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: Dysplasia
 

What is the prevalence of undetected carcinoma in resection specimens for high-grade dysplasia?

R. Romagnoli, C. Gutschow, J.-M. Collard (Brussels)

Dysplasia arising in Barrett's esophagus may be defined [1-3] as unequivocal neoplastic abnormalities in both the mucosal architecture and cellular morphology of the epithelium without any invasion of the lamina propria through the basement membrane. These abnormalities are mild and mainly located in the lower half of the epithelium in low-grade dysplasia (LGD), whereas they are more marked and extend over full thickness of the epithelium in high-grade dysplasia (HGD). Carcinoma arising in Barrett's esophagus is called invasive whenever neoplastic epithelial cells are found in the lamina propria beyond the basement membrane.

Reliable differentiation of HGD from invasive carcinoma on endoscopic biopsies may be impossible. For instance, a biopsy error rate for detecting invasive carcinoma in patients sent for esophagectomy because of the existence of HGD without endoscopically visible lesion may be as high as 43% [4] in spite of the fact that four-quadrant biopsies are taken every 2 cm throughout the whole length of the Barrett's area. Moreover, the use of large-bite "jumbo" spiked-biopsy forceps [5] does not seem to reduce the risk for erroneous staging. In the same way, there may be both inter- and intraobserver variations in the classification of dysplasia [6]. This is particularly true when the pathologist wavers between LGD an regenerative features. As for HGD, if no agreement exists among two independent, experienced pathologists, a second set of biopsies must be taken for further histologic analysis of the Barrett's area before making the final decision of an esophagectomy.

Table I shows the results of an in-depth review of both the medical and surgical literature on the subject: invasive carcinoma was found in about 40% of the resection specimens from patients who underwent esophagectomy because HGD had been evidenced in endoscopic biopsy material.

Table I. Prevalence of undetected invasive carcinoma in 228 patients who were offered an esophagectomy for HGD arising in Barrett's esophagus (data from the literature).

Data from 171 HGD patients from the literature for whom detailed histologic information was available indicate that 62 patients (36%) had, in fact, an invasive carcinoma that remained confined to the esophageal wall whereas 6 patients (3.5%) had an invasive carcinoma that had spread into loco-regional lymph nodes. Detailed information on the postoperative tumor-node staging [29] of these 68 invasive carcinoma patients is displayed in Table II. So, invasive carcinoma were classified as T1, T2 and T3 in 77.9%, 13.2% and 8.8%, respectively, and loco-regional lymph nodes were metastatic in 8.8% whereas they were histologically normal in 91.2%.

In addition to the discovery of an invasive carcinoma in the resected specimen of patients operated on for HGD, invasive carcinoma may be evidenced on the examination of a second set of biopsies taken a few weeks after a first set had settled the diagnosis of HGD. So, three of the 24 HGD patients we had to deal with in our department over a 14-year period had an invasive carcinoma disclosed on a second set of esophageal biopsies taken just to get some more histologic material and make sure of the presence of dysplastic lesions in the Barrett's area.

Table II. Staging according to T and N factors in 68 cancer patients from the literature for whom detailed histologic information is available.

There is no reliable endoscopic features for accurate prediction of the existence of an invasive carcinoma in a patient having HGD in endoscopic biopsy material. Indeed, data from the literature [3-5, 9-11, 13-15, 25, 26] indicate that, in comparison with the absence of any visible lesion in the Barrett's area, the presence of such a lesion (i.e. a nodule or an ulceration) does not increase the likelihood of finding an invasive carcinoma on postoperative examination of the resected specimen. Likewise, the predictive value of endosonography for the presence of an invasive carcinoma in patients having HGD has been shown to be rather low [30]. However, data from our institution [28] suggest that the adoption of a prompt surgical attitude by performing an esophagectomy as soon as HGD has been found on a first set of biopsies or at the latest, when an invasive carcinoma has been seen on biopsy samples taken a few weeks after the first histologic examination is much safer than the adoption of an expectant attitude towards HGD. Indeed, all 11 patients who underwent an esophagectomy a few weeks after HGD had been found for the first time were operated on for a mucosal disease. In contrast, four of our 13 patients in whom HGD was either followed up endoscopically for a long period (mean: 2 years) or disregarded until obstructive symptoms justified an endoscopic control, or who had been operated on after an invasive carcinoma had developped in the course of an endoscopic surveillance program of HGD, had metastatic lymph nodes in the resected specimen. This suggests that making the decision of an esophagectomy only after numerous successive sets of biopsies have shown the persistence of HGD, following a wait-and-see policy until neoplastic invasion beyond the basement membrane becomes evident in endoscopic biopsy material, or disregarding HGD until the patient re-consults for obstructive esophageal symptoms are three attitudes that expose to the risk of spontaneous progression of the disease to an advanced stage with poor long-term outcome [31].

References

1. Hameeteman W, Tytgat GNJ, Houthoff HJ, van den Tweel JG. Barrett's esophagus:development of dysplasia and adenocarcinoma. Gastroenterology 1989;96:1249-1256.

2. Riddell RH, Goldman H, Ransohoff DF, et al. Dysplasia in inflammatory bowel disease:standardized classification with provisional clinical applications. Hum Pathol 1983;14:931-968.

3. Reid BJ, Weinstein WM, Lewin KJ, et al. Endoscopic biopsy can detect high-grade dysplasia or early adenocarcinoma in Barrett's esophagus without grossly recognizable neoplastic lesions. Gastroenterology 1988;94:81-90.

4. Nigro JJ, Hagen JA, DeMeester TR, et al. Occult esophageal adenocarcinoma:extent of disease and implications for effective therapy. Ann Surg 1999;230:433-440.

5. 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.

6. 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.

7. Collard JM, Otte JB, Reynaert M, Michel L, Carlier MA, Kestens PJ. Esophageal resection and by-pass: a 6-year experience with a low postoperative mortality. World J Surg 1991;15:635-641.

8. Skinner DB, Walther BC, Riddell RH, Schmidt H, Iascone C, Demeester TR. Barrett's esophagus: comparison of benign and malignant cases. Ann Surg 1983;198:554-566.

9. Schmidt HG, Riddell RH, Walther B, Skinner DB, Riemann JF. Dysplasia in Barrett's esophagus. J Cancer Res Clin Oncol 1985;110:145-152.

10. Lee RG. Dysplasia in Barrett's esophagus:a clinicopathologic study of six patients. Am J Surg Pathol 1985;9:845-852.

11. Hamilton SR, Smith RRL. The relationship between columnar epithelial dysplasia and invasive adenocarcinoma arising in Barrett's esophagus. Am J Clin Pathol 1987;87:301-312.

12. Altorki NK, Sunagawa M, Little AG, Skinner DB. High-grade dysplasia in the columnar-lined esophagus. Am J Surg 1991;161:97-100.

13. McArdle JE, Lewin KJ, Randall G, Weinstein W. Distribution of dysplasia and early invasive carcinoma in Barrett's esophagus. Hum Pathol 1992;23:479-482.

14. Pera M, Trastek VF, Carpenter HA, Allen MS, Deschamps C, Pairolero PC. Barrett's esophagus with high-grade dysplasia: an indication for esophagectomy? Ann Thorac Surg 1992;54:199-204.

15. Levine DS, Haggitt RC, Blount PL, Rabinovitch PS, Rusch VW, Reid BJ. An endoscopic biopsy protocol can differentiate high-grade dysplasia from early adenocarcinoma in Barrett's esophagus. Gastroenterology 1993;105:40-50.

16. Streitz JM, Andrews CW, Ellis FH. Endoscopic surveillance of Barrett's esophagus:does it help? J Thorac Cardiovasc Surg 1993;105:383-388.

17. Peracchia A. Quoted. In: Perrachia A, Bonavina L, eds. Carcinoma del cardias. Roma: Studio Tipografico,1998;17-30.

18. Ortiz A, Martinez de Haro LF, Parrilla P, et al. Conservative treatment versus antireflux surgery in Barrett's oesophagus: long-term results of a prospective study. Br J Surg 1996;83:27427-8.

19. McDonald ML, Trastek VF, Allen MS, Deschamps C, Pairolero PC. Barrett's esophagus: does an antireflux procedure reduce the need for endoscopic surveillance? J Thorac Cardiovasc Surg 1996;111:1135-1140.

20. Edwards MJ, Gable DR, Lentsch AB, Richardson JD. The rationale for esophagectomy as the optimal therapy for Barrett's esophagus with high-grade dysplasia. Ann Surg 1996;223:585-591.

21. Heitmiller RF, Redmond M, Hamilton SR. Barrett's esophagus with high-grade dysplasia: an indication for prophylactic esophagectomy. Ann Surg 1996;224:66-71.

22. Cameron AJ, Carpenter HA. Barrett's esophagus, high-grade dysplasia, and early adenocarcinoma: a pathological study. Am J Gastroenterol 1997;92:586-591.

23. Ferguson MK, Naunheim KS. Resection for Barrett's mucosa with high-grade dysplasia:implications for prophylactic photodynamic therapy. J Thorac Cardiovasc Surg 1997;114:824-829.

24. Catrambone G, Leoncini G, Iurilli L, et al. Complications of Barrett's esophagus: indications for esophageal resection with special reference to high-grade dysplasia. Minerva Chir 1999;54:657-667.

25. Peters JH, Clark GWB, Ireland AP, Chandrasoma P, Smyrk TC, Demeester TR. Outcome of adenocarcinoma arising in Barrett's esophagus in endoscopically surveyed and nonsurveyed patients. J Thorac Cardiovasc Surg 1994;108:813-822.

26. Rice TW, Falk GW, Achkar E, Petras RE. Surgical management of high-grade dysplasia in Barrett's esophagus. Am J Gastroenterol 1993;88:1832-1836.

27. Nguyen NT, Schauer P, Luketich JD. Minimally invasive esophagectomy for Barrett's esophagus with high-grade dysplasia. Surgery 2000;127:284-290.

28. Collard JM, Gutschow C, Romagnoli R. High-grade dysplasia arising in Barrett's esophagus: endoscopic surveillance or immediate resection? In process of publication.

29. Hermanek P, Wittekind C. The pathologist and the residual tumor ( R ) classification. Pathol Res Pract 1994;190:115123.

30. Falk GW, Catalano MF, Sivak MV Jr, Rice TW, Van Dam J. Endosonography in the evaluation of patients with Barrett's esophagus and high-grade dysplasia. Gastrointest Endosc 1994;40:207-212.

31. Collard JM, Romagnoli R, Hermans BP, Malaise J. Radical esophageal resection for adenocarcinoma arising in Barrett's esophagus. Am J Surg 1997;174:307-311.


Publication date: August 2003 OESO©2015