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Barrett Esophagus

Basics

  • Metaplasia of distal esophageal mucosa from squamous to intestinalized columnar epithelium
  • Result of chronic GERD, with bile acids triggering metaplasia at gastroesophageal junction
  • Predisposes to esophageal adenocarcinoma (EAC)

Epidemiology

  • Predominant age >50 years; male > female
  • Present in 1-2% of adult population
  • Rare in pediatrics
  • Found in 10-15% undergoing endoscopy for reflux symptoms
  • Annual adenocarcinoma incidence in BE patients ~0.5%

Etiology and Pathophysiology

  • Chronic acid and bile reflux injure squamous epithelium → columnar metaplasia
  • Activation of CDX2 gene and HER2/neu oncogene promotes carcinogenesis
  • Elevated COX-2 associated with Barrett esophagus
  • Typical progression: normal → esophagitis → metaplasia (BE) → dysplasia → adenocarcinoma
  • Genetic predisposition exists with multiple identified markers

Risk Factors

  • Chronic GERD >5 years
  • Hiatal hernia
  • Age >50, male gender (higher in white males)
  • Smoking, intra-abdominal obesity
  • Family history of BE or esophageal adenocarcinoma

Diagnosis

History

  • Assess for GERD symptoms: heartburn, regurgitation
  • Atypical symptoms: chest pain, odynophagia, chronic cough, globus sensation
  • Alarm symptoms: weight loss, anorexia, dysphagia, hematemesis, melena
  • Up to 50% of BE patients may lack GERD symptoms

Physical Exam

  • No specific physical findings; similar to GERD

Diagnostic Tests

  • Endoscopy with multiple biopsies demonstrating intestinal metaplasia ≥1 cm proximal to gastroesophageal junction (GEJ)
  • Use Seattle protocol: four-quadrant biopsies at intervals plus biopsies of mucosal irregularities
  • Chromoendoscopy recommended to enhance detection
  • Capsule endoscopy less sensitive
  • Swallowable sponge devices with biomarkers are emerging screening tools
  • Dysplasia diagnosis requires confirmation by two GI pathologists

Treatment

Medical Therapy

  • Control GERD symptoms with daily proton pump inhibitors (PPI), lifelong therapy recommended
  • PPI dose titrated to symptom control; routine pH monitoring not recommended
  • Acid suppression may reduce progression risk but does not induce regression
  • Aspirin plus high-dose PPI may reduce progression risk (not routine)
  • Statins and COX-2 inhibitors under investigation for chemoprevention

Endoscopic Therapy

  • Low-grade dysplasia: endoscopic eradication (radiofrequency ablation or cryotherapy) or surveillance
  • High-grade dysplasia or intramucosal carcinoma: endoscopic mucosal resection ± ablation
  • Advanced carcinoma: referral to oncology and surgery for resection

Surgery

  • Esophagectomy reserved for invasive carcinoma or failed endoscopic therapy
  • Antireflux surgery does not reduce cancer risk

Surveillance

  • No dysplasia: endoscopy every 3-5 years
  • Low-grade dysplasia without ablation: every 6-12 months
  • Low-grade dysplasia after ablation: 1 year then every 2 years
  • High-grade dysplasia without ablation: every 3 months
  • After ablation: 3, 6, 12 months then annually
  • Discontinue surveillance if life expectancy ≤5 years

Diet and Lifestyle

  • Avoid reflux triggers: caffeine, alcohol, chocolate, peppermint, carbonated drinks, garlic, onions, spicy/fatty foods, citrus, tomato products
  • Smoking cessation, weight loss
  • Elevate head of bed, avoid supine position post meals, avoid tight clothing

Prognosis

  • Annual cancer risk: 0.12-0.6% overall
  • Low-grade dysplasia cancer risk ~0.7-0.8% per year
  • High-grade dysplasia cancer risk 5-9% per year
  • Surveillance and treatment adherence improve early detection

Complications

  • Same as GERD: strictures, bleeding, ulceration

Clinical Pearls

  • Highest BE incidence in white males >50 years old
  • BE is asymptomatic; surveillance guided by biopsy findings
  • Endoscopic eradication successful in >90% but may require multiple treatments
  • Esophagectomy reserved for invasive or refractory cases