Zentralbl Chir 2014; 139(4): 386-392
DOI: 10.1055/s-0033-1360296
Übersicht
Georg Thieme Verlag KG Stuttgart · New York

Barrett-Neoplasie: Wo liegt eigentlich das Problem?

Barrettʼs Neoplasia: Where is the Problem?
J. Krugmann
1   Institut für Pathologie, Klinikum Bayreuth, Bayreuth, Deutschland
,
M. Vieth
1   Institut für Pathologie, Klinikum Bayreuth, Bayreuth, Deutschland
,
H. Neumann
2   Medizinische Klinik I, Universität Erlangen-Nürnberg, Erlangen, Deutschland
› Author Affiliations
Further Information

Publication History

Publication Date:
13 August 2014 (online)

Zusammenfassung

Die Barrett-Schleimhaut ist charakterisiert durch einen metaplastischen Schleimhautersatz des Plattenepithels im distalen Ösophagus durch Zylinderepithel und geht mit einem erhöhten Risiko einer Karzinomentstehung einher. Bis heute gibt es keine weltweit einheitliche Definition der Erkrankung. Ebenso uneinheitlich ist die Abgrenzung einer niedriggradigen Dysplasie/intraepithelialen Neoplasie von einer hochgradigen Dysplasie/intraepithelialen Neoplasie. Die vorliegende Arbeit versucht, aus morphologischer Sicht Hilfestellungen für eine einheitliche und korrekte Diagnosestellung zu geben, diskutiert die Möglichkeiten der endoskopischen Diagnostik und beschreibt die aktuellen Biomarker der Barrett-Schleimhaut.

Abstract

The Barrett mucosa is characterised by metaplastic transformation in the distal oesophagus from squamous epithelium into columnar-lined cells and shows an increased risk for progression into adenocarcinoma. Up to date an international definition of Barrettʼs oesophagus is still lacking and it is also difficult to separate low-grade dysplasia/intraepithelial neoplasia from high-grade dysplasia/intraepithelial neoplasia. The present review describes the criteria for the histological diagnosis, discusses the possibilities of endoscopic diagnosis and highlights the biomarkers of the Barrett mucosa.

 
  • Literatur

  • 1 Kadri SR, Lao-Sirieix P, OʼDonovan M et al. Acceptability and accuracy of a non-endoscopic screening test for Barrettʼs oesophagus in primary care: cohort study. BMJ 2010; 341: c4372-c4380
  • 2 Fitzgerald RC, di Pietro M, Ragunath K et al. British Society of Gastroenterology guidelines on the diagnosis and management of Barrettʼs esophagus. Gut 2014; 63: 7-42
  • 3 Takubo K, Aida J, Naomoto Y et al. Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma. Hum Pathol 2009; 40: 65-74
  • 4 van Sandick JW, Baak JP, van Lanschot JJ et al. Computerized quantitative pathology for the grading of dysplasia in surveillance biopsies of Barrettʼs oesophagus. J Pathol 2000; 190: 177-183
  • 5 Clark GW, Smyrk TC, Burdile P et al. Is Barrettʼs metaplasia the source of adenocarcinoma oft he cardia?. Arch Surg 1994; 129: 609-615
  • 6 Cameron AJ, Lomboy CT, Pera M et al. Adenocarcinoma of the esophagogastric junction and Barrettʼs esophagus. Gastroenterology 1995; 109: 1541-1546
  • 7 Ruol A, Parenti A, Zaninotto G et al. Intestinal metaplasia ist he probable common precursor of adenocarcinoma in Barrettʼs esophagus and adenoocarcinoma oft he gastric cardia. Cancer 2000; 88: 2520-2528
  • 8 Cameron AJ, Arora AS. Barrettʼs esophagus and reflux esophagitis: is there a missing link?. Am J Gastroenterol 2002; 97: 273-278
  • 9 Tsuji N, Ishiguro S, Tsukamato Y et al. Mucin phenotypic expression and background mucosa of esophagogastric junctional adenocarcinoma. Gastric Cancer 2004; 7: 97-103
  • 10 Nunobe S, Nakanishi S, Taniguchi H et al. Two distinct pathways of tumorigenesis of adenocarcinomas oft he esophagogastric junction, related or unrelated to intestinal metaplasia. Pathol Int 2007; 57: 315-321
  • 11 Faller G, Stolte M. Barrettʼs oesophagus: time for consensus. Virchows Arch 2003; 443: 595-596
  • 12 Vieth M, Langner C, Neumann H et al. Barrettʼs esophagus. Practical issues for daily routine diagnosis. Pathol Res Pract 2012; 208: 261-268
  • 13 Liu W, Hahn H, Odze RD et al. Metaplastic esophageal columnar epithelium without goblet cells shows DNA content abnormalities similar to goblet cell-containing epithelium. Am J Gastroenterol 2009; 104: 816-824
  • 14 Vieth M, Barr H. Editorial: Defining a bad Barrettʼs segment: is it dependent on goblet cells?. Am J Gastroenterol 2009; 104: 825-827
  • 15 Vieth M, Schubert B, Lang-Schwarz C et al. Frequency of Barrettʼs neoplasia after initial negative endoscopy with biopsy: a long-term histopathological follow-up study. Endoscopy 2006; 38: 1201-1205
  • 16 Faller G, Borchard F, Ell C et al. Working Group for Gastroenterological Pathology of the German Society for Pathology. Histopathological diagnosis of Barrettʼs mucosa and associated neoplasias: results of a consensus conference of the Working Group for Gastroenterological Pathology of the German Society for Pathology on 22 September 2001 in Erlangen. Virchows Arch 2003; 443: 597-601
  • 17 Vakil N, van Zanten SV, Kahrilas P et al. Global Consensus Group. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol 2006; 101: 1900-1920
  • 18 Sharma P, Dent J, Armstrong D et al. The development and validation of an endoscopic grading system for Barrettʼs esophagus: the Prague C & M criteria. Gastroenterology 2006; 131: 1392-1399
  • 19 Spechler SJ, Sharma P, Souza RF et al. American Gastroenterological Association. American Gastroenterological Association technical review on the management of Barrettʼs esophagus. Gastroenterology 2011; 140: e18-e52
  • 20 Neumann H, Langner C, Neurath MF et al. Confocal laser endomicroscopy for diagnosis of Barrettʼs esophagus. Front Oncol 2012; 2: 42
  • 21 Krompecher E. Basalzellen, Metaplasie und Regeneration. Beitr z path Anat u z allg Path 1923; 72: 163-182
  • 22 Riddell RH. Grading of dysplasia. Eur J Cancer 1995; 31A: 1169-1178
  • 23 Odze RD, Flejou JF, Bofetta P et al. Adenocarcinoma of the oesophagogastric junction. In: Bosman FT, Carneiro F, Hruban RH et al. WHO classification of tumours of the digestive system. 4th ed. Lyon: 2010: 39-45
  • 24 Wang KK, Sampliner RE. Practice Parameterʼs Committee of the American College of Gastroenterology. Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barretts esophagus. Am J Gastroenterol 2008; 103: 788-797
  • 25 Montgomery E, Bronner MP, Goldblum JR et al. Reproducibility of the diagnosis of dysplasia in Barrettʼs oesophagus: a reaffirmation. Hum Pathol 2001; 32: 368-378
  • 26 Mueller J, Werner M, Stolte M. Barrettʼs esophagus: histopathologic definitions and diagnostic criteria. World J Surg 2004; 28: 148-154
  • 27 Curvers WL, Singh R, Wallace MB et al. Identification of predictive factors for early neoplasia in Barrettʼs esophagus after autofluorescence imaging: a stepwise multicenter structured assessment. Gastrointest Endosc 2009; 70: 9-17
  • 28 Munding J, Ziebarth W, Belyaev O et al. [Histological classification: evaluation of resection specimens of EMR/ESD–response evaluation after neoadjuvant therapy]. Zentralbl Chir 2013; 138 (Suppl. 02) e55-e62
  • 29 OʼConnor JB, Falk GW, Richter JE. The incidence of adenocarcinoma and dysplasia in Barrettʼs esophagus: report on the Cleveland clinics Barrettʼs esophagus registry adenocarcinoma and dyplasia in Barrettʼs esophagus. Am J Gastroenterol 1999; 94: 2037-2042
  • 30 Skacel MS, Petras RE, Gramlich TL et al. The diagnosis of low-grade dysplasia in Barrettʼs esophagus and ist implications for disease progression diagnosis of dysplasia in Barrettʼs esophagus. Am J Gastroenterol 2000; 95: 3383-3387
  • 31 Schnell TG, Sontag SJ, Chejfec G et al. Long-term nonsurgical management of Barrettʼs esophagus with high-grade dysplasia. Long-term nonsurgical management of Barrettʼs esophagus with high-grade dysplasia. Gastroenterology 2001; 120: 1607-1619
  • 32 Weston AP, Badr AS, Hassanein RS. Prospective multivariate analysis of clinical, endoscopic, and histological factors predictive oft he developement of Barrettʼs multifocal high grade dysplasia or adenocarcinoma. Am J Gastroenterol 1999; 94: 3413-3419
  • 33 Conio M, Blanchi S, Lapertosa G et al. Long-term endoscopic surveillance of patients with Barrettʼs esophagus. Incidence of dysplasia and adenocarcinoma: a prospective study surveillance of Barrettʼs esophagus: a prospective study. Am J Gastroenterol 2003; 98: 1931-1939
  • 34 Sharma P, Sampliner RE. Barrett esophagus. Curr Opin Gastroenterol 2002; 18: 471-478
  • 35 Curvers WL, ten Kate FJ, Krishnadath KK et al. Low-grade dysplasia in Barrettʼs esophagus: overdiagnosed and underestimated. Am J Gastroenterol 2010; 105: 1523-1530
  • 36 Dulai GS, Shekelle PG, Jensen DM et al. Dysplasia and risk of further neoplasticprogression in a regional veterans administration Barrettʼs cohort. Am J Gastroenterol 2005; 100: 775-783
  • 37 Srivastava A, Hornick JL, Li X et al. Extent of low-grade dysplasia is a risk factor for the developement of esophageal adenocarcinoma in Barrettʼs esophagus. Am J Gastroenterol 2007; 102: 483-493
  • 38 Lim CH, Treanor D, Dixon MF et al. Low-grade dysplasia in Barrettʼs esophagus has a high risk of progression. Endoscopy 2007; 39: 581-587
  • 39 Buttar NS, Wang KK. Mechanisms of disease: Carcinogenesis in Barrettʼs esophagus. Nat Clin Pract Gastroenterol Hepatol 2004; 1: 106-112
  • 40 Kaye PV, Haider SA, Ilyas M et al. Barrettʼs dysplasia and the Vienna classification: reproducibility, prediction of progression and impact of consensus reporting and p 53 immunohistochemistry. Histopathology 2009; 54: 699-712
  • 41 Weston AP, Sharma P, Topalovski M et al. Long-term follow-up of Barrettʼs high grade dysplasia. Am J Gastroenterol 2000; 95: 1888-1893
  • 42 Reid BJ, Levine DS, Longton G et al. Predictors of progression to cancer in Barrettʼs esophagus: baseline histology and flow cytometry identify low- and high risk patient subsets. Am J Gastroenterol 2000; 95: 1669-1676
  • 43 Downs-Kelly E, Mendelin JE, Bennett AE et al. Poor interobserver agreement in the distinction of high-grade dysplasia and adenocarcinoma in pretreatment Barrettʼs esophagus biopsies. Am J Gastroenterol 2008; 103: 2333-2340
  • 44 van Dekken H, Hop WC, Tilanus HW et al. Immunohistochemical evaluation of a panel of tumor cell markers during malignant progression in Barrett esophagus. Am J Clin Pathol 2008; 130: 745-753
  • 45 Dorer R, Odze RD. AMACR immunostaining is useful in detecting dysplastic epithelium in Barrettʼs esophagus, ulcerative colitis, and Crohnʼs disease. Am J Surg Pathol 2006; 30: 871-877
  • 46 Shy XY, Bharwandeen B, Leong AS. p 16, cyclin D1, Ki67, and AMACR as markers for dysplasia in Barrett esophagus. Appl Immunohistochem Mol Morph 2008; 16: 447-452
  • 47 Rabinovitch PS, Longton G, Blount PL et al. Aneuploidy and high expression of p 53 and Ki67 is associated with neoplastic progression Barrett esophagus. Cancer Biomark 2008; 4: 1-10
  • 48 Reid BJ, Prevo LJ, Galipeau PC et al. Predictors of progression in Barrettʼs esophagus II: baseline 17 p (p 53) loss of heterozygosity identified a patient subset at increased risk for neoplastic progression. Am J Gastroenterol 2001; 96: 2839-2848
  • 49 Rygiel AM, Milano F, Ten Kate FJ et al. Assessment of chromosomal gains as compared to DNA content changes is more useful to detect dysplasia in Barrettʼs esophagus brush cytology specimens. Genes Chromosomes Cancer 2008; 47: 396-404
  • 50 Bird-Lieberman EL, Dunn JM, Coleman HG et al. Population-based study reveals new risk-stratification biomarker panel for Barrettʼs esophagus. Gastroenterology 2012; 143: 927-935