Significance
Natural History, Incidence, and Mortality
Risk Factors
Natural History, Incidence, and Mortality
Annually, it is estimated that 16,470 Americans will be diagnosed with esophageal
cancer, and 14,280 will die of this malignancy.[1] Of the new cases, it is estimated that 12,970
will occur in men and 3,500 will occur in women.
Two histologic types account for the majority of malignant esophageal
neoplasms: adenocarcinoma and squamous carcinoma. The epidemiology of
these types varies markedly. In the 1960s, squamous cell cancers comprised
more than 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 six times more likely to occur in black males than in
white males.[3] 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 those aged 55 to 69
years is close to that of white men aged 70 years and older. In
black women aged 55 to 69 years, the incidence rate is slightly higher than
white women aged 70 years and older.
Risk Factors
While risk factors for squamous cell carcinoma of the esophagus have been
identified (such as tobacco, alcoholism, malnutrition, and infection with human
papillomavirus),[4] the risk factors associated with esophageal adenocarcinoma
are less defined. The most important epidemiological difference between
squamous cell cancer and adenocarcinoma, however, is the strong association
between gastroesophageal reflux disease (GERD) and adenocarcinoma. The results
of a population-based case-controlled study suggest that symptomatic
gastroesophageal reflux is a risk factor for esophageal adenocarcinoma. The
frequency, severity, and duration of reflux symptoms were positively associated
with increased risk of esophageal adenocarcinoma.[5-7]
Long-standing GERD predisposes to Barrett esophagus, the condition in which
an abnormal intestinal epithelium replaces the stratified squamous epithelium
that normally lines the distal esophagus.[8] The intestinal-type epithelium of
Barrett esophagus has a characteristic endoscopic appearance that differs
from squamous epithelium.[9] Dysplasia in Barrett epithelium represents an
alteration of the columnar epithelium that may progress to invasive
adenocarcinoma.[10]
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.[11]
According to this theory, H. pylori infections that cause pangastritis also
cause a decrease in gastric acid production that protects against GERD.[12]
Patients whose duodenal ulcers were treated successfully with antibiotics
developed reflux esophagitis twice as often as those in whom infection
persisted.[13]
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% confidence interval [CI], 2.2–6.4) 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.[14]
There exists a strong relationship between body mass index (BMI) and esophageal
adenocarcinoma. The adjusted odds ratio (OR) was 7.6 (95% CI, 3.8–15.2) among
persons in the highest BMI quartile compared with persons in the lowest. Obese
persons (those with BMI >30 kg/m2) had an OR of 16.2 (95% CI, 6.3–41.4) compared with the leanest persons (BMI <22 kg/m2). Esophageal squamous
cell carcinoma was not associated with BMI.[15]
References
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American Cancer Society.: Cancer Facts and Figures 2008. Atlanta, Ga: American Cancer Society, 2008. Also available online. Last accessed October 1, 2008.
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Blot WJ, McLaughlin JK: The changing epidemiology of esophageal cancer. Semin Oncol 26 (5 Suppl 15): 2-8, 1999.
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Devesa SS, Blot WJ, Fraumeni JF Jr: Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer 83 (10): 2049-53, 1998.
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Oesophagus. In: World Cancer Research Fund., American Institute for Cancer Research.: Food, Nutrition and the Prevention of Cancer: A Global Perspective. Washington, DC: The Institute, 1997, pp 118-129.
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Lagergren J, Bergström R, Lindgren A, et al.: Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 340 (11): 825-31, 1999.
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Wijnhoven BP, Tilanus HW, Dinjens WN: Molecular biology of Barrett's adenocarcinoma. Ann Surg 233 (3): 322-37, 2001.
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Skacel M, Petras RE, Gramlich TL, et al.: The diagnosis of low-grade dysplasia in Barrett's esophagus and its implications for disease progression. Am J Gastroenterol 95 (12): 3383-7, 2000.
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Spechler SJ, Goyal RK: The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett. Gastroenterology 110 (2): 614-21, 1996.
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Van Dam J, Brugge WR: Endoscopy of the upper gastrointestinal tract. N Engl J Med 341 (23): 1738-48, 1999.
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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): 1212-9, 1992.
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O'Connor HJ: Review article: Helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management. Aliment Pharmacol Ther 13 (2): 117-27, 1999.
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Graham DY, Yamaoka Y: H. pylori and cagA: relationships with gastric cancer, duodenal ulcer, and reflux esophagitis and its complications. Helicobacter 3 (3): 145-51, 1998.
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Labenz J, Blum AL, Bayerdörffer E, et al.: Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 112 (5): 1442-7, 1997.
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Lagergren J, Bergström R, Adami HO, et al.: Association between medications that relax the lower esophageal sphincter and risk for esophageal adenocarcinoma. Ann Intern Med 133 (3): 165-75, 2000.
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Lagergren J, Bergström R, Nyrén O: Association between body mass and adenocarcinoma of the esophagus and gastric cardia. Ann Intern Med 130 (11): 883-90, 1999.
[PUBMED Abstract]
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