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Barrett's Esophagus

BARRETT'S ESOPHAGUS
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Causes and Risk Factors

Barrett's esophagus develops as a result of abnormal changes (called metaplasia) in the lining of the esophagus. The exact cause for Barrett's esophagus is unknown; however, the condition is thought to be related to chronic acid reflux (also called heartburn or indigestion).

Acid reflux occurs when stomach acid and juices (i.e., enzymes that aid in digestion) back up (reflux) into the esophagus. Over time, severe acid reflux can cause gastroesophageal reflux disease (GERD) and can result in damage to and inflammation of the esophageal lining (i.e., reflux esophagitis). As this inflammation heals, the squamous (flat, scale-like) cells that line the esophagus may undergo abnormal changes, resulting in Barrett's esophagus.

Although GERD is the primary risk factor for Barrett's esophagus, the condition also can develop in people who do not experience frequent heartburn. In approximately 25% of cases, patients who have Barrett's esophagus do not have symptoms of acid reflux.

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Other risk factors for Barrett's esophagus include the following:

  • Age (more common in patients over the age of 60)
  • Cigarette smoking
  • Gender (more common in men)
  • Heredity (there may be a genetic link in some cases)
  • Medical conditions (e.g., diabetes, asthma, Zollinger-Ellison syndrome [characterized by high levels of stomach acid])
  • Medications (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs], antibiotics, antidepressants) and dietary supplements (e.g., iron, potassium, vitamin C)
  • Obesity/overweight
  • Race (more common in Caucasians and Hispanics)

Chemotherapy (using drugs to destroy harmful cells) can increase the risk for Barrett's esophagus. Chemotherapy drugs, which often target rapidly dividing cells, also can damage other cells in the body, including cells in the esophageal lining.


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    Original Date of Publication: 29 Feb 2008
    Reviewed by: Stanley J. Swierzewski, III, M.D.
    Last Reviewed: 22 Feb 2008

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    This page last modified: 28 Feb 2008

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