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Low-grade

Follow-up with shorter interval

High-grade

Follow-up with very short interval? Resection?

Intramucosal carcinoma (invasion of lamina propria)

established is the finding of high-grade dysplasia, because it seems to be a marker of high risk for concurrent carcinoma. Several studies report that when high-grade dysplasia is discovered, the likelihood of a concurrent invasive carcinoma is about 30%.1 ' However, in other studies, high-grade dysplasia is followed with more frequent endoscopic examinations, and some high-grade dysplasias are treated with different

types of ablation. In these centers, the indication for resection is carcinoma invading the lamina propria. Thus, the indications for resection vary from center to center, and no consensus exists on the appropriate end-point.

Complicating the situation is the lack of well-defined standards for surveillance. For instance, no standards dictate how often a patient should have esophagoscopy and biopsy, or how many biopsy samples should be taken, or at which sites they should be taken. Some pathologists believe that examination of brush cytologic specimens, in addition to biopsy specimens, increases diagnostic yield. Dysplasia and low-

stage carcinomas can be found in flat, innocuous-appearing mucosa as well as in abnormal-appearing mucosa, so there are often no endoscopic markers of where to perform a biopsy. One recommendation is to take four-quadrant biopsy samples at 2-cm increments along flat mucosa as well as of all endoscopic lesions. Likewise, the proper approach to take when high-grade dysplasia is found in a biopsy is not

clear-cut. For instance, should a pathologist who is expert in the field review every diagnosis of high-grade dysplasia? Some authors believe this should be done.1 ' 1 ' Does a diagnosis of high-grade dysplasia constitute an indication for esophagectomy? Should the follow-up period, whatever it may be, be shortened and rebiopsy and possibly brush cytology undertaken if esophagectomy is not performed? Furthermore, what constitutes a shortened follow-up interval? What should be done for patients with low-grade dysplasia? Does this lesion require a shorter period of follow-up? Some low-grade dysplasias evolve into high-grade lesions. Which ones will, and how long will this evolution take? At the moment, these questions have not been answered, the data are still inconclusive, and it is possible that anything that is done for these patients may be performed on the basis of a best estimate and on the clinical status of the individual.

To summarize, we know that many people in the general population suffer from chronic heartburn. In this population, and even in the population without heartburn, short-segment Barrett's mucosa appears to be common. We have not identified a set of clinical or histologic features that defines a high-risk clinical group within the population with Barrett's mucosa that requires cancer surveillance. Finally, once surveillance programs are undertaken, we are not absolutely certain what courses of action will be dictated by the biopsy changes that are found. In some centers, the finding of clear-cut, confirmed, high-grade columnar dysplasia is an indication for resection, because of the high risk of unsuspected, concurrent invasive adenocarcinoma. In other centers, the indication for resection is invasive carcinoma.

RELATIONSHIP BETWEEN BARRETT'S CARCINOMA AND OTHER ADENOCARCINOMAS OCCURRING ABOUT THE CARDIOESOPHAGEAL JUNCTION

Barrett's carcinoma is only one form of adenocarcinoma that occurs close to the cardioesophageal junction. Identical carcinomas occur on the gastric side within the cardiac mucosa; they are called cardiac carcinomas ( Fig. 14-20 and Fig. 14-21 ). 1 ' 1 ' 1 ' To complicate matters, there is a group of carcinomas that span and obliterate the junction, do not have any clear-cut Barrett's mucosa around them, and do not have any dysplasia on either the gastric side or the esophageal side ( Fig. 14-22 ). These carcinomas constitute a group ofjunctional carcinomas of uncertain origin. In our experience, more than 90% of the

Figure 14-20 Cardiac carcinomas such as this one arise immediately below the cardioesophageal junction. This tumor has a central ulcer with nodular, somewhat radiating folds below.

Figure 14-21 This cardiac carcinoma is mainly ulcerating. The large part of the ulcer is below the junction, but there is an extension into the totally squamous-lined distalmost esophagus.

Figure 14-22 This carcinoma crosses the cardioesophageal junction (arrows) and has almost equal components on both sides. It is impossible to tell whether it arose in the cardia or in a Barrett's mucosa.

References

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2. Cameron, A.J., Ott, B.J., and Payne, W.S.: The incidence of adenocarcinoma in columnar-lined (Barrett's) esophagus. N. Engl. J. Med., 313:851, 1985.

3. Cameron, A.J., Zinmeister, A.R., Ballard, D.J., and Carney, J.A.: Prevalence of columnar-lined (Barrett's) esophagus. Gastroenterology, 99:918, 1990.

4. Cameron, A.J., and Lomboy, C.T.: Barrett's esophagus: Age, prevalence, and extent of columnar epithelium. Gastroenterology, 103:1241, 1992.

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7. Geisinger, K.R., Teot, L.A., and Richter, J.E.: A comparative cytopathologic and histologic study of atypia, dysplasia, and adenocarcinoma in Barrett's esophagus. Cancer 69:8, 1992.

8. Gillen, P., Keeling, P., and Hennessy, T.P.J: Barrett's esophagus: Risk factors for malignancy (Abstract). Gut, 28:A1379, 1987.

9. Goldblum, J.R., Vicari, J.J., Falk, G.W., et al.: Inflammation and intestinal metaplasia of the gastric cardia: The role of gastroesophageal reflux and H. pylori. Gastroenterology, 114:633, 1998.

10. Gray, J.R., Coldman, A.J., and MacDonald, W.C.: Cigarette and alcohol use in patients with adenocarcinoma of the gastric cardia or lower esophagus. Cancer, 69:2221, 1992.

11. Haggitt, R.C.: Barrett's esophagus, dysplasia, and adenocarcinoma. Hum. Pathol., 25:982, 1994.

12. Hamilton, S.R., and Smith, R.R.L.: The relationship between columnar epithelial dysplasias and invasive adenocarcinoma arising in Barrett's esophagus. Am. J. Clin. Pathol., 87:301, 1987.

13. Hirota, W.K., Loughney, T.M., Lazas, D.J., et al.: Specialized intestinal metaplasia, dysplasia and cancer of the esophagus and esophagogastric junction: Prevalence and clinical data. Gastroenterology, 116:277, 1999.

14. Iftikhar, S.Y., James, P.D., Steele, R.J.C., et al.: Length of Barrett's oesophagus: An important factor in the development of dysplasia and adenocarcinoma. Gut, 33:1155, 1992.

15. Jabbari, M., Goresky, C.A., Lough, J., et al.: The inlet patch: Heterotopic gastric mucosa in the upper esophagus. Gastroenterology, 89:352, 1985.

16. Jass, J.R.: Mucin histochemistry of the columnar epithelium of the oesophagus: A retrospective study. J. Clin. Pathol., 34:866, 1981.

17. Kalish, R.J., Clancy, P.E., Orringer, M.B., et al.: Clinical epidemiologic and morphologic comparison between adenocarcinomas arising in Barrett's esophageal mucosa and in the gastric cardia. Gastroenterology, 86:461, 1984.

18. Lee, R.G.: Mucins in Barrett's esophagus: A histochemical study. Am. J. Clin. Pathol., 81:500, 1984.

19. Levine, D.S., Haggitt, R.C., Blount, P.L., et al.: An endoscopic biopsy protocol can differentiate high-grade dysplasia from early adenocarcinoma in Barrett's esophagus. Gastroenterology, 105:40, 1993.

20. McArdle, J.E., Lewin, K.J., Randzil, G., and Weinstein, W.: Distribution of dysplasia and early invasive carcinoma in Barrett's esophagus. Hum. Pathol., 23:479, 1992.

21. Naef, A.P., Savary, M., and Ozzello, L.: Columnar-lined lower esophagus: An acquired lesion with malignant predisposition. J. Thorac. Cardiovasc. Surg., 70:826, 1975.

22. Palli, D., Bianchi, S., Decarli, A., et al.: A case-control study of cancers of the gastric cardia in Italy. Br. J. Cancer, 65:263, 1992.

23. Paull, A., Trier, J.S., Dalton, M.D., et al.: The histologic spectrum of Barrett's esophagus. N. Engl. J. Med., 295:416, 1976.

24. Peuchmaur, M., Potet, F., and Goldfain, D.: Mucin histochemistry of the columnar epithelium of the oesophagus (Barrett's oesophagus): A prospective biopsy study. J. Clin. Pathol., 37:607, 1984.

25. Reid, B.J., Haggitt, R.C., Rubin, C.E., et al.: Criteria for dysplasia in Barrett's esophagus: A cooperative consensus study (Abstract). Gastroenterology, 88:1552, 1985.

26. Reid, B.J., and Rubin, C.E.: When is the columnar-lined esophagus premalignant? (Abstract). Gastroenterology, 88:1552, 1985.

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Herbal Remedies For Acid Reflux

Herbal Remedies For Acid Reflux

Gastroesophageal reflux disease is the medical term for what we know as acid reflux. Acid reflux occurs when the stomach releases its liquid back into the esophagus, causing inflammation and damage to the esophageal lining. The regurgitated acid most often consists of a few compoundsbr acid, bile, and pepsin.

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