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BackgroundAbdominal obesity is a risk factor for Barrett's esophagus independent of GERD symptoms, but little is understood about the biological mechanisms between obesity and the carcinogenic pathway of esophageal adenocarcinoma.AimsTo evaluate whether ghrelin and leptin may partially explain the association between obesity and Barrett's esophagus.MethodsWe conducted a case-control study using patients with a new diagnosis of Barrett's esophagus (cases) and two control groups frequency matched to cases for age, gender, and geographic region: (1) patients with gastroesophageal reflux disease (GERD) and (2) a sample of the general population. We generated odds ratios using logistic regressions to evaluate quartiles of serum ghrelin or serum leptin, adjusting for known risk factors for Barrett's esophagus. We evaluated potential interaction variables using cross products and ran stratified analyses to generate stratum-specific odds ratios.ResultsA total of 886 participants were included in the analysis. Higher ghrelin concentrations were associated with an increased risk of Barrett's esophagus, when compared to the population controls, but not the GERD controls. Ghrelin concentrations were not associated with the frequency of GERD symptoms, but ghrelin's relationship with Barrett's esophagus varied significantly with the frequency of GERD symptoms. Leptin concentrations were positively associated with at least weekly GERD symptoms among the population controls and were inversely associated with Barrett's esophagus only among the GERD controls. Adjusting for waist circumference did not change the main associations.ConclusionHigher levels of ghrelin were associated with an increased risk of Barrett's esophagus among the general population. In contrast, leptin was positively associated with frequent GERD symptoms, but inversely associated with the risk of Barrett's esophagus among the GERD controls.

Racial differences among hepatocellular carcinoma survival have been reported, but the etiology behind these disparities remains unclear. Using multi-variable logistic regression analysis, our restrospective cohort study investigated the demographic disparities in survival among localized hepatocellular carcinoma in the United States. From 1998 to 2001, 2,776 cases of localized hepatocellular carcinoma were identified. Significant racial/ethnic disparities in overall survival and utilization of therapies were identified. Compared with non-Hispanic white males, black females were 56% less likely to survive 3 years (OR 0.44; 95% CI 0.21–0.93). Treatment-specific models also demonstrated disparities, e.g., compared with non-Hispanic whites, Asians receiving transplantation were 77% more likely to survive 3 years (OR, 1.77; 95% CI 1.28–2.44). There are significant racial/ethnic disparities in 3-year survival among patients with localized hepatocellular carcinoma. These differences are partially explained by demographic differences in utilization of therapy and in stage-specific survival for each therapy.