Kyoto international consensus report on anatomy, pathophysiology and clinical significance of the gastro-oesophageal junction

Abstract

Objective: An international meeting was organised to develop consensus on (1) the landmarks to define the gastro-oesophageal junction (GOJ), (2) the occurrence and pathophysiological significance of the cardiac gland, (3) the definition of the gastro-oesophageal junctional zone (GOJZ) and (4) the causes of inflammation, metaplasia and neoplasia occurring in the GOJZ.

Design: Clinical questions relevant to the afore-mentioned major issues were drafted for which expert panels formulated relevant statements and textural explanations.A Delphi method using an anonymous system was employed to develop the consensus, the level of which was predefined as ≥80% of agreement. Two rounds of voting and amendments were completed before the meeting at which clinical questions and consensus were finalised.

Results: Twenty eight clinical questions and statements were finalised after extensive amendments. Critical consensus was achieved: (1) definition for the GOJ, (2) definition of the GOJZ spanning 1 cm proximal and distal to the GOJ as defined by the end of palisade vessels was accepted based on the anatomical distribution of cardiac type gland, (3) chemical and bacterial (Helicobacter pylori) factors as the primary causes of inflammation, metaplasia and neoplasia occurring in the GOJZ, (4) a new definition of Barrett's oesophagus (BO).

Conclusions: This international consensus on the new definitions of BO, GOJ and the GOJZ will be instrumental in future studies aiming to resolve many issues on this important anatomic area and hopefully will lead to better classification and management of the diseases surrounding the GOJ.

Keywords: BARRETT'S CARCINOMA; BARRETT'S OESOPHAGUS; GASTRO-OESPHAGEAL JUNCTION; GASTROESOPHAGEAL REFLUX DISEASE; HELICOBACTER PYLORI.

Figure 1

Landmarks of gastro-oesophageal junction (GOJ). (A) Schema of the landmarks used for GOJ. Endoscopic view of the GOJ. (1) palisade vessels, (2) squamocolumnar junctional line (Z line), (3) proximal end of the gastric folds, (4) gastric sling fibres and (5) angle of His. (B) Palisade vessels (thin arrows), squamocolumnar junctional line (Z-line) (arrow heads) and the end of gastric folds (thick arrows) are shown. These three landmarks (distal end of palisade vessels, Z-line and proximal end of gastric folds) are closely aligned with each other in normal subjects. (This endoscopic Image was provided by Prof. MF.).

Figure 2

Changes of endoscopic images at the GOJ depending on the different observation conditions. (A) This white light image was taken with deflated condition. Note that oesophageal mucosa on the left side of this image forms as a fold-like configuration, but can be identified as oesophageal mucosa as the whitish colour of the squamous epithelium. Whereas the columnar metaplasia seen at the upper right folds with columnar metaplasia, such a fold-like configuration can be miss-interpreted as PEGF. (B) When the distal end of the oesophagus was inflated with moderate amount of air, the distal end of the gastric folds was clearly recognisable. Although palisade vessels can be seen on the right side of the same fold pointed out in A, they are not visible on the other side of this image, indicating a very short area of metaplastic mucosa. (C) Image taken under further air insufflation during deep inhalation, separation between the PEGF and SCJ became more obvious, partly due to flattening of the gastric mucosa. On the right side of this image, DEPV in the columnar mucosa distal to the squamous epithelium became clearly visible, indicating the presence of metaplastic mucosa in this case. (These endoscopic images were provided by Prof. TG.). DEPV, distal end of palisade vessel; GOJ, gastro-oesophageal junction; PEGF, proximal end of gastric fold; SCJ, squamocolumnar junction.

Figure 3

Histological features of oesophagus at the gastro-oesophageal junction. In this specimen, histological features unique to the oesophagus are depicted; namely double muscularis mucosa consisting of the superficial muscularis mucosae (m) and the deep muscularis mucosae (M), squamous epithelium (S) and the duct (D) connected to the oesophageal submucosal gland (oesophageal gland proper; ESG). Note the right side of the epithelium is covered by columnar epithelium containing goblet cells. Presence of double muscularis mucosae, and the oesophageal submucosal gland underneath the epithelium indicate that the columnar epithelium is not gastric mucosa but metaplastic oesophageal mucosa. (This histology photo was provided by professor KM.).

Figure 4

Pathophysiological mechanisms of columnar metaplasia at the gastro-oesophageal junction zone (GOJZ). Two independent mechanisms, gastroduodenal reflux in high gastric acidity (type I) and hypo- or achlorhydria due to advanced atrophy caused by H. pylori infection (type II) were postulated for causing columnar metaplasia at the GOJZ. Type I may be subdivided further into two subtypes, gastroduodenal reflux in H. pylori-negative patients without gastric atrophy (type Ia), and gastroduodenal reflux in H. pylori-positive patients with mild gastritis limited in the antrum (type Ib). Nitrosative and oxidative stress occurring at the GOJ may also contribute the inflammation. In H. pylori-positive subjects, inflammation around the GOJ may be higher than the gastric corpus and can be a cause of atrophic and/or intestinal metaplastic change. However, more frequent pattern of gastric atrophy is pangastritis progressing from the distal stomach toward proximal direction. Theoretically autoimmune gastritis (AIG) may involve GOJZ. However, detailed investigation on histological changes at the GOJZ in AIG is scarce, and hence this hypothetical subtype is not depicted in this figure. Curved black arrows indicate reflux (gastric acid and bile acid). Vermillion areas indicate inflammations and/or metaplasia caused by these factors.