Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

  Browse by Author
  Browse by Movies
OESO©2015
 
Volume: Barrett's Esophagus
Chapter: The definition of Barrett's esophagus
 

Consensus of a Panel at the end of the 6th OESO World Congress

A. Watson (Chairman), R.E. Sampliner, H.D. Appelman, S.J. Spechler, N.A. Shepherd

The lack of a universally accepted definition of Barrett's esophagus has resulted in confusion and difficulties in comparing different studies on this condition. preeminent among reasons for this is the fact that Barrett's original description in 1950 related to two conditions, namely a congenital short esophagus with intrathoracic gastric columnar lining and congenital gastric heterotropia in the esophagus, with ulceration [1]. Three years later Allison provided sound anatomical reasons why columnar lining could occur in the distal esophagus, as an acquired condition which appeared to be prevalent in patients with gastroesophageal reflux (GER) [2]. Subsequently, several authors confirmed the association of columnar lining of the esophagus with clinical GER [3, 4] and subsequent studies confirmed the development of a columnar lined esophagus (CLE) as a response to GER in an animal model [5].

It became apparent from the histological standpoint that the CLE embraced a spectrum of different cellular types, principally comprising a gastric fundic type epithelium, a junctional type epithelium, which had similarities to gastric mucosa but did not secrete digestive juices, although possessing the ability to withstand acid-peptic digestion, and a distinctive type of intestinal metaplasia, characterised by the presence of goblet cells [6]. The malignant potential of the CLE was subsequently described [7, 8], which conferred great importance on the condition and consequently on its accurate diagnosis. For this reason, and in order to eliminate any confusion between CLE and the normal junctional columnar epithelium, as well as difficulty in identifying the precise esophagogastric junction (EGJ) in cases of hiatal hernia (HH), an arbitrary minimal length of 3 cm of CLE from the EGJ was recommended before the diagnosis of CLE should be made [9]. Until the last few years, Barrett's esophagus was defined as any histological type of columnar epithelium with a minimum length of 3 cm above the EGJ.

If viewed from the standpoint of the risk of developing adenocarcinoma, it became apparent that this applied only to CLE with intestinal metaplasia (IM) and that CLE with fundic epithelium had no malignant potential [10, 11]. However, endoscopic appearances did not distinguish between the various histological types and all comprised "Barrett's esophagus" and were all included in the initial surveillance programmes, which resulted in a much lower incidence of adenocarcinoma than more recent series which have documented the risk in patients with IM. The problem of definition has become more clouded with the realisation that short segments of CLE with IM, less than 3 cm in length, can be associated with the development of adenocarcinoma and even in short, noncircumferential tongues of columnarisation [12]. These two entities have each been referred to as "short segment Barrett's" since the length of these segments, which have malignant potential, fall short of the 3 cm required to fulfil the traditional definition. Subsequent studies have shown that such short and usually circumferential segments of CLE with intestinal metaplasia are visible in 42% of adenocarcinoma of the cardia when detailed pathological examination is undertaken [13, 14]. Furthermore, pathophysiological studies have shown that patients with these short segments of columnarisation have gastroesophageal reflux disease (GERD), the pathophysiological severity of which is intermediate between that in patients with erosive esophagitis and those with "traditional Barrett's CLE" [15].

The problem of definition has been further compounded by numerous reports of microscopic intestinal metaplasia around the EGJ, present in up to 36% of patients undergoing endoscopy for a variety of gastrointestinal symptoms, and some have referred to this phenomenon also as "short-segment Barrett's" or "ultra-short segment Barrett's" [16-18]. In Spechler's series [16], only patients with "traditional Barrett's esophagus" and those with microscopic IM at the cardia were studied, those patients with confluent or circumferential columnarisation seen endoscopically being excluded from the study. The bulk of evidence suggests that microscopic IM at the cardia is not associated with GER, but associated principally with increasing age and Helicobacter infection. It is believed to have a different histogenesis from intestinal metaplasia in confluent and circumferential areas of columnarisation in the esophagus, and its risk of malignant change appears to be extremely low [19]. In these circumstances, there is confusion in using the term "short segment Barrett's" interchangeably between endoscopically visible confluent or circumferential columnarisation with intestinal metaplasia and microscopic intestinal metaplasia around the cardia, and furthermore it would appear entirely inappropriate to apply the term "Barrett's esophagus" at all to the latter group, in the absence of endoscopically visible columnarisation, GERD and a significant malignant risk.

In making a confident diagnosis of "Barrett's esophagus" or the reflux-induced columnarisation of the esophagus which contains IM and consequently carries a malignant risk, both endoscopic and histopathological components are necessary [20]. The endoscopist needs to confirm that there is visible columnar epithelium above the EGJ and that biopsies are taken from this as opposed to the gastric cardia and the histopathologist needs to confirm the presence of columnar metaplasia. Whilst it is the demonstration of the presence of IM which confers the risk of malignant transformation, there is a body of pathological opinion which believes that IM is always present in macroscopic columnarisation if a sufficient number of biopsies are taken over an adequate period of time. Care is needed on the part of the endoscopist in identifying short segments of columnarisation as the precise EGJ can be difficult to identify, particularly in the presence of a HH, and measurements and precise identification on the site of biopsy in relation to the EGJ can be difficult in the living, moving esophagus at endoscopy. The most widely accepted definition of the EGJ is where the proximal limit of the longitudinal gastric mucosal folds, the distal limit of the longitudinal esophageal vessels and the point of flaring from the tubular esophagus into the more dilated stomach co-exist in the absence of air insufflation.

The definition of "Barrett's esophagus" proposed by the American College of Gastroenterology [21] acknowledges these factors and states "Barrett's esophagus is a change in the esophageal epithelium of any length that can be recognised at endoscopy and is confirmed to have intestinal metaplasia by biopsy". Such a definition, although eminently satisfactory in clinical practice, requires the performance of endoscopy and biopsy before Barrett's esophagus can be said to exist, whereas in reality, the vast majority of patients with Barrett's esophagus never present clinically [22]. The following definition would serve to overcome this problem: "Barrett's esophagus" is an esophagus in which any portion of the normal squamous lining has been replaced by a metaplastic columnar epithelium which is visible macroscopically. In order to make a positive diagnosis of "Barrett's esophagus", a segment of columnar metaplasia of any length must be visible endoscopically above the EGJ and confirmed or corroborated histologically.

A major question is whether this condition should continue to be referred to as "Barrett's esophagus" in view of its application to differing situations where either a significant or negligible malignant risk exists, and that the above-described entity is different to that described by Barrett in 1950 in which the malignant risk, the relevance of IM and of short segment columnarisation were not recognised. An alternative proposal is to replace the eponym by a more descriptive term such as "columnar-lined esophagus", and to qualify as to whether tongues or circumferential, and by length. It is believed that a distinction between "short-segment" and "traditional segment" columnarisation is arbitrary, although it is recognised that increasing length of the columnarised segment reflects increasing severity of GERD and risk of malignant transformation.

Conclusions and recommendations

Current usage of the term “Barrett’s esophagus” is confusing and when applied to cases where there is no or minimal risk of malignant change, causes unnecessary anxiety.

There is a need to specifically define the columnar metaplasia which carries a risk of malignant transformation and has implications regarding surveillance.

A proposed definition of this condition is “an esophagus in which any portion of the normal squamous lining has been replaced by a metaplastic columnar epithelium which is visible macroscopically”. In order to make a positive diagnosis, a segment of columnar metaplasia of any length must be visible endoscopically above the EGJ and confirmed or corroborated histologically. o In order to minimise confusion and undue anxiety, consideration should be given to replacing the term "Barrett's esophagus" by a more descriptive term such as "columnar-lined esophagus" which can be qualified as to whether tongues or circumferential, and by length which would obviate the arbitrary distinction between "short-segment" and "traditional segment" disease.

References

1. Barrett NR. Chronic peptic ulcer of the oesophagus and "oesophagitis". Br J Surg 1950;38:175-182.

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

3. Moersch R, Ellis FH, McDonald JR. Pathologic changes occurring in severe reflux oesophagitis. Surg Gynecol Obstet 1959;108:476-484.

4. Hayward J. The lower end of the oesophagus. Thorax 1961;16:36-41.

5. Bremner CG, Lynch VP, Ellis FH. Barrett's esophagus: congenital or acquired? An experimental study of esophageal mucosal regeneration in the dog. Surgery 1970;68:209-216.

6. Paull A, Trier JS, Dalton MD, Camp RC, Loeb P, Goyal RP. The histological spectrum of Barrett's oesophagus. N Engl J Med 1976;295:476-480.

7. Naef AP, Savary M. Ozzello L. Columnar-lined lower esophagus: an acquired lesion with malignant predisposition: report on 140 cases of Barrett's esophagus with 12 adenocarcinomas. J Thorac Cardiovasc Surg 1975;70:826-834.

8. Haggitt RC, Tryzelaar J, Ellis FH, et al. Adenocarcinoma complicating columnar epithelium-lined (Barrett's) esophagus. Am J Clin Pathol 1978;70:1-5.

9. Skinner DB, Walther BC, Riddell RH, Schmidt H, Iascone C, DeMeester TR. Barrett's esophagus: comparison of benign and malignant cases. Ann Surg 1983;198:554-565.

10. Reid BJ, Haggitt RC, Rubin LE, Rabinovitch PS. Barrett's esophagus: correlation between flow cytometry and histology in detection of patients at risk for adenocarcinoma. Gastroenterology 1987;93:1-11.

11. Spechler SJ, Goyal RK. The columnar-lined esophagus, intestinal metaplasia and Norman Barrett. Gastroenterology 1996;110:614-621.

12. Schnell TG, Sontag SJ, Chejfec G. Adenocarcinoma arising in tongues or short segments of Barrett's esophagus. Dig Dis Sci 1992;37:137-143.

13. Cameron AJ, Lomboy CT, Pera M, Carpenter HA. Adenocarcinoma of the esophagogastric junction and Barrett's esophagus. Gastroenterology 1995;109:1541-1546.

14. Clark GWB, Smyrk TC, Burdiles P, et al. Is Barrett's metaplasia the source of adenocarcinomas of the cardia? Arch Surg 1994;129:609-614.

15. Clark GWB, Ireland AP, Peters JH, Chandrasoma P, DeMeester TR, Bremner CG. Short-segment Barrett's esophagus: a prevalent complication of gastroesophageal reflux disease with malignant potential. J Gastrointest Surg 1997;1:113122.

16. Spechler SJ, Zeroogian JM, Antonioli DA, Wang HH, Goyal RK. Prevalence of metaplasia at the gastro-oesophageal junction. Lancet 1994;344:1533-1536.

17. Trudgill NJ, Suvarna SK, Kapur KC, Riley SA. Intestinal metaplasia at the squamocolumnar junction in patients attending for diagnostic gastroscopy. Gut 1997;41:585-589.

18. Nandurkar S, Talley NJ, Martin CJ, Ng THK, Adams S. Short segment Barrett's oesophagus: prevalence, diagnosis and associations. Gut 1997;40:710-715.

19. Weston AP, Krmpotich P, Makdisi WF, et al. Short segment Barrett's esophagus; clinical and histological features associated endoscopic findings, and association with gastric intestinal metaplasia. Am J Gastroenterol 1996;91;5:981986.

20. Shepherd NA, Biddlestone LR. The histopathology and cytopathology of Barrett's oesophagus. In: Manek S, ed. Bulletin Cellular Pathology. Rila Publications 1999;1:39-44.

21. Sampliner RE. Practice guidelines on the diagnosis, surveillance and therapy of Barrett's esophagus. Am J Gastroenterol 1988;93:1028-1031.

22. Cameron AJ, Zinsmeister AR, Ballard DJ, Carney JA. Prevalence of columnar-lined Barrett's esophagus. Comparison of population-based clinical and autopsy findings. Gastroenterology 1990;99:918-22.


Publication date: August 2003 OESO©2015