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Asbjørn Mohr Drewes

Barrett's esophagus: prevalence-incidence and etiology-origins

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisKonferenceartikelForskningpeer review

  • Gary W Falk
  • ,
  • Brian C Jacobson
  • ,
  • Robert H Riddell
  • ,
  • Joel H Rubenstein
  • ,
  • Hala El-Zimaity
  • ,
  • Asbjørn Mohr Drewes
  • Katie S Roark
  • ,
  • Stephen J Sontag
  • ,
  • Thomas G Schnell
  • ,
  • Jack Leya
  • ,
  • Gregorio Chejfec
  • ,
  • Joel E Richter
  • ,
  • Gareth Jenkins
  • ,
  • Aaron Goldman
  • ,
  • Katerina Dvorak
  • ,
  • Gerardo Nardone
Although the prevalence of Barrett's esophagus (BE) is rising no data exist for racial minorities on prevalence in the general population. Minorities have a lower prevalence than Caucasians, and yet age, smoking, abdominal obesity, and Helicobacter pylori are all risk factors. Metabolic changes induced by adipocytokines and the apparently strong association between obesity, central adiposity, and BE may lead to reconsideration of some aspects of the natural history of BE. There is lack of experimental evidence on acid sensitivity and BE, which is hyposensitive compared to esophageal reflux disease. Reactive nitrogen and oxygen species lead to impaired expression of tumor suppressor genes, which can lead to cancer development; thus, antioxidants may be protective. Gastroesophageal reflux disease may be considered an immune-mediated disease starting at the submucosal layer; the cytokine profile of the mucosal immune response may explain the different outcome of gastroesophageal reflux.
OriginalsprogEngelsk
TidsskriftNew York Academy of Sciences. Annals
Vol/bind1232
Nummer1
Sider (fra-til)1-17
Antal sider17
ISSN0077-8923
DOI
StatusUdgivet - 1 sep. 2011

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