- Metaplasia of the distal esophageal mucosa from native stratified squamous epithelium to abnormal columnar (intestinalized) epithelium; likely a consequence of chronic GERD
- Predisposes to the development of adenocarcinoma of the esophagus
- Predominant age is >50 years, more common in men; estimated to be present in 1–2% of adult population
- Very rare in pediatric population
- 10–15% of patients undergoing endoscopy for evaluation of reflux symptoms
- Incidence of esophageal adenocarcinoma (EAC) is rising in the United States (1); since 1970s
- Attributed to changes in smoking and obesity rather than reclassification or overdiagnosis
- Annual incidence of adenocarcinoma in all Barrett patients estimated at 0.5% per year
Potentially as many 1.5 to 2 million U.S. adults
Etiology and Pathophysiology
- Chronic gastric reflux injures the esophageal mucosa, triggering columnar metaplasia. Refluxed bile acids likely induce differentiation in gastroesophageal junction (GEJ) cells.
- Columnar cells in the esophagus have higher malignant potential than squamous cells. Activation of CDX2 gene and overexpression of HER2/neu (ERBB2) oncogene promotes carcinogenesis.
- Elevated levels of COX-2 are associated with Barrett esophagus (BE).
- Classic progression: normal epithelium → esophagitis/reflux exposure → metaplasia (BE) → dysplasia (low → high-grade) → adenocarcinoma
Familial predisposition to GERD and BE with multiple genetic markers have been identified.
- Chronic reflux (>5 years); hiatal hernia
- Age >50 years; male gender
- Incidence in white males is much higher than white women and black men.
- Smoking history; intra-abdominal obesity
- Family history—at least one first-degree relative with BE or EAC
Weight loss, smoking cessation, robust intake of fruits and vegetables, and moderate wine consumption may decrease risk of BE and lower progression to esophageal cancer.
Commonly Associated Conditions
GERD, obesity, hiatal hernia
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