Summary Of Evidence

Significance

Evidence Of Benefit

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SUMMARY OF EVIDENCE

There is no evidence to establish that screening would result in a decrease in mortality from esophageal cancer in the U.S. population (Level of Evidence: 5). Endoscopy is sometimes used to screen for esophageal cancer. There are serious but uncommon side effects associated with endoscopy, which may include the following: perforation, cardiopulmonary events, and aspiration and bleeding requiring hospitalization.

Level of Evidence:

5: Opinions of respected authorities based on clinical experience, descriptive studies, or reports of expert committees

SIGNIFICANCE

Incidence and Mortality

Two histologic types account for the majority of malignant esophageal neoplasms, i.e., adenocarcinoma and squamous carcinoma. The epidemiology of these types varies markedly. In the 1960s, squamous cell cancers comprised over 90% of all esophageal tumors. The incidence of esophageal adenocarcinomas has risen considerably over the past 2 decades, such that it is now more prevalent than squamous cell cancer in the United States and Western Europe, with most tumors located in the distal esophagus.[2] Although the overall incidence of squamous cell carcinoma of the esophagus is declining, this histologic type remains 6 times more likely to occur in black males than in white males.[1] Incidence rates generally increase with age in all racial/ethnic groups but squamous cell cancer is consistently more common in blacks than in whites. Among black men, the incidence rate for the 55 to 69 year age group is close to that of white men in the 70 and older age group. In black women aged 55 to 69 years, the incidence rate is slightly higher than that of white women in the 70 years and older age group.

Risk Factors

Long-standing GERD predisposes to Barrett's esophagus, the condition in which an abnormal intestinal epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus.[7] The intestinal-type epithelium of Barrett's esophagus has a characteristic endoscopic appearance that differs from squamous epithelium.[8] Dysplasia in Barrett's epithelium represents an alteration of the columnar epithelium that may progress to invasive adenocarcinoma.[9]

An interesting hypothesis relates the rise in incidence of esophageal adenocarcinoma to a declining prevalence of Helicobacter pylori infection in Western countries. Reports have suggested that gastric infection with H. pylori may protect the esophagus from GERD and its complications.[10] According to this theory, H. pylori infections that cause pangastritis also cause a decrease in gastric acid production that protects against GERD.[11] Patients whose duodenal ulcers were treated successfully with antibiotics developed reflux esophagitis twice as often as those in whom infection persisted.[12]

Past use of lower esophageal sphincter (LES)-relaxing drugs was positively associated with risk of esophageal adenocarcinoma. Among daily, long-term users (> 5 years) of LES-relaxing drugs, the estimated incidence rate ratio was 3.8 (95%), (95% CI, 2.2 to 6.4) compared with persons who had never used these drugs. Gastric cardia adenocarcinoma and esophageal squamous cell carcinoma were not associated with use of LES-relaxing drugs.[13]

There exists a strong relationship between body mass index (BMI) and esophageal adenocarcinoma. The adjusted odds ratio was 7.6 (95% CI, 3.8 to 15.2) among persons in the highest BMI quartile compared with persons in the lowest. Obese persons (those with BMI 30kg/m2) had an odds ratio of 16.2 (95% CI, 6.3 to 41.4) compared with the leanest persons (BMI < 22mg/m2). Esophageal squamous cell carcinoma was not associated with BMI.[14]

References:

1. American Cancer Society: Cancer Facts and Figures-2002. Atlanta, Ga: American Cancer Society, 2002.
2. Blot WJ, McLaughlin JK: The changing epidemiology of esophageal cancer. Seminars in Oncology 26(5 suppl 15): 2-8, 1999.
3. Oesophagus. In: World Cancer Research Fund in association with American Institute for Cancer Research: Food, Nutrition and the Prevention of Cancer: a Global Perspective. Washington, DC: American Institute for Cancer Research, 1997, pp 118-129.
4. Lagergren J, Bergstrom R, Lindgren A, et al.: Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. New England Journal of Medicine 340(11): 825-831, 1999.
5. Wijnhoven BP, Tilanus HW, Dinjens WN: Molecular biology of Barrett's adenocarcinoma. Annals of Surgery 233(3): 322-337, 2001.
6. Skacel M, Petras RE, Gramlich TL, et al.: The diagnosis of low-grade dysplasia in Barrett's esophagus and its implications for disease progression. American Journal of Gastroenterology 95(12): 3383-3387, 2000.
7. Spechler SJ, Goyal RK: The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett. Gastroenterology 110(2): 614-621, 1996.
8. Van Dam J, Brugge WR: Endoscopy of the upper gastrointestinal tract. New England Journal of Medicine 341(23): 1738-1748, 1999.
9. Reid BJ, Blount PL, Rubin CE, et al.: Flow-cytometric and histological progression to malignancy in Barrett's esophagus: prospective endoscopic surveillance of a cohort. Gastroenterology 102(4 pt 1): 1212-1219, 1992.
10. O'Connor HJ: Helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management. Alimentary Pharmacology and Therapeutics 13(2): 117-127, 1999.
11. Graham DY, Yamaoka Y: H. pylori and cagA: relationships with gastric cancer, duodenal ulcer, and reflux esophagitis and its complications. Helicobacter 3(3): 145-151, 1998.
12. Labenz J, Blum AL, Bayerdorffer E, et al.: Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 112(5): 1442-1447, 1997.
13. Lagergren J, Bergstrom R, Adami HO, et al.: Association between medications that relax the lower esophageal sphincter and risk for esophageal adenocarcinoma. Annals of Internal Medicine 133(3): 165-175, 2000.
14. Lagergren J, Bergstrom R, Nyren O: Association between body mass and adenocarcinoma of the esophagus and gastric cardia. Annals of Internal Medicine 130(11): 883-890, 1999.

EVIDENCE OF BENEFIT

Squamous Cell Cancer

Efforts at early detection of squamous cell cancer of the esophagus have concentrated on cytological or endoscopic screening of populations in countries where there is a high incidence. Although these programs have demonstrated that it is possible to detect squamous cell cancers in an early asymptomatic stage, no data on efficacy (e.g., mortality reduction) have been published. Esophageal cytological screening studies have been reported from China,[11,12] Iran,[13] South Africa,[14,15] Italy,[16] and Japan.[17] In the United States, such efforts have been focused on individuals perceived to be at higher risk.[18,19] Studies of primary endoscopic screening have been reported from France [20] and Japan.[21]

Comparisons of both Chinese and U.S. cytological diagnosis with concurrent histological findings showed low (14%-36%) sensitivities for the cytological detection of biopsy-proven cancers. Specificity ranged from 90% to 99% with a positive predictive value from 23% to 94%.[22] The development of uniform and accurate cytological criteria will require formal cytological-histological correlation studies of esophageal lesions. Such studies should become more feasible with the increasing availability of endoscopy in high-risk populations.

The efficacy of surveillance cytology or endoscopy for high-risk patients with tylosis or long-standing achalasia is not known.

Adenocarcinoma of the Esophagus

Barrett's esophagus is strongly associated with gastroesophageal reflux disease (GERD), and the changes of Barrett's esophagus can be found in approximately 10% of patients who have GERD. GERD, however, is very common; surveys have found that approximately 20% of adult Americans experience symptoms of GERD, such as heartburn, at least once each week.[26] The likelihood of finding Barrett's esophagus on endoscopy is related to the duration of symptoms of gastroesophageal reflux. In a series of 701 individuals, 4% of those with symptoms for less than 1 year, had Barrett's esophagus on endoscopy, whereas Barrett's esophagus was found in 21% of those with more than 10 years of symptoms of GERD. It has been estimated that physicians identify only approximately 5% of the population who have Barrett's esophagus.[27]

Surveillance of Barrett's esophagus involves the use of tests to identify preneoplastic changes or curable neoplasms in patients who are known to have Barrett's esophagus. Certain factors are essential in the implementation of an effective surveillance protocol, including low risk of the surveillance method, correct histological diagnosis of dysplasia, proof that surgical resection for high-grade dysplasia will decrease the risk of cancer, and successful resection of cancer. The interval between endoscopic evaluations is typically determined by histologic findings, in accordance with published guidelines by gastroenterological committees.[28] GERD should be treated prior to surveillance endoscopy to minimize confusion caused by inflammation in the interpretation of biopsy specimens. The technique of random, 4-quadrant biopsies taken every 2 cm in the columnar-lined esophagus for standard histological evaluation has been recommended by some clinicians. For patients with no dysplasia, surveillance endoscopy at an interval of every 2 to 3 years has been recommended.[28] For patients with low-grade dysplasia, surveillance every 6 months for the first year has been recommended, followed by annual endoscopy if the dysplasia has not progressed in severity. For patients with high-grade dysplasia, 2 options have been recommended: either surgical resection or repeated endoscopic evaluation until the diagnosis of intramucosal carcinoma is made. Although widely adopted in clinical practice, these practices are based on uncontrolled series and the opinion of expert gastrointestinal endoscopists and pathologists.

Other techniques to potentially identify dysplastic epithelium that could then be sampled extensively include chromoendoscopy [29] and laser-induced fluorescence spectroscopy.[30]

References:

1. Bollschweiler E, Schroder W, Holscher AH, et al.: Preoperative risk analysis in patients with adenocarcinoma or squamous cell carcinoma of the oesophagus. British Journal of Surgery 87(8): 1106-1110, 2000.
2. Aggestrup S, Holm JC, Sorensen HR: Does achalasia predispose to cancer of the esophagus? Chest 102(4): 1013-1016, 1992.
3. Abemayor E, Moore DM, Hanson DG: Identification of synchronous esophageal tumors in patients with head and neck cancer. Journal of Surgical Oncology 38(2): 94-96, 1988.
4. Ellis A, Field JK, Field EA, et al.: Tylosis associated with carcinoma of the oesophagus and oral leukoplakia in a large Liverpool family--a review of six generations. European Journal of Cancer. Part B, Oral Oncology 30B(2): 102-112, 1994.
5. Risk JM, Mills HS, Garde J, et al.: The tylosis esophageal cancer (TOC) locus: more than just a familial cancer gene. Diseases of the Esophagus 12(3): 173-176, 1999.
6. Isolauri J, Markkula H: Lye ingestion and carcinoma of the esophagus. Acta Chirurgica Scandinavica 155(4-5): 269-271, 1989.
7. Ferguson A, Kingstone K: Coeliac disease and malignancies. Acta Paediatrica. Supplement 412: 78-81, 1996.
8. Rolon PA, Castellsague X, Benz M, et al.: Hot and cold mate drinking and esophageal cancer in Paraguay. Cancer Epidemiology, Biomarkers and Prevention 4(6): 595-605, 1995.
9. Lagergren J, Wang Z, Bergstrom R, et al.: Human papillomavirus infection and esophageal cancer: a nationwide seroepidemiologic case-control study in Sweden. Journal of the National Cancer Institute 91(2): 156-162, 1999.
10. Sur M, Cooper K: The role of the human papilloma virus in esophageal cancer. Pathology 30(4): 348-354, 1998.
11. Shen Q, Liu SF, Dawsey SM, et al.: Cytologic screening for esophageal cancer: results from 12,877 subjects from a high-risk population in China. International Journal of Cancer 54(2): 185-188, 1993.
12. Dawsey SM, Lewin KJ, Wang GQ, et al.: Squamous esophageal histology and subsequent risk of squamous cell carcinoma of the esophagus. A prospective follow-up study from Linxian, China. Cancer 74(6): 1686-1692, 1994.
13. Dowlatshahi K, Daneshbod A, Mobarhan S: Early detection of cancer of oesophagus along Caspian Littoral. Report of a pilot project. Lancet 1(8056): 125-126, 1978.
14. Jaskiewicz K, Venter FS, Marasas WF: Cytopathology of the esophagus in Transkei. Journal of the National Cancer Institute 79(5): 961-965, 1987.
15. Tim LO, Leiman G, Segal I, et al.: A suction-abrasive cytology tube for the diagnosis of esophageal carcinoma. Cancer 50(4): 782-784, 1982.
16. Aste H, Saccomanno S, Munizzi F: Blind pan-esophageal brush cytology. Diagnostic accuracy. Endoscopy 16(5): 165-167, 1984.
17. Nabeya K: Markers of cancer risk in the esophagus and surveillance of high-risk groups. In: Sherlock P, Morson BC, Barbara L, et al., eds.: Precancerous Lesions of the Gastrointestinal Tract. New York, NY: Raven Press, 1983, pp 71-86.
18. Dowlatshahi K, Skinner DB, DeMeester TR, et al.: Evaluation of brush cytology as an independent technique for detection of esophageal carcinoma. Journal of Thoracic and Cardiovascular Surgery 89(6): 848-851, 1985.
19. Jacob P, Kahrilas PJ, Desai T, et al.: Natural history and significance of esophageal squamous cell dysplasia. Cancer 65(12): 2731-2739, 1990.
20. Meyer V, Burtin P, Bour B, et al.: Endoscopic detection of early esophageal cancer in a high-risk population: does Lugol staining improve videoendoscopy? Gastrointestinal Endoscopy 45(6): 480-484, 1997.
21. Yokoyama A, Ohmori T, Makuuchi H, et al.: Successful screening for early esophageal cancer in alcoholics using endoscopy and mucosa iodine staining. Cancer 76(6): 928-934, 1995.
22. Dawsey SM, Shen Q, Nieberg RK, et al.: Studies of esophageal balloon cytology in Linxian, China. Cancer Epidemiology, Biomarkers and Prevention 6(2): 121-130, 1997.
23. Drewitz DJ, Sampliner RE, Garewal HS: The incidence of adenocarcinoma in Barrett's esophagus: a prospective study of 170 patients followed 4.8 years. American Journal of Gastroenterology 92(2): 212-215, 1997.
24. Shaheen NJ, Crosby MA, Bozymski EM, et al.: Is there publication bias in the reporting of cancer risk in Barrett's esophagus? Gastroenterology 119(2): 333-338, 2000.
25. Spechler SJ: Barrett's esophagus: an overrated cancer risk factor. Gastroenterology 119(2): 587-589, 2000.
26. Locke GR III, Talley NJ, Fett SL, et al.: Prevalence and clinical spectrum of gastroesophageal reflux: a population-based study in Olmsted County, Minnesota. Gastroenterology 112(5): 1448-1456, 1997.
27. Spechler SJ: Barrett's esophagus: should we brush off this ballooning problem? Gastroenterology 112(6): 2138-2142, 1997.
28. DeVault KR, Castell DO, and the Practice Parameters Committee of the American College of Gastroenterology: Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. The Practice Parameters Committee of the American College of Gastroenterology. American Journal of Gastroenterology 94(6): 1434-1442, 1999.
29. Canto MI, Setrakian S, Petras RE, et al.: Methylene blue selectively stains intestinal metaplasia in Barrett's esophagus. Gastrointestinal Endoscopy 44(1): 1-7, 1996.
30. Panjehpour M, Overholt BF, Vo-Dinh T, et al.: Endoscopic fluorescence detection of high-grade dysplasia in Barrett's esophagus. Gastroenterology 111(1): 93-101, 1996.

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