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

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OESO©2015
 
Volume: Barrett's Esophagus
Chapter: Pathophysiology
 

What are the advantages of a new simplified classification system of dysplasia?

R.H Riddell (Hamilton)

Is there a new simplified classification system for the classification of dysplasia? There are certainly new systems and new correlations with dysplasia but not a new simplified classification.
Which classification systems of dysplasia are currently in use?

Those in vogue are the following

1. Negative, Indefinite, Dysplasia - 3 step, Mild, Moderate, Severe (in practice this becomes a stage system because of the use of "mild to moderate dysplasia" and "moderate to severe dysplasia". This inevitably decreases kappa value for inter and intraobserver variability). Although still used, especially in parts of Europe, most of the literature regarding surveillance and carcinoma uses the 2-grade system as follows [1].
2. Negative, Indefinite, Dysplasia - 2 step, low-grade dysplasia (LGD), high-grade dysplasia (HGD) (in practice, although this could be a 3-grade system with "low to highgrade dysplasia" as a third option, this rarely is used). Because the management algorithm tends to have a node at HGD or worse for potential esophagectomy, and give the lack of reproducibility [2] of LGD versus Indefinite, there is a tendency to merge indefinite for dysplasia with LGD.

A simplified system could therefore be:

3. Negative Indefinite/LGD/HGD There are potential problems with this system:
- it is not new,
- it may not work.

Why may it not work? The Seattle protocol assumes:
- that patients with LGD or less are at virtually no increased risk of Ca,
- that it is feasible to wait until patients develop evidence of invasion before recommending esophagectomy without increased mortality from Ca and also minimizing the number of patients coming to esophagectomy - with its associated morbidity and potential mortality (3-5%).

At least 2 studies [3, 4] suggest that the Seattle protocol can still result in mortality from unrecognized carcinomas found only in resection specimens. This raises the issue of whether LGD should be used as the endpoint for surveillance and for treatment. The difficulty is that if LGD cannot be readily distinguished from indefinite for dysplasia, then unless they have similar implications for the development of carcinoma, which may be the case, they need to be distinguished. In this regard the utility of p53 immunostaining or computerized quantitative pathology for the grading of dysplasia in surveillance biopsies of Barrett's esophagus[1, 5-13] is obvious.

New systems

The Vienna system resembles the 2-grade system with high and low-grade dysplasia (noninvasive neoplasia, but includes a category of "suspicious for invasive carcinoma that may be very useful in Barrett's esophagus. It also uses the morphological entity of carcinoma in situ, recognizing that in the world of molecular biology, once uniformly defined, this may have specific molecular associations and implications. In Barrett's esophagus, this term is clinically included with HGD. The Vienna classification system is developed for use throughout the gastrointestinal tract [14]. It consists of the following".
1. Negative for dysplasia/neoplasia (includes reactive lesions).
2. Indefinite for dysplasia/neoplasia.
3. Non-invasive neoplasia-low-grade (synonymous with low-grade dysplasia). Low-grade adenoma/dysplasia (includes mild and moderate dysplasia in a 3 grade system).
4. Non-invasive neoplasia-high-grade (synonymous with high-grade dysplasia):
 4.1 High-grade adenoma / dysplasia (includes severe dysplasia in a 3-grade system),
 4.2 Non-invasive carcinoma (carcinoma in situ),
 4.3 Suspicious for invasive carcinoma.
5. Invasive neoplasia:
 5.1 Intramucosal carcinoma (invasive into the lamina propria),
 5.2 Invasion into the submucosa or beyond.

References

1. Van Sandick JW, Baak JP, van Lanschot JJ, et al. Computerized quantitative pathology for the grading of dysplasia in surveillance biopsies of Barrett's oesophagus. J Pathol 2000;190:177-183.

2. Reid BJ, Haggitt RC, Rubin CE, et al. Observer variation in the diagnosis of dysplasia in Barrett's esophagus. Hum Pathol 1988;19:166-178.

3. Van Sandick JW, Van Lanschot JJB, Kuiken BW, Tytgat GNJ, Offerhaus GJA, Obertop H. Impact of endoscopic biopsy surveillance of Barrett's oesophagus on pathological stage and clinical outcome of Barrett's carcinoma. Gut 1998;43:216-222.

4. Falk GW, Rice TW, Goldblum JR, Richter JE. Jumbo biopsy forceps protocol still misses unsuspected cancer in Barrett's esophagus with high-grade dysplasia. Gastrointest Endosc 1999;49:170-176.

5. Schneider PM, Stoeltzing O, Roth JA, et al. P53 mutational status improves estimation of prognosis in patients with curatively resected adenocarcinoma in Barrett's esophagus. Clin Cancer Res 2000;6:3153-3158.

6. Bani-Hani K, Martin IG, Hardie LJ, et al. Prospective study of cyclin D1 overexpression in Barrett's esophagus: association with increased risk of adenocarcinoma. J Natl Cancer Inst 2000;92:1316-1321.

7. Mueller J, Werner M, Siewert JR. Malignant progression in Barrett's esophagus: pathology and molecular biology. Rec Res Cancer Res 2000;155:29-41.

8. Galipeau PC, Prevo LJ, Sanchez CA, Longton GM, Reid BJ. Clonal expansion and loss of heterozygosity at chromosomes 9p and 17p in premalignant esophageal (Barrett's) tissue. J Natl Cancer Inst 1999;91:2087-2095.

9. Gimenez A, De Haro LM, Parrilla P, Bermejo J, Perez-Guillermo M, Ortiz MA. Immunohistochemical detection of p53 protein could improve the management of some patients with Barrett esophagus and mild histologic alterations. Arch Pathol Lab Med 1999;123:1260-1263.

10. Eisen GM, Montgomery EA, Azumi N, et al. Qualitative mapping of Barrett's metaplasia: a prerequisite for intervention trials. Gastrointest Endosc 1999;50:814-818.

11. Klump B, Hsieh CJ, Holzmann K, et al. Diagnostic significance of nuclear p53 expression in the surveillance of Barrett's esophagus; a longitudinal study. Z Gastroenterol 1999;37:1005-1011.

12. Prevo LJ, Sanchez CA, Galipeau PC, Reid BJ. p53-mutant clones and field effects in Barrett's esophagus. Cancer Res 1999;59:4784-4787.

13. Hanas JS, Lerner MR, Lightfoot SA, et al. Expression of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) and p53 tumor suppressor in dysplastic progression and adenocarcinoma in Barrett esophagus. Cancer 1999;86:756-763.

14. Schlemper RJ, Riddell RH, Kato Y, et al. The Vienna classification of gastrointestinal epithelial neoplasia. Gut 2000;47:251-255.


Publication date: August 2003 OESO©2015