Natural History, Incidence, and Mortality
In 2013, it is estimated that 17,990 Americans will be diagnosed with esophageal cancer, and 15,210 will die of this malignancy. Of the new cases, it is estimated that 14,440 will occur in men and 3,550 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 for 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. 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. 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), 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. The intestinal-type epithelium of Barrett esophagus has a characteristic endoscopic appearance that differs from squamous epithelium. Dysplasia in Barrett epithelium represents an alteration of the columnar epithelium that may progress to invasive adenocarcinoma.
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. According to this theory, H. pylori infections that cause pangastritis also cause a decrease in gastric acid production that protects against GERD. Patients whose duodenal ulcers were treated successfully with antibiotics developed reflux esophagitis twice as often as those in whom infection persisted.
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.
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.References
- American Cancer Society.: Cancer Facts and Figures 2013. Atlanta, Ga: American Cancer Society, 2013. Available online. Last accessed October 24, 2013.
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