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Update: histopathology-based definition of gastroesophageal reflux disease and Barrett's esophagus

Übersicht zur Histologie-basierten Definition der gastroösophagealen Refluxkrankheit

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Zusammenfassung

GRUNDLAGEN: Die gastroösophageale Refluxkrankheit (GERD) ist mit Zylinderepithel- und Barrett-Ösophagus (BE) assoziiert, aus dem sich ein Adenokarzinom entwickeln kann. Derzeit wird GERD entsprechend einer Mischung aus Symptomen, Endoskopie, Histopathologie und Funktionsdiagnostik definiert. Wir suchten nach einer primär histologie-basierten Definition von GERD. METHODIK: Übersicht rezenter Literatur zu GERD-Histopathologie. ERGEBNISSE: Multi-Level Biopsien vom ösophagogastralen Übergang und die neue Paull-Chandrasoma Histopathologie-Klassifikation von CLE definieren jene mit Reflux und Karzinomrisiko. Man unterscheidet drei abnormale, nondysplastische Mukosatypen zwischen Plattenepithel und Magenschleimhaut: Kardia Mukosa (CM), Oxyntokardia Mukosa (OCM) und CM mit intestinaler Metaplasie (=Barrett's esophagus, mit 0,5% jährlichem Krebsrisiko). Die Häufigkeit von intestinaler Metaplasia (IM) beträgt 15–24 % an einem endoskopisch normalen ösophagogastralen Übergang und findet sich in 100% bei endoskopisch sichtbarem CLE≥5 cm. IM entsteht an der Mukosagrenze (Platten-, Zylindereptithel). Der sog. dilatierte Endstadium Ösophagus ist ein neues Konzept und definiert das GERD-Frühstadium und entsteht durch transiente, Magendehnungs-induzierte Erschlaffungen des unteren Ösophagusphinkters. Permanente Schädigung führt zur Auskleidung mit Zylinderepithel und magenartigem Aussehen. Die Mehrzahl der sog. Kardiakarzinome entstehen auf Basis des dilatierten Endstadium Ösophagus. SCHLUSSFOLGERUNGEN: CLE entsteht durch Reflux und wird zur Krankheit, wenn er mit die Lebensqualität beeinträchtigenden Symptomen und/oder intestinaler Metaplasie bzw. Dysplasie (Krebsrisiko) vergesellschaftet ist. CLE, IM und Dysplasie können endoskopisch nicht ausgeschlossen werden, dies gelingt nur mittels Histopathologie von Biopsien aus dem ösophagogastralen Übergang.

Summary

BACKGROUND: Gastroesophageal reflux disease (GERD) is associated with columnar lined esophagus (CLE) and Barrett's esophagus (BE), which may progress towards esophageal adenocarcinoma. Currently a mixture of symptoms, endoscopic and histopathologic criteria and results obtained from esophageal function tests define GERD. We searched for a histopathology-based definition of GERD. METHODS: Review on GERD-histopathology. RESULTS: Multilevel biopsies and the novel Paull-Chandrasoma histopathology-classification of CLE define those with reflux and risk for development of esophageal adenocarcinoma (those with Barrett's esophagus and dysplasia) and list three abnormal nondysplastic epithelia between squamous and gastric oxyntic mucosa: cardiac mucosa (CM), oxyntocardiac mucosa (OCM), and CM with intestinal metaplasia (=Barrett's esophagus, with 0.5% annual cancer risk). Frequency of intestinal metaplasia (IM) is 15–24% at an endoscopically normal junction and increases towards 100% if CLE is ≥5 cm. IM develops at the squamocolumnar junction. Dilated end stage esophagus (DESE) is a novel concept and defines the early stage of reflux disease. The pathophysiology of DESE involves gastric distention-induced shortenings of the lower esophageal sphincter (LES) with reflux favoring damage and columnar metaplasia of the most distal esophagus. Over time permanent LES shortening and proximal dislocation of the squamocolumnar junction result in gastric-type appearance of DESE, which is mistaken for proximal stomach. The majority of adenocarcinomas of the "esophagogastric" junction arise within DESE. CONCLUSIONS: CLE is abnormal, results from reflux and is a disease if associated with life quality-impairing symptoms and/or intestinal metaplasia and dysplasia (cancer risk). Presence of CLE, IM, and dysplasia cannot be excluded from endoscopy, but requires histopathology of biopsies from the squamocolumnar junction.

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  1. Division of General Surgery, Department of Surgery, Medical University of Vienna, Vienna, Austria

    J. Lenglinger, M. Eisler, G. Prager, J. Zacherl & M. Riegler

  2. Department of Pathology, Medical University of Vienna, Vienna, Austria

    F. Wrba

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  1. J. Lenglinger
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  2. M. Eisler
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Lenglinger, J., Eisler, M., Wrba, F. et al. Update: histopathology-based definition of gastroesophageal reflux disease and Barrett's esophagus. Eur Surg 40, 165–175 (2008). https://doi.org/10.1007/s10353-008-0415-z

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