Page 2 - 03- Barrett Esophagus

BARRETT ESOPHAGUS
Daniel J. Stein, MD, MPH

BASICS

DESCRIPTION
Metaplasia of the distal esophageal mucosa from native stratified squamous epithelium to
abnormal columnar (intestinalized) epithelium; likely a consequence of chronic
gastroesophageal reflux disease (GERD)
Predisposes to the development of adenocarcinoma of the esophagus
EPIDEMIOLOGY
Predominant age >50 years, more common in men
Estimated to be present in 1–2% of adult population
Very rare in pediatric population
Incidence
10–15% of patients undergoing endoscopy for evaluation of reflux symptoms
Incidence of esophageal adenocarcinoma (EAC) is rising in the United States (1); 6-fold
increase (to 2.5 cases per 100,000) since 1970s
Annual incidence of adenocarcinoma in all Barrett patients estimated at 0.5% per year
Attributed to changes in smoking and obesity rather than reclassification or overdiagnosis

Prevalence
Difficult to ascertain, may be as many as 1.5 to 2 million adults in the U.S. (extrapolated from a
1.6% prevalence in Swedish general population)
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, a mediator of inflammation and regulator of epithelial cell growth,
are associated with Barrett esophagus (BE) (1).
Classic progression: normal epithelium → esophagitis/reflux exposure → metaplasia (BE) →
dysplasia (low or high grade) → adenocarcinoma

Genetics
Familial predisposition to GERD and BE with multiple genetic markers have been identified.
Acquired genetic changes lead to adenocarcinoma and are being investigated as biomarkers for
risk stratification and early detection.

RISK FACTORS
Chronic reflux (>5 years)
Hiatal hernia
Age >50 years