Epidemiology of Barrett's Esophagus and Esophageal Adenocarcinoma

Abstract

Barrett's esophagus (BE) is the precursor to esophageal adenocarcinoma (EAC), a disease with increasing burden in the Western world, especially in white men. Risk factors for BE include obesity, tobacco smoking, and gastroesophageal reflux disease (GERD). EAC is the most common form of esophageal cancer in the United States. Risk factors include GERD, tobacco smoking, and obesity, whereas nonsteroidal antiinflammatory drugs and statins may be protective. Factors predicting progression from nondysplastic BE to EAC include dysplastic changes on esophageal histology and length of the involved BE segment. Biomarkers have shown promise, but none are approved for clinical use.

Keywords: Barrett’s esophagus; Epithelium; Esophageal adenocarcinoma; Gastroesophageal reflux disease.

Figure 1

Forrest plots summarizing the association between smoking and the risk of BE, using population controls. Smoking exposure is grouped by categories. Large unfilled diamonds represent the pooled estimates across all studies within that category. The width of the diamonds represents the 95% CIs. Black squares indicate the point estimate for each individual study. KPNC, Kaiser Permanente Northern California; UNC, University of North Carolina. Adapted from Cook et al, “Cigarette Smoking Increases Risk of Barrett’s Esophagus: An Analysis of the Barrett’s and Esophageal Adenocarcinoma Consortium.” Gastroenterol 142 (2012): 744–753; with permission.

Figure 2

Incidence and Incidence-based mortality from esophageal adenocarcinoma, 1975 – 2009. Produced from SEER 9 data. From Hur et al “Trends in Esophageal Adenocarcinoma Incidence and Mortality,” Cancer 119(6): 1149-58; with permission.

Figure 3

Incidence and incidence-based mortality by stage, for (A) Local, (B) Regional, and (C) Distant spread of disease. Produced from SEER 9 data. From Hur et al “Trends in Esophageal Adenocarcinoma Incidence and Mortality,” Cancer 119 (6): 1149-58; with permission.

Figure 4

Predicted incidence rates of EAC through 2030 for all males. Figure depicts yearly SEER data (black line) overlying simulation models from Massachusetts General Hospital (MGH) and the Fred Hutchinson Cancer Research Center (FHCRH), as well as the University of Washington and the Microsimulation Screening Analysis model (UW-MISCAN). From Kong et al, “Exploring the recent trend in esophageal adenocarcinoma incidence and mortality using comparative simulation modeling.” Cancer Epidemiol Biomarkers 23 (2014): 997-1006; with permission.

Figure 5

Restricted cubic regression splines depicting the relationship between body mass index and adenocarcinomas of the esophagus and esophageal junction. From Hoyo et al, “Body mass index in relation to oesophageal and oesophagogastric junction adenocarcinomas: a pooled analysis from the international BEACON consortium.” Int J. Epidemiol 41 (2012): 1706-1718; with permission.