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News

Central adiposity associated with increased risk of esophageal cancer

November's issue of the Clinical Gastroenterology & Hepatology reports that central adiposity is associated with an increased risk of esophageal inflammation, metaplasia, and adenocarcinoma.

News image

Central adiposity has been implicated as a risk factor for Barrett's esophagus and esophageal adenocarcinoma, possibly promoting the progression from inflammation to metaplasia and neoplasia.

Dr Prasad Iver and colleagues from Minnesota, USA performed a systematic review and meta-analysis of studies to evaluate the association between central adiposity and erosive esophagitis, Barrett's esophagus, and esophageal adenocarcinoma.

The team specifically explored body mass index (BMI)–independent and gastroesophageal reflux (GERD)–independent effects of central adiposity on the risk of these outcomes.

The researchers performed a systematic search of multiple databases through 2013.

Studies were included if they reported effect of central adiposity on the risk of erosive esophagitis, Barrett's esophagus, and esophageal adenocarcinoma.

The research team identified 40 relevant articles.

For 98% of scenarios, at least 1 treatment was appropriate
Clinical Gastroenterology & Hepatology

Compared with patients with normal body habitus, patients with central adiposity had a higher risk of erosive esophagitis, and Barrett's esophagus.

The researchers found that association between central adiposity and Barrett's esophagus persisted after adjusting for BMI.

Reflux-independent association of central adiposity and Barrett's esophagus was observed in studies that used GERD patients as controls or adjusted for GERD symptoms.

In 6 studies, the team found that central adiposity was associated with higher risk of esophageal adenocarcinoma, compared with normal body habitus.

Dr Iver's team concludes, "On the basis of a meta-analysis, central adiposity, independent of BMI, is associated with esophageal inflammation, metaplasia, and neoplasia."

"Its effects are mediated by reflux-dependent and reflux-independent mechanisms."

Clin Gastroenterol Hepatol 2013: 11(11): 1399-1412.e7
24 October 2013

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