rats. Rats, Wistar. Sulfones / therapeutic use

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  • (PMID = 17727884.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cyclooxygenase 2 Inhibitors; 0 / Lactones; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; PQ6CK8PD0R / Ascorbic Acid
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3. Looby E, Abdel-Latif MM, Athié-Morales V, Duggan S, Long A, Kelleher D: Deoxycholate induces COX-2 expression via Erk1/2-, p38-MAPK and AP-1-dependent mechanisms in esophageal cancer cells. BMC Cancer; 2009;9:190
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  • BACKGROUND: The progression from Barrett's metaplasia to adenocarcinoma is associated with the acquirement of an apoptosis-resistant phenotype.
  • The bile acid deoxycholate (DCA) has been proposed to play an important role in the development of esophageal adenocarcinoma, but the precise molecular mechanisms remain undefined.
  • The aim of this study was to investigate DCA-stimulated COX-2 signaling pathways and their possible contribution to deregulated cell survival and apoptosis in esophageal adenocarcinoma cells.
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Apoptosis / drug effects. Barrett Esophagus / enzymology. Barrett Esophagus / metabolism. Barrett Esophagus / pathology. Cell Growth Processes / drug effects. Cell Line, Tumor. Collagen Type XI / metabolism. DNA, Neoplasm / metabolism. Enzyme Induction / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proto-Oncogene Proteins c-fos / metabolism. Proto-Oncogene Proteins c-jun / metabolism. Signal Transduction / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19534809.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / COL11A2 protein, human; 0 / Collagen Type XI; 0 / DNA, Neoplasm; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-jun; 0 / Transcription Factor AP-1; 0 / fos-related antigen 1; 005990WHZZ / Deoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2704223
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4. Vona-Davis L, Riggs DR, Jackson BJ, McFadden DW: Antiproliferative and apoptotic effects of rofecoxib on esophageal cancer in vitro(1). J Surg Res; 2004 Jun 15;119(2):143-8
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  • BACKGROUND: The incidence of Barrett's adenocarcinoma has increased dramatically in the United States, whereas squamous cell carcinoma of the esophagus remains a worldwide problem.
  • Cyclooxygenase (COX)-2 may play an important role in gastrointestinal carcinogenesis and is overexpressed in both Barrett's metaplasia and adenocarcinoma.
  • We hypothesized that a selective and commercially available COX-2 inhibitor, rofecoxib (Vioxx), would inhibit growth of Barrett's adenocarcinoma and squamous cell carcinoma of the esophagus by apoptotic pathways.
  • MATERIALS AND METHODS: Two esophageal adenocarcinoma cell lines (SEG-1 and BIC) and two esophageal squamous cell cancer lines (KYSE 150 and KYSE 410) were treated with rofecoxib at doses ranging from 8.0 to 125 microg/well.
  • RESULTS: Rofecoxib, NS-398, and Catechin treatments all resulted in significant antiproliferative effects in both adenocarcinoma and squamous cell carcinoma of the esophagus in vitro.
  • Further in vivo and human studies are warranted to evaluate the safety and clinical utility of these agents in patients with all cancers of the esophagus.
  • [MeSH-major] Adenocarcinoma. Apoptosis / drug effects. Cyclooxygenase Inhibitors / pharmacology. Esophageal Neoplasms. Lactones / pharmacology
  • [MeSH-minor] Cell Division / drug effects. Cell Line, Tumor / cytology. Cell Line, Tumor / drug effects. Cyclooxygenase 1. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Humans. In Vitro Techniques. Isoenzymes / antagonists & inhibitors. Membrane Proteins. Nitrobenzenes / pharmacology. Prostaglandin-Endoperoxide Synthases. Sulfonamides / pharmacology. Sulfones

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  • [ErratumIn] J Surg Res. 2004 Aug;120(2):326
  • (PMID = 15145696.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Lactones; 0 / Membrane Proteins; 0 / Nitrobenzenes; 0 / Sulfonamides; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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5. Gil J, Błaszak A, Wojtuń S, Wojtkowiak M: [Endoscopic methods of gastro-esophageal reflux disease (GERD) treatment and their complications]. Pol Merkur Lekarski; 2007 May;22(131):429-33
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  • It is caused by the fact of change and development of diagnostic and therapeutic methods.
  • Alternative methods of treatment are still searched beacause patients do not accept many years long drug treatment or surgical procedures.
  • Chronic character of GERD is associated with intestinal metaplasia and adenocarcinoma of the esophagus in its distal part.
  • [MeSH-minor] Animals. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Esophagogastric Junction / pathology. Esophagogastric Junction / surgery. Fundoplication / methods. Humans. Laser Coagulation. Laser Therapy. Metaplasia. Monitoring, Ambulatory. Postoperative Complications. Proton Pump Inhibitors. Proton Pumps / drug effects

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  • (PMID = 17679388.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors; 0 / Proton Pumps
  • [Number-of-references] 25
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6. Anderson LA, Johnston BT, Watson RG, Murphy SJ, Ferguson HR, Comber H, McGuigan J, Reynolds JV, Murray LJ: Nonsteroidal anti-inflammatory drugs and the esophageal inflammation-metaplasia-adenocarcinoma sequence. Cancer Res; 2006 May 1;66(9):4975-82
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  • [Title] Nonsteroidal anti-inflammatory drugs and the esophageal inflammation-metaplasia-adenocarcinoma sequence.
  • Observational studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of esophageal adenocarcinoma, but it is not known at what stage they may act in the esophageal inflammation-metaplasia-adenocarcinoma sequence.
  • In an all-Ireland case-control study, we investigated the relationship between the use of NSAIDs and risk of reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma.
  • Patients with esophageal adenocarcinoma, long-segment Barrett's esophagus and population controls were recruited from throughout Ireland.
  • Data were collected on known and potential risk factors for esophageal adenocarcinoma and on the use of NSAIDs, including aspirin, at least 1 year before interview.
  • Associations between use of NSAIDs and the stages of the esophageal inflammation-metaplasia-adenocarcinoma sequence were estimated by multiple logistic regression.
  • In total, 230 reflux esophagitis, 224 Barrett's esophagus, and 227 esophageal adenocarcinoma and 260 population controls were recruited.
  • Use of aspirin and NSAIDs was associated with a reduced risk of Barrett's esophagus [odds ratio [OR; 95% confidence interval (95% CI)], 0.53 (0.31-0.90) and 0.40 (0.19-0.81), respectively] and esophageal adenocarcinoma [OR (95% CI), 0.57 (0.36-0.93) and 0.58 (0.31-1.08), respectively].
  • Barrett's esophagus and esophageal adenocarcinoma patients were less likely than controls to have used NSAIDs.
  • Selection or recall bias may explain these results and the results of previous observational studies indicating a protective effect of NSAIDs against esophageal adenocarcinoma.
  • If NSAIDs have a true protective effect on the esophageal inflammation-metaplasia-adenocarcinoma sequence, they may act early in the sequence.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Barrett Esophagus / prevention & control. Esophageal Neoplasms / prevention & control. Esophagitis, Peptic / prevention & control
  • [MeSH-minor] Acetaminophen / administration & dosage. Aged. Aged, 80 and over. Aspirin / administration & dosage. Case-Control Studies. Esophagus / drug effects. Esophagus / pathology. Female. Humans. Male. Metaplasia. Middle Aged


7. Tseng HH, Hsu PI, Chen HC, Lai KH, Lo GH, Lo CC, Chou NH, Mok KT, Chen IS, Chou NH, Yang HB, Liu L, Hsu PN: Compartment theory in Helicobacter pylori-associated gastric carcinogenesis. Anticancer Res; 2003 Jul-Aug;23(4):3223-9
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  • This study was aimed at examining the compartment alterations through the Helicobacter pylori (H. pylori)-related chronic gastritis-intestinal metaplasia-carcinoma sequence, and investigating the long-term effect of bacterial eradication on the compartment changes.
  • PATIENTS AND METHODS: Gastric biopsy specimens were obtained from subjects with H. pylori-negative normal mucosa (N = 12), H. pylori-positive non-metaplastic gastritis (N = 42), H. pylori-positive intestinal metaplasia (N = 21) and intestinal-type adenocarcinoma (N = 20).
  • RESULTS: The mean PCNA labeling indices (L.I.) of non-metaplastic gastritis, intestinal metaplasia and adenocarcinoma were significantly higher than that of normal mucosa (31.1, 49.2 and 40.7 vs. 21.4; p < 0.01, 0.001 and 0.001, respectively).
  • In patients with intestinal metaplasia, there was a full expansion (phase 1 change) of proliferating zone to the middle compartment of gastric pits (ratio of L.I. between middle and lower compartment = 1.00).
  • The proliferating cells were evenly distributed in adenocarcinoma (complete loss of compartmentalization).
  • [MeSH-major] Adenocarcinoma / microbiology. Gastritis / microbiology. Helicobacter Infections / complications. Helicobacter Infections / drug therapy. Helicobacter pylori. Stomach Neoplasms / microbiology
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles. Aged. Cell Cycle / physiology. Cell Division / physiology. Chronic Disease. Disease Progression. Drug Therapy, Combination. Female. Gastric Mucosa / microbiology. Gastric Mucosa / pathology. Humans. Lansoprazole. Male. Metaplasia / microbiology. Metaplasia / pathology. Metronidazole / therapeutic use. Middle Aged. Omeprazole / analogs & derivatives. Omeprazole / therapeutic use. Tetracycline / therapeutic use

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  • (PMID = 12926056.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0K5C5T2QPG / Lansoprazole; 140QMO216E / Metronidazole; F8VB5M810T / Tetracycline; KG60484QX9 / Omeprazole
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8. Combet E, Paterson S, Iijima K, Winter J, Mullen W, Crozier A, Preston T, McColl KE: Fat transforms ascorbic acid from inhibiting to promoting acid-catalysed N-nitrosation. Gut; 2007 Dec;56(12):1678-84
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  • BACKGROUND: The major potential site of acid nitrosation is the proximal stomach, an anatomical site prone to a rising incidence of metaplasia and adenocarcinoma.
  • [MeSH-minor] Catalysis / drug effects. Humans. Hydrochloric Acid / pharmacology. Hydrogen-Ion Concentration. In Vitro Techniques. Models, Biological. Nitric Oxide / metabolism. Nitrosation / drug effects. Oxygen / metabolism

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  • (PMID = 17785370.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipids; 0 / Nitrosamines; 31C4KY9ESH / Nitric Oxide; PQ6CK8PD0R / Ascorbic Acid; QTT17582CB / Hydrochloric Acid; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2095705
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9. Murphy JO, Ravi N, Byrne PJ, McDonald GS, Reynolds JV: Neither antioxidants nor COX-2 inhibition protect against esophageal inflammation in an experimental model of severe reflux. J Surg Res; 2007 Sep;142(1):20-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Reflux-induced injury and oxidative stress result in esophageal inflammation and the potential for progression to intestinal metaplasia and adenocarcinoma.
  • RESULTS: Esophagitis was present in all 63 animals completing the study and severe in 27 (43%).
  • No animal developed metaplasia or tumor.
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Esophagus / pathology. Esophagus / surgery. Female. Inflammation / pathology. Inflammation / prevention & control. Jejunum / pathology. Jejunum / surgery. Models, Animal. Random Allocation. Rats. Rats, Wistar. Ulcer / pathology. Ulcer / prevention & control

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  • (PMID = 17543990.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cyclooxygenase 2 Inhibitors; 0 / Lactones; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; PQ6CK8PD0R / Ascorbic Acid
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