Trends in esophageal adenocarcinoma incidence and mortality.

BACKGROUND: Over the past several decades, the incidence of esophageal adenocarcinoma (EAC) has rapidly increased. The purpose of this analysis was to examine temporal trends in EAC incidence and mortality within the US population and, in addition, to explore these trends within subgroups of the population. METHODS: The National Cancer Institute (NCI) Surveillance, Epidemiology and End Results (SEER 9) data were used to examine incidence and incidence-based (IB) mortality in EAC from 1975 to 2009. Secular trends in incidence and IB mortality by cancer stage, sex, and race were further characterized using the NCI's Joinpoint Regression program. RESULTS: Based on SEER 9 data, EAC incidence and IB mortality continues to increase in the United States. However, since the mid-1990s, the overall rate of increase in both EAC incidence and IB mortality appears to be slowing. In addition, in early-stage cancers, there is a noticeable leveling off of IB mortality rates and divergence from incidence starting in the late 1990s. Over the study period, the average annual percentage increase in incidence was 6.1% in men and 5.9% in women. CONCLUSIONS: EAC incidence and IB mortality rates continue to rise in the United States, although at a slower rate in more recent years. In early-stage cancers, IB mortality and incidence rates have diverged primarily because IB mortality rates have plateaued beginning in the late 1990s. Although EAC continues to be less common in women, the rate of increase in EAC incidence is similar in both sexes.

Aspirin protects against Barrett's esophagus in a multivariate logistic regression analysis.

BACKGROUND & AIMS: Better criteria are needed to identify patients who should be screened for Barrett's esophagus (BE) to reduce overtesting and improve the cost effectiveness. There is evidence that chemopreventive agents such as nonsteroidal anti-inflammatory drugs, particularly aspirin, reduce the risk of esophageal adenocarcinoma (EAC), but little is known about their effects on BE. We analyzed characteristics of patients with BE for factors that might be used in screening and management. METHODS: In this case-controlled study, we identified 434 patients with BE diagnosed at the first endoscopy (incident cases) at a single institution (1997-2010). BE cases were matched with controls on the basis of indication for endoscopy, year of endoscopy, and endoscopist. Risk factors analyzed included age, sex, body mass index, medical and social history, and medications. We performed a multivariate logistic regression analysis to identify clinical risk factors for BE. RESULTS: In a multivariate regression model, men had a greater risk for developing BE (odds ratio, 3.2; 95% confidence interval, 2.3-4.4), whereas current aspirin users had a lower risk than nonusers (odds ratio, 0.56; 95% confidence interval, 0.39-0.80). A subset analysis, limited to patients who had endoscopies for symptoms of gastroesophageal reflux disease, yielded similar findings. No interactions were found between aspirin use and smoking or use of acid-suppressive medications. CONCLUSIONS: In a case-controlled study of 434 patients with BE, current aspirin use appeared to reduce the risk of BE; previous studies associated aspirin use with a reduced risk of EAC. Although efforts were made to minimize biases in our analysis, the possibility of residual confounding remains.

The impact of obesity on the rise in esophageal adenocarcinoma incidence: estimates from a disease simulation model.

BACKGROUND: The United States has experienced an alarming and unexplained increase in the incidence of esophageal adenocarcinoma (EAC) since the 1970s. A concurrent increase in obesity has led some to suggest a relationship between the two trends. We explore the extent of this relationship. METHODS: Using a previously validated disease simulation model of white males in the United States, we estimated EAC incidence 1973 to 2005 given constant obesity prevalence and low population progression rates consistent with the early 1970s. Introducing only the observed, rising obesity prevalence, we calculated the incremental incidence caused by obesity. We compared these with EAC incidence data from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) registry to determine obesity's contribution to the rise therein. Incidences were converted to absolute numbers of cases using U.S. population data. RESULTS: Using constant obesity prevalence, we projected a total of 30,555 EAC cases cumulatively over 1973 to 2005 and 1,151 in 2005 alone. Incorporating the observed obesity trend resulted in 35,767 cumulative EACs and 1,608 in 2005. Estimates derived from SEER data showed 111,223 cumulative and 7,173 cases in 2005. We conclude that the rise in obesity accounted for 6.5% of the increase in EAC cases that occurred from 1973 to 2005 and 7.6% in the year 2005. CONCLUSION: Using published OR for EAC among obese individuals, we found that only a small percentage of the rise in EAC incidence is attributable to secular trends in obesity. IMPACT: Other factors, alone and in combination, should be explored as causes of the EAC epidemic.