Visceral Obesity and the Risk of Barrett’s EsophagusAkiyama T.a · Yoneda M.b · Maeda S.b · Nakajima A.b · Koyama S.a · Inamori M.b
aDepartment of Gastroenterology, Tokyo Metropolitan Hiroo Hospital, Tokyo, and bGastroenterology Division, Yokohama City University School of Medicine, Yokohama, Japan Digestion 2011;83:142–145 (DOI:10.1159/000321810)
It still remains controversial whether simple obesity, as measured by the body mass index (BMI), is an independent risk factor for Barrett’s esophagus (BE). Recent studies have shown abdominal obesity, as defined by the waist circumference (WC) and the waist-to-hip ratio (WHR), to be a risk factor for BE, independent of the BMI, with the association between BMI and BE being no longer observed after adjustment for the WC and WHR. Moreover, visceral obesity, as directly measured by the surface area of the visceral adipose tissue (VAT) on abdominal CT images, has also been reported to have an association with the risk of BE. In addition to the mechanical effects of abdominal obesity, that is, increase of the intra- abdominal pressure by the large amount of adipose tissue, circulating factors secreted from the VAT, such as tumor necrosis factor-α, interleukin-6, leptin, and adiponectin, have also been proposed to be pathogenetically linked to BE and esophageal adenocarcinoma. Obesity is associated with the risk of BE, and this risk appeared to be mediated for the most part by abdominal obesity, especially visceral obesity. This raises several questions regarding the pathogenesis of obesity-related BE. Larger studies with prospective enrollment of patients are required for further examination of this issue.
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