Ryan AM et al. (2008) Barrett esophagus: prevalence of central adiposity, metabolic syndrome, and a proinflammetory state. Ann Surg 247: 909–915

Previous studies have shown that obesity increases the risk of esophageal adenocarcinoma. A widely accepted theory suggests that obesity-related reflux causes chronic inflammation and metaplasia, which might progress to adenocarcinoma. To explore the associations between obesity, metabolic syndrome, inflammatory precursors and tumor development, Ryan and colleagues assessed patients with Barrett esophagus (a premalignant condition characterized by specialized intestinal metaplasia in the lower esophagus).

The study included 102 patients with Barrett esophagus (mean age 56 years). Examinations included measurements of serum glucose, total and HDL cholesterol, triglycerides, insulin, C-reactive protein, adipokines, cytokines and growth factor levels after an overnight fast, as well as anthropometric, body composition and blood-pressure measurements.

Metabolic syndrome was diagnosed in 46% of the patients, who had higher BMI, greater waistline, higher blood pressure and higher risk of hyperinsulinemia than patients without metabolic syndrome. Further findings associated with metabolic syndrome included elevated levels of C-reactive protein and leptin and lower levels of adiponectin. Severity of symptoms correlated with the length of specialized intestinal metaplasia; the prevalence of obesity, metabolic syndrome and hyperinsulinemia and the levels of IL-6 were significantly higher in patients with long-segment Barrett esophagus than in patients with short-segment metaplasia.

The authors conclude that obesity, metabolic syndrome, central adiposity and Barrett esophagus are strongly linked. They hypothesize that changes in adipokine and cytokine levels related to the metabolic syndrome might contribute to the progress of metaplasia.