Objective-To evaluate the demographics and incidence of Barrett's oesophagus diagnosis using community-based data. Design-Observational study.Setting-Kaiser Permanente, Northern California health-care membership, 1994-2006. Patients-Members with an electronic diagnosis of Barrett's oesophagus.Main outcome measures-Incidence and prevalence of a new Barrett's oesophagus diagnosis by race, sex, age and calendar year.Results-4205 persons met the study definition for a diagnosis of Barrett's oesophagus. The annual incidence in 2006 was highest among non-Hispanic whites (39/100 000 race-specific member-years, 95% confidence interval (95% CI) 35 to 43), with lower rates among Hispanics (22/100 000, 95% CI 16 to 29), Asians (16/100 000, 95% CI 11 to 22), and blacks (6/100 000, 95% CI 2 to 12). The annual incidence was higher among men than women (31 vs 17/100 000, respectively, year 2006; p<0.01). The incidence increased with age from 2 per 100 000 for persons aged 21-30 years, to a peak of 31 per 100 000 member-years for persons aged 61-70 years (year 2006). There was no increase in the incidence of new diagnoses until the last two observation years, which coincided with changes in data collection methods and may be due to bias. The overall prevalence among active members increased almost linearly to 131/100 000 member-years by 2006.Conclusions-The demographic distributions of Barrett's oesophagus differ markedly by race, age and sex and were comparable to those for oesophageal adenocarcinoma. Thus, demographic disparities in oesophageal adenocarcinoma risk may arise partly from the risk of having Barrett's oesophagus, rather than from differing risks of progression from Barrett's oesophagus to cancer. There has been an almost linear increase in the prevalence of diagnosed disease. The incidence of oesophageal adenocarcinoma has increased over 500% within the United States during the last three decades, with similar increases noted in other countries. The rates vary substantially by race (more common among Caucasians), gender (more common among men), and geography and are not explained solely by changes in classification. 1-6 The carcinogenic sequence may progress through several steps, from normal to Barrett's oesophagus to oesophageal adenocarcinoma. Barrett's oesophagus is a metaplastic change in the oesophageal lining that effectively identifies persons at markedly increased risk for oesophageal adenocarcinoma. The annual incidence of oesophageal adenocarcinoma among patients with Barrett's oesophagus is approximately 0.5%, a risk approximately 30-to 40-fold greater than that of the general population. 7-10 A key question has thus become whether the increased cancer incidence is primarily from an increase in the prevalence of Barrett's oesophagus, from an increased risk of Barrett's oesophagus progressing to oesophageal adenocarcinoma, or whether other cancer pathways are involved.There is relatively little detailed data on the demographic distribution of Barrett's oesophagus, its temporal changes in incide...

Objective-Gastric colonization with the Helicobacter pylori bacterium is a proposed protective factor against oesophageal adenocarcinoma, but its point of action is unknown. We evaluated its associations with Barrett's oesophagus, a metaplastic change that is a probable early event in the carcinogenesis of oesophageal adenocarcinoma. Design-A case-control studySetting-The Kaiser Permanente Northern California population, a large health services delivery organization Patients-Persons with a new Barrett's oesophagus diagnosis (cases) were matched to subjects with gastrooesophageal reflux disease (GORD) without Barrett's oesophagus and to population controls. Main Measures-Subjects completed direct in-person interviews and antibody testing forHelicobacter pylori and its cagA protein.Results-Serologic data were available on 318 Barrett's oesophagus cases, 312 GORD patients, and 299 population controls. Patients with Barrett's oesophagus were substantially less likely to have antibodies for Helicobacter pylori (odds ratio [OR] = 0.42, 95% confidence interval [CI] 0.26-0.70) than population controls; this inverse association was stronger among those with lower body mass indexes (BMI<25 OR=0.03, 95% CI 0.00 -0.20) and those with cagA+ strains (OR=0.08, 95% CI 0.02-0.35). The associations were diminished after adjustment for GORD symptoms. The H. pylori status was not an independent risk factor for Barrett's oesophagus compared to the GORD controls. Conclusions-Helicobacter pylori infection and cagA+ status were inversely associated with a new diagnosis of Barrett's oesophagus. The findings are consistent with the hypothesis that Helicobacter pylori colonization protects against Barrett's oesophagus and that the association may be at least partially mediated through GORD.

Background & Aims-Little is known about the effects of alcohol use and sociodemographics on the risk of Barrett's esophagus, a precursor to esophageal adenocarcinoma. We evaluated the association between alcohol use, alcohol type, sociodemographic profiles, other lifestyle factors and the risk of Barrett's esophagus.

OBJECTIVE The present study evaluated the associations between antioxidants, fruit and vegetable intakes and the risk of Barrett’s esophagus, a potential precursor to esophageal adenocarcinoma. METHODS We conducted a case-control study within the Kaiser Permanente Northern California population. Incident Barrett’s esophagus cases (n=296) were matched to persons with gastroesophageal reflux disease (GERD) (GERD controls, n=308) and to population controls (n=309). Nutrient intake was measured using a validated 110-item food frequency questionnaire. The antioxidant results were stratified by dietary vs. total intake of antioxidants. RESULTS Comparing cases to population controls, dietary intake of vitamin C and beta-carotene were inversely associated with the risk of Barrett’s esophagus [4th vs. 1st quartile, adjusted odds ratio [OR]=0.48 95% confidence interval [CI] (0.26–0.90); OR=0.56 95%CI(0.32–0.99), respectively], and the inverse association was strongest for vitamin E [OR=0.25 95%CI (0.11–0.59)]. The inverse trends for antioxidant index (total and dietary) and fruit and vegetable intake were statistically significant, while most total intakes were not associated with reduced risk. The use of antioxidant supplements did not influence the risk of Barrett’s esophagus, and antioxidants and fruits and vegetables were inversely associated with a GERD diagnosis. CONCLUSION Dietary antioxidants, fruit and vegetable are inversely associated with the risk of Barrett’s esophagus, while no association was observed for supplement intake. Our results suggest that fruits and vegetables themselves or associated undetected confounders may influence early events in the carcinogenesis of esophageal adenocarcinoma.

Introduction-We examined the association between smoking and the risk of Barrett's esophagus (BE), a metaplastic precursor to esophageal adenocarcinoma.