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    Lack of differential pattern in central adiposity and metabolic syndrome in Barrett's esophagus and gastroesophageal reflux disease.

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    Authors
    Healy, L A
    Ryan, A M
    Pidgeon, G
    Ravi, N
    Reynolds, J V
    Affiliation
    Department of Clinical Surgery, St. James' Hospital and Trinity College, Dublin, , Ireland.
    Issue Date
    2012-02-01T10:45:48Z
    MeSH
    Adenocarcinoma/etiology
    Barrett Esophagus/*complications/pathology
    Esophageal Neoplasms/etiology
    Female
    Gastroesophageal Reflux/*complications/pathology
    Humans
    Male
    Metabolic Syndrome X/*complications/pathology
    Metaplasia/etiology
    Middle Aged
    Obesity, Abdominal/*complications/metabolism/pathology
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    Citation
    Dis Esophagus. 2010 Jul;23(5):386-91. Epub 2010 Mar 26.
    Journal
    Diseases of the esophagus : official journal of the International Society for, Diseases of the Esophagus / I.S.D.E
    URI
    http://hdl.handle.net/10147/207826
    DOI
    10.1111/j.1442-2050.2010.01052.x
    PubMed ID
    20353443
    Abstract
    Obesity is an established risk factor for esophageal adenocarcinoma, although the mechanism is unclear. A pathway from reflux to inflammation through metaplasia is the dominant hypothesis, and an added role relating to visceral adiposity and the metabolic syndrome has been mooted in Barrett's esophagus (BE) patients. Whether BE differs from gastroesophageal reflux disease (GERD) in obesity and metabolic syndrome profiles is unclear, and this was the focus of this study. Patients with proven BE or GERD were randomly selected from the unit data registry and invited to attend for metabolic syndrome screening, anthropometry studies including segmental body composition analysis, and laboratory tests including fasting lipids, insulin, and C-reactive protein. Metabolic syndrome was defined using the National Cholesterol Education Program (NCEP) and the International Diabetes Federation (IDF) criteria. One hundred and eighteen BE patients and 113 age- and sex-matched GERD controls were studied. The incidence of obesity (body mass index >30 kg/m(2)) was 36% and 38%, respectively, with the pattern of fat deposition predominantly central and an estimated trunk fat mass of 13 and 14 kg, respectively. Using the NCEP criteria, metabolic syndrome was significantly more common in the BE cohort (30% vs 20%, P < 0.05), but there was no significant difference using IDF criteria (42% vs 37%, P= 0.340). Central obesity and the metabolic syndrome are common in both Barrett's and GERD cohorts, but not significantly different, suggesting that central obesity and the metabolic syndrome does not per se impact on the development of BE in a reflux population. In BE, the importance of obesity and the metabolic syndrome in disease progression merits further study.
    Language
    eng
    ISSN
    1442-2050 (Electronic)
    1120-8694 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1111/j.1442-2050.2010.01052.x
    Scopus Count
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    St. James's Hospital

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