Barrett's Oesophagitis

Synonyms: Barrett's Oesophagitis, Barrett's Columnar Lined Oesophagus

Barrett's oesophagus is an acquired condition in which any portion of the normal squamous lining has been replaced by a metaplastic columnar epithelium which is visible macroscopically.

• It is often subdivided into short segment (less than 3cm) or long segment (more than 3cm).¹
• A segment of columnar metaplasia of any length must be visible endoscopically above the oesophago-gastric junction and confirmed or corroborated histologically.²
• Barrett's oesophagus results from chronic gastro-oesophageal reflux. The metaplastic columnar epithelium is at risk of increasing grades of dysplasia leading to invasive adenocarcinoma of the oesophagus.³

• Barrett's oesophagus is found in about 1% of the older adult population and in 3% to 5% of persons with gastro-oesophageal reflux disease.⁴
• It is more common in men and much more common in caucasians (rare in people of African ancestry). The prevalence increases with age.
• Most cases remain undiagnosed and the prevalence may be much higher than appreciated.
• The development of metaplasia to columnar epithelium does not correlate accurately with the degree of oesophageal acid reflux and other genetic and environmental factors are clearly involved. Both non-steroidal anti-inflammatory drugs (by non-selectively blocking COX receptors⁵) and Helicobacter pylori⁶ appear to be protective and associated with a lower risk of developing oesophageal adenocarcinoma.

Risk factors

• Patients with chronic gastro-oesophageal reflux disease are at increased risk of developing the changes of Barrett's oesophagus. The risk increases with longer duration and increased frequency of gastro-oesophageal symptoms.⁷
• Hiatus hernia is a risk factor and the size of the hernia is correlated with the length of Barrett's oesophagus.⁸
• Some studies indicate a higher prevalence of obesity, smoking and alcohol intake.⁸ Risk factors for progression to adenocarcinoma include male gender, age over 45 years, extended segment (>8cm) disease, duration of reflux history, early age of onset of GORD, duodeno-gastrooesophageal reflux, mucosal damage (ulceration and stricture) and family history.²

• Some patients may not have any symptoms. Symptoms of gastro-oesophageal reflux and strictures are less common in the affected oesophageal segment.
• The classic history is a middle-aged white man with a long history of gastro-oesophageal reflux and, occasionally, dysphagia.¹

• Histological corroboration of endoscopically visible columnarisation is the most accurate method of diagnosis.² In cases of erosive oesophagitis, it is important to first treat the oesophagitis to ensure there is no Barrett's mucosa underneath the inflammation.
• When high-grade dysplasia or cancer is found on surveillance endoscopy, endoscopic ultrasound is advisable to evaluate for surgical resectability.¹
• A patient with a columnar-lined distal oesophagus without confirmed intestinal metaplasia on biopsy must be followed up with further endoscopies and biopsies.

• The role of surveillance endoscopy is controversial.² Oesophageal cancers arising in Barrett's detected by surveillance are often early and have an excellent prognosis. There are a few studies that suggest that, among those patients who develop oesophageal adenocarcinoma, survival is higher in those who had been undergoing endoscopic surveillance.⁹ It is recommended that when surveillance is considered appropriate, it should be performed every 2 years.²
• Low-grade dysplasia should be managed by extensive re-biopsy after intensive acid suppression for 8-12 weeks. If persisting, surveillance should be six monthly for as long as it remains stable. If apparent regression occurs on two consequent examinations, surveillance internals may be increased to 2-3 yearly.²
• High-grade dysplasia is associated with a focus of invasive adenocarcinoma in 30-40% of patients. Photodynamic therapy appears to be effective in downgrading the dysplasia when used for high-grade dysplasia. However, its efficacy in preventing the progression of Barrett's oesophagus to invasive cancer is not clear.¹⁰
• If high-grade dysplasia persists after intensive acid suppression, oesophagectomy in a specialised unit is currently recommended in patients considered fit for surgery. In those unfit for surgery, endoscopic ablation or mucosal resection should be considered.²

Non-drug

The recommended lifestyle advice is the same as that recommended for patients with gastro-oesophageal reflux disease.

• Reduce weight.
• Stop smoking.
• Reduce alcohol intake.
• Raise the head of the bed at night.
• Take small, regular meals
• Avoid hot drinks, alcohol, and eating within 3 hours of going to bed.
• Avoid drugs that affect oesophageal motility (nitrates, anti-cholinergics, tricyclic antidepressants) or damage the mucosa (NSAIDs, potassium salts, alendronate).

Drug

• Available data indicate that long-term PPI therapy is effective. Twice daily PPI therapy may be recommended for patients who do not respond clinically to once daily therapy. There are no studies that provide evidence that higher doses of PPI therapy provides any increased benefit for prevention of oesophageal adenocarcinoma.¹
• Recent review of data indicates that chemoprevention may be the most promising approach for reduction of adenocarcinoma risk. Studies have shown a protective association between NSAIDs and oesophageal cancer.¹¹
• Ablative therapy The goal of ablative therapy is to destroy the Barrett epithelium to a sufficient depth to eliminate the intestinal metaplasia and allow regrowth of squamous epithelium.¹² A number of modalities have been tried, e.g. photodynamic therapy, argon plasma coagulation, multipolar electrocoagulation and various forms of lasers. There is no direct evidence to suggest that there is a reduction in cancer risk in patients after mucosal ablation therapy. Long term outcomes have been disappointing in terms of relapse after treatment, but this form of treatment is still considered to offer the prospect of developing improved intervention for the future.¹³

Surgical

• Anti-reflux surgeries, e.g. Nissen fundoplication, have not been shown to prevent the progression of Barrett's oesophagus to oesophageal cancer.¹
• However oesophagectomy is often recommended when severe dysplasia is confirmed.¹⁴

• The most significant complication is the development of adenocarcinoma in the oesophagus. Recent data suggest that the risk of dysplasia is strongly associated with increasing age of the patient and the segment length of Barrett's oesophagus.¹⁵
• Although Barrett's oesophagus is the only known precursor to oesophageal adenocarcinoma, most patients with Barrett's oesophagus do not develop cancer.¹⁶
• Barrett's oesophagus has a 2-25% risk of mild-severe dysplasia and a 2-5% risk of developing adenocarcinoma. 40-50% of those patients with Barrett's oesophagus and severe dysplasia go on to develop oesophageal adenocarcinoma within 5 years.¹³

• Barrett's is a premalignant condition and increases the risk of oesophageal adenocarcinoma to 30-60 times that of the general population.¹⁷
• Most patients will not develop oesophageal cancer and will die of other causes.
• In a cohort study of patients with Barrett's oesophagus but not undergoing surveillance, only 2.5% of 155 patients died as a result of oesophageal cancer, with a mean of 9 years follow-up.¹

• Chronic heartburn is a risk factor for oesophageal adenocarcinoma and the risk increases with increasing severity and duration of heartburn. However, the absolute risk in individual patients is less than 1 in 1000 per annum and there is no evidence that endoscopic screening of heartburn patients to detect cancer is worthwhile.²
• However, in view of the increasing incidence of oesophageal adenocarcinoma, the poor results of treatment for established adenocarcinoma and the likely development of better diagnostic tools in the future, screening may be considered worthwhile in the future.¹⁸