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Review on novel concepts of columnar lined esophagus

Übersicht zu neuen Konzepten des Zylinderepithel-Ösophagus

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Summary

Background

Columnar lined esophagus (CLE) is a marker for gastroesophageal reflux and associates with an increased cancer risk among those with Barrett’s esophagus. Recent studies fostered the development of integrated CLE concepts.

Methods

Using PubMed, we conducted a review of studies on novel histopathological concepts of nondysplastic CLE.

Results

Two histopathological concepts—the squamo-oxyntic gap (SOG) and the dilated distal esophagus (DDE), currently model our novel understanding of CLE. As a consequence of reflux, SOG interposes between the squamous lined esophagus and the oxyntic mucosa of the proximal stomach. Thus the SOG describes the histopathology of CLE within the tubular esophagus and the DDE, which is known to develop at the cost of a shortened lower esophageal sphincter and foster increased acid gastric reflux. Histopathological studies of the lower end of the esophagus indicate, that the DDE is reflux damaged, dilated, gastric type folds forming esophagus and cannot be differentiated from proximal stomach by endoscopy. While the endoscopically visible squamocolumnar junction (SCJ) defines the proximal limit of the SOG, the assessment of the distal limit requires the histopathology of measured multilevel biopsies. Within the SOG, CLE types distribute along a distinct zonation with intestinal metaplasia (IM; Barrett’s esophagus) and/or cardiac mucosa (CM) at the SCJ and oxyntocardiac mucosa (OCM) within the distal portion of the SOG. The zonation follows the pH-gradient across the distal esophagus. Diagnosis of SOG and DDE includes endoscopy, histopathology of measured multi-level biopsies from the distal esophagus, function, and radiologic tests. CM and OCM do not require treatment and are surveilled in 5 year intervals, unless they associate with life quality impairing symptoms, which demand medical or surgical therapy. In the presence of an increased cancer risk profile, it is justified to consider radiofrequency ablation (RFA) of IM within clinical studies in order to prevent the progression to dysplasia and cancer. Dysplasia justifies RFA ± endoscopic resection.

Conclusions

SOG and DDE represent novel concepts fusing the morphological and functional aspects of CLE. Future studies should examine the impact of SOG and DDE for monitoring and management of gastroesophageal reflux disease (GERD).

Zusammenfassung

Hintergrund

Zylinderepithel-Ösophagus (engl. columnar lined esophagus; CLE) zeigt gastroösophagealen Reflux und bedingt bei jenen mit einem Barrett Ösophagus ein erhöhtes Krebsrisiko. Rezente Studien beschreiben ein integriertes morphofunktionales CLE Konzept.

Methodik

Diese PubMed basierte Analyse gibt eine Übersicht zu neuen histopathologischen Konzepten zu CLE ohne Dysplasie.

Ergebnisse

Unsere neue Vorstellung zu CLE wird anhand von zwei neuen histopathologischen Konzepten dargestellt: dem Mukosasegment zwischen Plattenepithel und oxntischer Magenschleimhaut (engl. squamo-oxntic gap; SOG) und dem dilatierten distalen Ösophagus (engl. dilated distal esophagus; DDE). Als Folge des Reflux entsteht das SOG zwischen dem von Plattenepithel ausgekleideten Ösophagus und des von oxyntischer Mukosa ausgekleideten proximalen Magens. SOG beschreibt die Histologie des CLE im tubulären Ösophagus und DDE, welcher auf Kosten des durch den Reflux verkürzten unteren Ösophagussphinkters entsteht und damit vermehrten Rückfluss des sauren Mageninhalts begünstigt. Morphologische Untersuchungen des Ausgangs der Speiseröhre zeigten, dass der DDE Reflux-geschädigter, dilatierter, magenähnliche Falten bildender Ösophagus ist und in der Endoskopie nicht vom proximalen Magen unterschieden werden kann. Während die proximale Grenze des SOG der endoskopisch definierbaren Platten-Zylinderepithelgrenze entspricht, kann die untere Grenze des SOG nur mittels Fusion von Biopsie-Lokalisation und der Histologie von aus diesem Bereich entnommenen Gewebeproben bestimmt werden. Im SOG ordnen sich die CLE Typen entsprechend einer typischen proximalen-distalen Verteilung mit intestinaler Metaplasie (IM, Barrett Ösophagus) ± Kardia Schleimhaut (CM) an der Platten-Zylinderepithelgrenze und Oxyntokardia (OCM) Mukosa im distalen Abschnitt des SOG. Die Ausrichtung folgt dem Reflux-bedingte pH Gradienten entlang des unteren Ösophagus. Die Diagnose von SOG und DDE erfolgt mittels Endoskopie, Histologie von Multi-Level Biopsien aus dem Ausgang der Speiseröhre sowie Funktionstests und Röntgenuntersuchungen. CM und OCM an sich bedürfen keiner Therapie und sollen in 5 Jahren nachuntersucht werden, nur assoziierte Reflux Beschwerden, welche die Lebensqualität beeinträchtigen, sollen medikamentös oder chirurgisch behandelt werden. Bei entsprechendem Krebsrisiko ist es gerechtfertigt, bei IM ohne Dysplasie eine Radiofrequenzablation (RFA) im Rahmen klinischer Studien zu erwägen, um damit die Entstehung von Dysplasie und Karzinom zu verhindern. Dysplasie rechtfertigt eine RFA ± endoskopischer Resektion.

Schlussfolgerungen

SOG und DDE sind neue Konzepte, welche Morphologie und Funktion des Zylinderepithel-Ösophagus integrieren. Die Zukunft wird zeigen, welche Bedeutung diese neuen Konzepte für Diagnose und Therapie der gastroösophagealen Refluxkrankheit haben.

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References

  1. Dent J, El-Serag HB, Wallander MA, et al. Epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut. 2005;54:710.

    PubMed  CAS  Google Scholar 

  2. Ruigomez A, Wallander MA, Johansson S, et al. Natural history of gastroesophageal reflux disease diagnosed in UK general practice. Aliment Pharmacol Ther. 2004;20:751.

    PubMed  CAS  Google Scholar 

  3. Kotzan J, Wade W, Yu HH. Assessing NSAID prescription use as a predisposing factor for gastroesophageal reflux disease in a Med-icaid population. Pharm Res. 2001;18:1376.

    Google Scholar 

  4. Becher A, Dent J. Systematic review: ageing and gastro-oesophageal reflux disease symptoms, esophageal function and reflux oesophagitis. Aliment Pharmacol Ther. 2011;33(4):442–54.

    PubMed  CAS  Google Scholar 

  5. Kamolz T, Velanovich V. The impact of disease and treatment on health-related quality of life in patients suffering from GERD. In: Granderath FA, Kamolz T, Pointner R, editors. Gastroesophageal reflux disease, principles of disease, diagnosis and treatment. New York: Springer Wien; 2006. S. 287–98.

    Google Scholar 

  6. Velanovich V. The development of the GERD-HRQL symptom severity instrument. Dis Esophagus. 2007;20:130.

    PubMed  CAS  Google Scholar 

  7. Ronkainen J, Aro P, Storskrubb T, et al. Gastro-oesophageal reflux symptoms and health-related quality of life in the adult general population—the Kalixanda study. Aliment Pharmacol Ther. 2006;23:1725.

    PubMed  CAS  Google Scholar 

  8. Vakil N, van Zanten SV, Kahrilas P, et al. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol. 2006;101:1900.

    PubMed  Google Scholar 

  9. Labenz J, Jaspersen D, Kulig M, et al. Risk factors for erosive esophagitis: a multivariate analysis based on the ProGERD study initiative. Am J Gastroenterol. 2004;99:1652.

    PubMed  Google Scholar 

  10. Sharma P, Dent J, Armstrong D, et al. The development and validation of an endoscopic grading system for Barrett’s esophagus: the Prague C & M criteria. Gastroenterology. 2006;131:1392.

    PubMed  Google Scholar 

  11. Chandrasoma PT. Columnar lined esophagus: what it is and what it tells us. Eur Surg. 2006;38(3):197–209.

    Google Scholar 

  12. Lenglinger J, Eisler M, Wrba F, et al. Update: histopathology-based definition of gastroesophageal reflux disease and Barrett’s esophagus. Eur Surg. 2008;40(4):165–75.

    Google Scholar 

  13. Lenglinger J, Izay B, Eisler M, et al. Barrett’s esophagus: size of the problem and diagnostic value of a novel histopathology classification. Eur Surg. 2009;41(1):26–39.

    Google Scholar 

  14. Goldblum JR. Controversies in the diagnosis of Barrett esophagus ad Barrett-related dysplasia. Arch Pathol Lab Med. 2010;134:1479–84.

    PubMed  Google Scholar 

  15. Odze RD. What the gastroenterologist needs to know about the histology of Barrett’s esophagus. Curr Opin Gastroenterol. 2011;27(4):389–96.

    PubMed  Google Scholar 

  16. Öberg S, Peters JH, DeMeester TR, et al. Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg. 1997;226(4):522–32.

    PubMed  Google Scholar 

  17. Ayazi S, Tanhankar A, DeMeester SR, et al. The impact of gastric distension on the lower esophageal sphincter and its exposure to acid gastric juice. Ann Surg. 2010;252:57–62.

    PubMed  Google Scholar 

  18. Bredenoord AJ. High-resolution manometry—bliss upon bliss for the esophagology? Eur Surg. 2007;39(3):176–86.

    Google Scholar 

  19. Savarino E, Gemignani L, Pohl D, et al. Oesophageal motility and bolus transit abnormalities increase in parallel with the severity of gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2011;34(4):476–86.

    PubMed  CAS  Google Scholar 

  20. Lagergren J, Bergström R, Lindgren A, et al. Symptomatic gastro-esophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med. 1999;340:825.

    PubMed  CAS  Google Scholar 

  21. Spechler SJ, Fitzgerald RC, Prasad GA, Wang KK. History, molecular mechanism, and endoscopic treatment of Barrett’s esophagus. Gastroenterology. 2010;138(3):854–69.

    PubMed  Google Scholar 

  22. Spechler SJ. Screening and surveillance for Barrett’s esophagus—an unresolved dilemma. Nat Clin Pract Gastroenterol Hepatol. 2007;4(9):470–1.

    PubMed  Google Scholar 

  23. Ronkainen J, Aro P, Storskrubb T, et al. High prevalence of gastro- esophageal reflux symptoms and esophagitis with or without symptoms in the general adult Swedish population: a Kalixanda study report. Scand J Gastroenterol. 2005;40:275.

    PubMed  Google Scholar 

  24. Rex DK, Cummings OW, Shaw M, et al. Screening for Barrett’s esophagus in colonoscopy patients with and without heartburn. Gastroenterology. 2003;125:1670–7.

    PubMed  Google Scholar 

  25. Gerson LB, Shetler K, Triadafilopoulos G. Prevalence of Barrett’s esophagus in asymptomatic individuals. Gastroenterology. 2002;123:461–7.

    PubMed  Google Scholar 

  26. Dulai GS, Guha S, Kahn KL, et al. Preoperative prevalence of Barrett’s esophagus in esophageal adenocarcinoma: a systematic review. Gastroenterology. 2002;122:26–33.

    PubMed  Google Scholar 

  27. Oezcelik A, DeMeester SR. General anatomy of the esophagus. Thorac Surg Clin. 2011;21(2):289–97.

    PubMed  Google Scholar 

  28. DeHertogh G, Ectors N, van Eyken P, Geboes K. Review article: the nature of oesophageal injury in gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2006;24(Suppl 2):17–26.

    Google Scholar 

  29. Glickman JN, Fox V, Antolini DA, et al. Morphology of the cardia and significance of carditis in pediatric patients. Am J Surg Pathol. 2002;26(8):1032–9.

    PubMed  Google Scholar 

  30. Chandrasoma PT, Der R, Ma Y, et al. Histology of the gastroesophageal junction. An autopsy study. Am J Surg Pathol. 2000;24(3):402–9.

    PubMed  CAS  Google Scholar 

  31. Allison PR, Johnstone AS. The oesophagus lined with gastric mucous membrane. Thorax. 1953;8:87–101.

    PubMed  CAS  Google Scholar 

  32. Chandrasoma P, Wijetunge S, Ma Y, DeMeester S, et al. The dilated distal esophagus: a new entity that is the pathologic basis of early gastroesophageal reflux disease. Am J Surg Pathol. 2011;35(12):1873–81.

    PubMed  Google Scholar 

  33. Bonavina L, Saino GI, Bona D, et al. Magnetic augmentation of the lower esophageal sphincter: results of a feasibility clinical trial. J Gastroinest Surg. 2008;12:2133–40.

    Google Scholar 

  34. Rieder F, Biancani P, Harnett K, et al. Inflammatory mediators in gastroesophageal reflux disease: impact on esophageal motility, fibrosis, and carcinogenesis. Am J Physiol. 2010;298:G571–81.

    CAS  Google Scholar 

  35. Souza RF, Huo X, Mittal V, et al. Gastroesophageal reflux might cause esophagitis through a cytokine-mediated mechanism rather than caustic acid injury. Gastroenterology. 2009;137:1776–84.

    PubMed  CAS  Google Scholar 

  36. Sarosi G, Brown G, Jaiswal K, et al. Bone marrow progenitor cells contribute to esophageal regeneration and metaplasia in a rat model of Barrett’s esophagus. Dis Esoph. 2008;21:43–50.

    CAS  Google Scholar 

  37. Marsman WA, van Sandick JW, Tygat GNJ, ten Kate FJW, van Lanschot JJB. The presence and mucin histochemistry of cardiac type mucosa at the esophagogastric junction. Am J Gastroenterol. 2004;99:212–7.

    PubMed  CAS  Google Scholar 

  38. Lenglinger J, Ringhofer C, Eisler M, Sedivy R, Wrba F, Zacherl J, Cosentini EP, Prager G, Heafner M, Riegler M. Histopathology of columnar lined esophagus in patients with gastroesophageal reflux disease. Wien Klin Wochenschr. 2007;119(13/14):405–11.

    PubMed  Google Scholar 

  39. Ringhofer C, Lenglinger J, Izay B, et al. Histopathology of the endoscopic esophagogastric junction in patients with gastroesophageal reflux disease. Wien Klin Wochenschr. 2008;120(11):350–9.

    PubMed  Google Scholar 

  40. Petterson GB, Bombeck CT, Nyhus LM. Influence of hiatal hernia on lower esophageal sphincter function. Ann Surg. 1981;193(2):214–20.

    Google Scholar 

  41. Hill LD, Kozarek RA, Kraemer SJ, Aye RW, Mercer CD, Low DE, Pope CE II. The gastroesophageal flap valve: in vitro and in vivo observations. Gastrointest Endosc. 1996;44(5):541–7.

    PubMed  CAS  Google Scholar 

  42. Korn O, Csendes A, Burdiles P, Braghetto I, Stein HJ. Anatomic dilatation of the cardia and competence of the lower esophageal sphincter: a clinical and experimental study. J Gastrointest Surg. 2000;4(4):398–406.

    PubMed  CAS  Google Scholar 

  43. Mattioli S, D’Ovidio F, Pilotti V, Di Simone MP, Lugaresi ML, Bassi F, Brusori S. Hiatus hernia and intrathoracic migration of esophagogastric junction in gastroesophageal reflux disease. Dig Dis Sci. 2003;48(9):1823–31.

    PubMed  Google Scholar 

  44. Kahrilas PJ, Shi G, Manka M, Joehl RJ. Increased frequency of transient lower esophageal sphincter relaxation induced by gastric distention in reflux patients with hiatal hernia. Gastroenterology. 2000;118(4):688–95.

    PubMed  CAS  Google Scholar 

  45. Jones MP, Sloan SS, Rabine JC, Ebert CC, Huang CF, Kahrilas PJ. Hiatal hernia size is the dominant determinant of esophagitis presence and severity in gastroesophageal reflux disease. Am J Gastroenterol. 2001;96(6):1711–7.

    PubMed  CAS  Google Scholar 

  46. Miholic J, Hafez J, Lenglinger J, et al. Hiatal hernia, Barrett’s esophagus and long term symptom control after laparoscopic fundoplication for gastroesophageal reflux disease. Surg Endosc. 2012. (ahead of print)

  47. Csendes A, Smok G, Burdiles P, Quesada F, Huertas C, Rojas J, Korn O. Prevalence of Barrett’s esophagus by endoscopy and histologic studies: a prospective evaluation of 306 control subjects and 376 patients with symptoms of gastroesophageal reflux. Dis Esophagus. 2000;13:5–11.

    PubMed  CAS  Google Scholar 

  48. Hirota WM, Loughney TM, Lazas DJ, Maydonovitch CL, Rholl V, Wong RKH. Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus and esophagogastric junction: prevalence and clinical data. Gastroenterology. 1999;116:277–85.

    PubMed  CAS  Google Scholar 

  49. Barrett NR. Chronic peptic ulcer of the oesophagus and “oesophagitis”. Br J Surg. 1950;38:175–82.

    PubMed  CAS  Google Scholar 

  50. Barrett NR. The lower esophagus lined by columnar epithelium. Surgery. 1957;41:881–94.

    PubMed  CAS  Google Scholar 

  51. Sarbia M, Donner A, Gabbert HE. Histopathology of the gastroesophageal junction: a study on 36 operation specimens. Am J Surg Pathol. 2002;26:1207–12.

    PubMed  Google Scholar 

  52. Jain R, Aquino D, Harford WV, et al. Cardiac epithelium is found infrequently in the gastric cardia. Gastroenterology. 1998;114:A160 (Abstract).

    Google Scholar 

  53. Chandrasoma P, Wijetunge S, DeMeester SR, et al. The histologic squamo-oxyntic gap: an accurate and reproducible diagnostic marker of gastroesophageal reflux disease. Am J Surg Pathol. 2010;34(11):1574–81.

    PubMed  Google Scholar 

  54. Glickman JN, Spechler SJ, Souza RF, et al. Multilayered epithelium in mucosal biopsy specimens from the gastroesphageal junction region is a histologic marker of gastroesophageal reflux disease. Am J Surg Pathol. 2009;33:818–25.

    PubMed  Google Scholar 

  55. Shi L, Der R, Ma Y, et al. Gland ducts and multilayered epithelium in mucosal biopsies from gastroesophageal-junction region are useful in characterizing esophageal location. Dis Esoph. 2005;18(2):87–92.

    CAS  Google Scholar 

  56. Bhat S, Coleman HG, Yousef F, et al. Risk of malignant progression in Barrett’s esophagus patients: results from a large population-based study. J Natl Cancer Inst. 2011;103:1049–57.

    PubMed  Google Scholar 

  57. Guindi M, Riddell RH. Histology of Barrett’s esophagus and dysplasia. Gastrointest Endosc Clin N Am. 2003;13(2):349–68.

    PubMed  Google Scholar 

  58. Wijetunge S, Ma Y, DeMeester S, et al. Association of adenocarcinomas of the distal esophagus, “gastroesophageal junction”, and “gastric cardia” with gastric pathology. Am J Surg Pathol. 2010;34(10):1521–7.

    PubMed  Google Scholar 

  59. Chandrasoma P, Wickramasinghe K, Ma Y, DeMeester T. Adenocarcinomas of the distal esophagus and “gastric cardia” are predominantly esophageal carcinomas. Am J Surg Pathol. 2007;31(4):569–75.

    PubMed  Google Scholar 

  60. SD Oh, DeMeester SR. Pathophysiology and treatment of Barrett’s esophagus. World J Surg. 2010;16(30):3762–72.

    Google Scholar 

  61. Milano F, van Baal JWPM, Buttar NS, et al. Bone morphogenetic protein 4 expressed in esophagitis induces a columnar phenotype in esophageal squamous cells. Gastroenterology. 2007;132:2412–21.

    PubMed  CAS  Google Scholar 

  62. Castillo D, Puig S, Iglesias M, et al. Activation of the BMP4 pathway and early expression of CDX2 characterize non-specialized columnar metaplasia in a human model of Barrett’s esophagus. J Gastrointest Surg. 2012;16(2):227–37.

    PubMed  Google Scholar 

  63. Reflux DeMeesterSR. Barrett’s and adenocarcinoma of the esophagus: can we disrupt the pathway? J Gastroinest Surg. 2010;14:941–5.

    Google Scholar 

  64. Theodorou D, Ayazi S, DeMeester SR, et al. Intraluminal pH and goblet cell density in Barrett’s esophagus. J Gastrointest Surg. 2012;16(3):469–74.

    PubMed  Google Scholar 

  65. Sharma P, Falk GW, Weston AP, et al. Dysplasia and cancer in a large multicenter cohort of patients with Barrett’s esophagus. Clin Gastroenterol Hepatol. 2006;4:566–72.

    PubMed  Google Scholar 

  66. Hvid-Jensen F, Pedersen L, Mohr Drewes A, et al. Incidence of adenocarcinoma among patients with Barrett’s esophagus. N Engl J Med. 2011;365:1375–83.

    PubMed  CAS  Google Scholar 

  67. De Jonge PJ, van Blankenstein M, Looman CW, et al. Risk of malignant progression in patients with Barrett’s oesophagus: Dutch nationwide cohort study. Gut. 2010;59(8):1030–6.

    PubMed  Google Scholar 

  68. Jung KW, Talley NJ, Romero Y, et al. Epidemiology and natural history of intestinal metaplasia of the gastroesophageal junction and Barrett’s esophagus: a population-based study. Am J Gastroenterol. 2011;106:1447–55.

    PubMed  Google Scholar 

  69. Sikkema M, De Jonge PJF, Steyerberg EW, Kuipers EJ. Risk of esophageal adenocarcinoma and mortality in patients with Barrett’s esophagus: a systematic review and meta-analysis. Clin Gastroenterol Hepatol. 2010;8:235–44.

    PubMed  Google Scholar 

  70. Desai TK, Krishnan K, Samala N, et al. The incidence of oesophageal adenocarcinoma in non-dysplastic Barrett’s oesophagus: a meta-analysis. Gut. 2012;61:970–6.

    PubMed  Google Scholar 

  71. Ronkainen J, Aro P, Storskrubb T, et al. Prevalence of Barrett’s esophagus in the general population: an endoscopy study. Gastroenterology. 2005;129:1825–31.

    PubMed  Google Scholar 

  72. Hayeck TJ, Kong CY, Spechler SJ, et al. The prevalence of Barrett’s esophagus in the US: estimates from a simulation model confirmed by SEER data. Dis Esoph. 2010;23(6):451–7.

    CAS  Google Scholar 

  73. Thomas T, Abrams KR, De Caestecker JS, Robinson RJ. Meta analysis: cancer risk in Barrett’s oesophagus. Aliment Pharm. 2007;26:1465–77.

    CAS  Google Scholar 

  74. Rubenstein JH, Mattek N, Eisen G. Age- and sex-specific yield of Barrett’s esophagus by endoscopy indication. Gastrointest Endosc. 2010;71:21–7.

    PubMed  Google Scholar 

  75. Curvers WL, ten Kate FJ, Krishnadath KK, et al. Low-grade dysplasia in Barrett’s esophagus: overdiagnosed and underestimated. Am J Gastroenterol. 2010;105(7):1523–30.

    PubMed  Google Scholar 

  76. Rutegard M, Shore R, Lu Y, et al. Sex differences in the incidence of gastrointestinal adenocarcinomas in Sweden 1970–2006. Eur J Cancer. 2010;46:1093–100.

    PubMed  Google Scholar 

  77. Lagergren J, Mattsson F. No further increase in the incidence of esophageal adenocarcinoma in Sweden. In J Cancer. 2011;129:513–6.

    CAS  Google Scholar 

  78. Löfdahl HE, Lane A, Lu Y, et al. increased population prevalence of reflux and obesity in the United Kingdom compared with Sweden: a potential explanation for the difference in incidence of esophageal adenocarcinoma. Gastroenterol Hepatol. 2011;23:128–32.

    Google Scholar 

  79. Eypasch E, Williams JI, Wood-Dauphinee S, et al. Gastrointestinal quality of life index: development, validation and application of a new instrument. Br J Surg. 1995;82:216–22.

    PubMed  CAS  Google Scholar 

  80. Theisen J, Stein HJ, Feith M, et al. Preferred location for the development of esophageal adenocarcinoma within a segment of intestinal metaplasia. Surg Endosc. 2006;20(2):235–8.

    PubMed  CAS  Google Scholar 

  81. Corley DA, Levin TR, Habel LA, et al. Surveillance and survival in Barrett’s adenocarcinomas: a population based study. Gastroenterology. 2002;122:633–40.

    PubMed  Google Scholar 

  82. Weickert U, Wolf A, Schröder C, et al. Frequency, histopathological findings, and clinical significance of cervical heterotopic gastric mucosa (gastric inlet patch): a prospective study in 300 patients. Dis Esoph. 2011;24(2):63–8.

    CAS  Google Scholar 

  83. Rosztoczy A, Izbeki F, Nemeth IB, et al. Detailed esophageal function and morphological analysis shows high prevalence of gastroesophageal reflux disease and Barrett’s esophagus in patients with cervical inlet patch. Dis Esoph. 2011;22:1442–2050.

    Google Scholar 

  84. Chong VA, Jalihal A. Caervical inleet patch: case series and literature review. South Med J. 2006;99(8):865–9.

    PubMed  Google Scholar 

  85. Tutuian R, Castell DO. Combined multichannel intraluminal impedance and manometry clarifies esophageal function abnormalities: study in 350 patients. Am J Gastroenterol. 2004;99(6):1011–9.

    PubMed  Google Scholar 

  86. Agrawal A, Roberts J, Sharma N, et al. Symptoms with acid and nonacid reflux may be produced by different mechanisms. Dis Esoph. 2009;22(5):467–70.

    CAS  Google Scholar 

  87. Woodland P, Al-Zinaty M, Yazaki E, Sifrim D. In vivo evaluation of acid-induced changes in oesophageal mucosa integrity and sensitivity in non-erosive reflux disease. Gut. 2012. (ahead of print)

  88. Bredenoord AJ, Tutuian R, Smout AJ, Castell DO. Technology review: esophageal impedance monitoring. Am J Gastroenterol. 2007;102(1):187–94.

    PubMed  Google Scholar 

  89. Kwiatek MA, Pandolfino JE, Hirano I, Kahrilas PJ. Esophagogastric junction distensibility assessed with an endoscopic functional luminal imaging probe (EndoFLIP). Gastrointest Endosc. 2010;72(2):272–8.

    PubMed  Google Scholar 

  90. Kwiatek MA, Kahrilas K, Soper NJ, et al. Esophagogastric junction distensibility after fundoplication assessed with a novel functional luminal imaging probe. J Gastrointest Surg. 2010;14(2):268–76.

    PubMed  Google Scholar 

  91. Scharitzer M, Pokieser P, Schober E, et al. Morphological findings in dynamic swallowing studies of symptomatic patients. Eur Radiol. 2002;12(5):1139–44.

    PubMed  Google Scholar 

  92. Kauppi JT, Oksala N, Salo JA, et al. Locally advanced esophageal adenocarcinoma: response to neoadjuvant chemotherapy and survivial predicted by (18F)FDG-PET/CT. Acta Oncol. 2012;636–44.

  93. Klayton T, Li T, Yu JQ, et al. The role of qualitative and quantitative analysis of F18-FDG positron emission tomography in predicting pathologic response following chemoradiotherapy in patients with esophageal carcinoma. J Gastrointest Cancer. 2012. (ahead of print)

  94. Covotta F, Piretta L, Badiali D, et al. Functional magnetic resonance in the evaluation of oesophageal motility disorders. Gastroenterol Res Pract. 2011;367639.

  95. Griffin JM, Reed CE, Denlinger CE. Utility of restaging endoscopic ultrasound after neoadjuvant therapy for esophageal cancer. Ann Thorac Surg. 2012;93(6):1855–9.

    PubMed  Google Scholar 

  96. Lord RVN, DeMeester SR, Peters JH, et al. Hiatal hernia, lower esophageal sphincter incompetence, and effectiveness of Nissen fundoplication in the spectrum of gastroesophageal reflux disease. J Gastrointest Surg. 2008;13(4):602–10.

    PubMed  Google Scholar 

  97. Oelschlager BK, Ma KC, Soares RV, et al. A broad assessment of clinical outcomes after laparoscopic antireflux surgery. Ann Surg. 2012;256:87–94.

    PubMed  Google Scholar 

  98. Triadafilopoulos G. Proton pump inhibitor in Barrett’s esophagus: pluripotent but controversial. Eur Surg. 2008;40(2):58–65.

    Google Scholar 

  99. Fein M, Seyfried F. Is there a role for anything other than a Nissen’s operation? J Gastrointest Surg. 2010;14(Suppl 1):67–74.

    Google Scholar 

  100. Shan CX, Zhang W, Zheng XM, et al. Evidence-based appraisal in laparoscopic Nissen and Toupet fundoplications for gastroesophageal reflux disease. World J Gastroenterol. 2010;16(24):3063–71.

    PubMed  Google Scholar 

  101. Galmiche JP, Hatlebakk J, Attwood S, et al. Laparoscopic antireflux surgery vs esomeprazole treatment for chronic GERD. The LOTUS randomized clinical trial. JAMA. 2011;305(19):1969–77.

    PubMed  CAS  Google Scholar 

  102. Shaheen NJ, Sharma P, Overholt BF, et al. Radiofrequency ablation in Barrett’s esophagus with dysplasia. N Engl J Med. 2009;360:2277–88.

    PubMed  CAS  Google Scholar 

  103. Shaheen NJ, Overholt BF, Sampliner RE, et al. Durability of radiofrequency ablation in Barrett’s esophagus with dysplasia. Gastroenterology. 2011;141:460–68.

    PubMed  Google Scholar 

  104. Fleischer DE, Overholt BF, Sharma VK, et al. Endoscopic ablation of Barrett’s esophagus: a multicenter study with 2.5-year follow up. Gastrointest Endosc. 2008;68(5):867–76.

    PubMed  Google Scholar 

  105. Lyday WD, Corbett FS, Kuperman DA, et al. Radiofrequency ablation of Barrett’s esophagus: outcomes of 429 patients from a multicenter community practice registry. Endoscopy. 2010;42:272–8.

    PubMed  CAS  Google Scholar 

  106. Fleischer DE, Overholt BF, Sharma VK, et al. Endoscopic radiofrequency ablation for Barrett’s esophagus: 5-year outcomes from a prospective multicenter trial. Endoscopy. 2010;42(10):781–9.

    PubMed  CAS  Google Scholar 

  107. Fleischer DE, Odze R, Overholt BF, et al. The case for endoscopic treatment of non-dysplastic and low grade dysplastic Barrett’s esophagus. Dig Dis Sci. 2010;55:1918–31.

    PubMed  Google Scholar 

  108. Van Vilsteren FGI, Pouw RE, Seewald S, et al. Stepwise radical endoscopic resection versus radiofrequency ablation for Barrett’s oesophagus with high-grade dysplasia or early cancer: a multicenter randomized trial. Gut. 2011;60(6):765–73.

    PubMed  Google Scholar 

  109. Liu W, Hahn H, Odze RD, Goyal RK. Metaplastic esophageal columnar epithelium without goblet cells shows DNA content abnormalities similar to goblet cell-containing epithelium. Am J Gastroetnerol. 2009;104(4):816–24.

    CAS  Google Scholar 

  110. Hahn HP, Blount PL, Ayub K, et al. Intestinal differentiation in metaplastic, nongoblet columnar epithelium in the esophagus. Am J Surg Pathol. 2009;33(7):1006–15.

    PubMed  Google Scholar 

  111. Sikkema M, Looman CWN, Steyerberg EW, et al. Predictors for neoplastic progression in patients with Barrett’s esophagus: a prospective cohort study. Am J Gastroenterol. 2011;106(7):1231–8.

    PubMed  CAS  Google Scholar 

  112. Parrilla P, Martinez deHLF, Ortiz A, et al. Long-term results of a randomized prospective study comparing medical and surgical treatment of Barrett’s esophagus. Ann Surg. 2003;237(3):291–8.

    PubMed  Google Scholar 

  113. Rossi M, Barreca M, de Bartoli N, et al. Efficacy of Nissen fundoplication versus medical therapy in the regression of low-grade dysplasia in patients with Barrett’s esophagus. Ann Surg. 2006;243:58–63.

    PubMed  Google Scholar 

  114. Zaninotto G, Parente P, Salvador R, et al. Long term follow up of Barrett’s epithelium: medical versus antireflux surgical therapy. J Gastrointest Surg. 2011. (ahead print)

  115. O’Connell K, Velanovich V. Effects of Nissen fundplication on endoscopic endoluminal radiofrequency ablation of Barrett’s esophagus. Surg Endosc. 2011;25(3):830–34.

    PubMed  Google Scholar 

  116. Goers TA, Leao P, Cassera MA, et al. Concomitant endoscopic radiofrequency ablation and laparoscopic reflux operative results in more effective and efficient treatment of Barrett’s esophagus. J Am Coll Surg. 2011;213(4):486–92.

    PubMed  Google Scholar 

  117. Schoppmann SF, Prager G, Langer FB, et al. Open versus minimally invasive esophagectomy: a single-center case controlled study. Surg Endosc. 2010;24(12):3044–53.

    PubMed  Google Scholar 

  118. Rubenstein JH, Mattek N, Eisen G. Age- and sex-specific yield of Barrett’s esophagus by endoscopy indication. Gastrointest Endosc. 2010;71:21–7.

    PubMed  Google Scholar 

  119. Wykypiel H, Wetscher GJ, Klingler P, Glaser K. The Nissen fundoplication: indication, technical aspects and postoperative outcome. Langenbecks Arch Surg. 2005;390:495–502.

    PubMed  CAS  Google Scholar 

  120. Kadri S, Lao-Sirieix P, Fitzgerald RC. Developing a nonendoscopic screening test for Barrett’s esophagus. Biomark Med. 2011;5(3):397–404.

    PubMed  Google Scholar 

  121. Fikrova P, Stetina R, Hronek M, et al. Application of the comet assay method in clinical studies. Wien Klin Wochenschr. 2011;123(23–24):693–99.

    PubMed  CAS  Google Scholar 

  122. Shukla R, Abidi WM, Richards-Kortum R, et al. Endoscopic imaging: how far are we from real-time histology? World J Gastroinest Endosc. 2011;3(10):183–194.

    Google Scholar 

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Lenglinger, J., See, S., Beller, L. et al. Review on novel concepts of columnar lined esophagus. Wien Klin Wochenschr 125, 577–590 (2013). https://doi.org/10.1007/s00508-013-0418-z

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