Summary
Barrett esophagus is a precancerous condition in which the stratified squamous epithelium of the distal esophageal mucosa is replaced by nonciliated columnar epithelium and goblet cells (intestinal metaplasia). Gastroesophageal reflux disease (GERD) is the most common cause. Major risk factors include male sex, age > 50 years, obesity, smoking, and a family history of the condition. Barrett esophagus is a precursor lesion to esophageal adenocarcinoma. While Barrett esophagus does not cause symptoms, some individuals may experience symptoms of GERD, such as heartburn or regurgitation. Patients with chronic GERD and three or more additional risk factors for Barrett esophagus should undergo esophagogastroduodenoscopy (EGD) screening. Endoscopic findings include salmon-pink mucosa extending proximal to the gastroesophageal junction (GEJ). The diagnosis is confirmed via biopsy; histopathology shows intestinal metaplasia. Management includes daily proton pump inhibitor therapy for all patients. Periodic endoscopic surveillance is recommended for patients without dysplasia, while those with low-grade or high-grade dysplasia are candidates for endoscopic eradication therapy.
Epidemiology
-
Prevalence
- Up to 12% of individuals with GERD symptoms [1]
- ∼ 5% of the general population [2]
- Sex: ♂ > ♀ [2]
- Age: more common in individuals aged > 50 years [2]
Epidemiological data refers to the US, unless otherwise specified.
Etiology
GERD is the most common cause. [1]
Risk factors for Barrett esophagus [1]
- Chronic GERD symptoms (weekly symptoms for ≥ 5 years)
- Male sex
- Age > 50 years
- White race
- Tobacco smoking
- Obesity
- Family history of Barrett esophagus or a first-degree relative with esophageal adenocarcinoma
Pathophysiology
- Reflux esophagitis → damage to the mucosa of the distal esophagus by stomach acid → replacement of stratified squamous epithelium by nonciliated columnar epithelium and goblet cells (intestinal metaplasia, Barrett metaplasia) [3]
- The physiological transformation zone between squamous and columnar epithelium (Z line) shifts upward (proximal to the GEJ). [4]
Clinical features
- Intestinal metaplasia does not cause symptoms.
- Symptoms of GERD may be present, e.g.: [5]
Barrett esophagus is asymptomatic; any presenting symptoms are due to underlying GERD. [3]
Diagnosis
Approach [1][6]
-
Screen for Barrett esophagus with EGD in patients with both: [1][6]
- Chronic GERD symptoms (weekly for ≥ 5 years)
- ≥ 3 additional risk factors for Barrett esophagus
- Repeat screening for Barrett esophagus is not recommended if the initial screen is negative.
- Repeat the EGD if initial histology is negative despite endoscopic suspicion for Barrett esophagus. [1]
- Characteristic mucosal lesions: Repeat in 1–2 years.
- Severe erosive esophagitis: Repeat after 8–12 weeks of PPI therapy.
EGD [1]
- Findings: salmon-pink mucosal lesions extending proximally from the GEJ into the pale pink esophagus
- Indication for biopsies: characteristic lesions that displace the Z line ≥ 1 cm [1]
Histopathology [1]
- Diagnostic confirmation: intestinal metaplasia (columnar epithelium with goblet cells)
- Severity is characterized by:
Long-segment Barrett esophagus is associated with a higher risk of cancer than short-segment Barrett esophagus. [1]
Management
General principles [1][7]
- All patients: daily PPI therapy
- Patients with confirmed dysplasia: endoscopic eradication therapy followed by surveillance
- Patients without dysplasia or with indefinite histopathology: endoscopic surveillance
Refer patients with confirmed dysplasia to a high-volume center for management. [8]
Endoscopic eradication therapy [1][8]
- Indications
- Preparation: Initiate twice-daily PPI therapy.
- Procedure: resection of all visible mucosal lesions followed by radiofrequency ablation to achieve complete eradication of intestinal metaplasia and dysplasia
While endoscopic eradication is recommended for Barrett esophagus with low-grade dysplasia, endoscopic surveillance is a reasonable alternative.
Antireflux surgery to prevent progression to esophageal adenocarcinoma is not routinely recommended. [1]
Endoscopic surveillance [1][6][7]
Surveillance intervals depend on histology and whether endoscopic eradication was performed.
- No previous endoscopic eradication therapy [1][7]
- Previous endoscopic eradication therapy [1][8]
Barrett esophagus is a precursor lesion to esophageal adenocarcinoma and thus requires close surveillance.