Barrett Esophagus

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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
  • Male gender
  • White ethnicity—incidence in white males is much higher than white women and African American men
  • Smoking history
  • Intra-abdominal obesity
  • Family history—at least one first-degree relative with BE or EAC

General Prevention

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 (1)[C].

Commonly Associated Conditions

GERD, obesity, hiatal hernia

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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
  • Male gender
  • White ethnicity—incidence in white males is much higher than white women and African American men
  • Smoking history
  • Intra-abdominal obesity
  • Family history—at least one first-degree relative with BE or EAC

General Prevention

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 (1)[C].

Commonly Associated Conditions

GERD, obesity, hiatal hernia

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