Barrett’s Oesophagus

Link to teaching module

Discuss Barrett’s oesophagus?

  • Norman Barrett (1903–1979) described the condition in 1957. He was an Australian born British thoracic surgeon.
  • Mean incidence of approx 1.17% with 30 new cases per 250000 population. Prevalence is variably reported but as high as 25% in asymptomatic patients over 50.
  • Barrett’s oesophagus” (more appropriately referred to as columnar-lined oesophagus [CLO]) is an oesophagus in which any portion of the normal squamous lining has been replaced by a metaplastic columnar epithelium which is visible macroscopically.
  • The length of Barrett’s oesophagus has been defined as the distance between the transition from oesophageal mucosa to gastric mucosa (Z-line) and the upper end of the gastric folds.
  • Barrett’s can be divided into long and short (<3cm) segments. Ultra short refers to macroscopically normal oesophagus but with the presence of intestinal metaplasia on biopsy, now termed intestinal metaplasia of the cardia.
  • The average age at diagnosis is between 60 – 68 years. 65% of patients are male.
  • Some degree of dysplasia is found at diagnosis in 10-18% and in a further 12% at 3-5 years. 57% of patients with high grade dysplasia will develop malignancy shortly after diagnosis. The risk of progression from Barrett’s to malignancy is approx 0.5-1% per patient per year.
  • Important clinical risk factors for progression to adenocarcinoma include male gender, age >45, “extended segment (>8cm) disease, duration of reflux history, early age of onset of GORD, duodeno-gastro-oesophageal reflux, mucosal damage (ulceration and stricture) and uncommonly, family history.

Discuss the evidence for surveillance in Barrett’s oesophagus?
Evidence for surveillance

  • Of patients with Barrett’s, approximately 1% per year develops adenocarcinoma, which is 30 – 125 times the rate of the general population.
  • It is usually asymptomatic until locally advanced and has a poor prognosis unless detected early.
  • Several retrospective studies have suggested that the cancers picked up through surveillance are at an earlier stage than those that present with symptoms, and that the survival of patients under surveillance is improved (2-4)

Evidence against surveillance

  • No evidence to suggest that screening whole population is effective. Even with screening of high risk groups only, 2000 people would need to be screened to detect one adenocarcinoma (5)
  • Previous retrospective studies looking at mortality rates are subject to ‘lead-time bias’ – that is, the apparently longer survival may just represent identification of more patients at an earlier point in the natural history of the disease rather than a real survival advantage.
  • Most patients will die from causes other than adenocarcinoma (6)

Discuss the cost effectiveness of surveillance for Barrett’s oesophagus?
Several studies have suggested that it is not cost effective and may do more harm than good (7, 8).

Discuss the British Society of Gastroenterology recommendations for surveillance?

  • Endoscopic screening of patients with chronic heartburn to detect CLO is not recommended.
  • The benefits and risks of surveillance should be discussed with patients in whom CLO is newly diagnosed.
  • Benefits- detecting early stage tumours and improving cancer survival, however efficacy is unproven. Clinicians should make it clear that for most patients the actual risk of death from oesophageal cancer is small.
  • Disadvantages of endoscopic surveillance-physical and psychological morbidity, and the fact that surveillance cannot guarantee to detect every tumour that may develop.
  • When surveillance is considered appropriate, it should be performed every 2 years.
  • A Markov model based on UK NHS costing estimate the cost of two yearly surveillance at £19,000 per life year saved.  At present there is insufficient evidence to either promote or reject surveillance programmes in CLO on economic grounds alone.
  • In surveillance endoscopy, quadrantic biopsies should be taken every 2cm in the columnar segment together with biopsies of any visible lesion.
  • The length of the CLO segment has been linked to an increased risk of developing dysplasia or carcinoma development but the relationship seems weak. Consequently, modifying clinical management according to CLO segment length is not warranted at present.
  • There is no upper age limit for stopping surveillance. This should be discussed with patient with regard to co-morbid factors, fitness for oesophageal resection. However, the goal posts are constantly being moved with the advent of endoscopic ablative techniques. Median age limit in the Netherlands is 75.

Discuss the management of dysplasia detected on biopsies?

The British Society of Gastroenterology recommends

Low-grade dysplasia- 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.

High-grade dysplasia- is associated with a focus of invasive adenocarcinoma in 30–40% of patients. For this reason, if the changes persist after intensive acid suppression and are confirmed by two expert pathologists, 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.

‘Indefinite for dysplasia’- is diagnosed when there are changes suggestive of dysplasia but inflammatory changes make the distinction impossible. Endoscopy should be repeated with extensive biopsies following a course of PPI therapy. If this, together with a subsequent endoscopy and multiple biopsies at 6 months fail to reveal definite evidence of dysplasia, then the patient can return to routine surveillance.

What is the role of PPI in Barrett’s oesophagus?

Longitudinal cohort studies of patients with Barrett’s oesophagus suggest that use of PPI may be associated with reduced risk of dysplasia. It may be that chronic inflammation associated with GORD promotes carcinogenesis.  However, PPI’s has not been shown to reduce the length or progression of Barrett’s, or to reduce acid exposure adequately in up to 30-40% of patients despite high dose PPI.
In clinical practice, most patients are advised long term PI based on the premise that chronic acid exposure leads to Barrett’s oesophagus.

What is the role of antireflux surgery in Barrett’s oesophagus?

There is insufficient evidence to suggest it reduces incidence of adenocarcinoma.

Discuss the pathogenesis of Barrett’s oesophagus?

  • Acid/pepsin and duodenal refluxate causes acute and chronic inflammation, which in turn stimulates oesophageal stem cells to promote columnar metaplasia
  • Cytokine profile of Barrett’s oesophagus differs from oesophagitis, with an anti-inflammatory response characterized by increased levels of T Helper 2 cytokines and a reduction in signalling through the transforming growth factor β (TGF-β) pathway
  • Barrett’s oesophagus has a higher proportion of Th2 effector cells (plasma and mast cells) than Th1 effector cells (macrophages and CD8+ T cells) when compared with reflux oesophagitis

Discuss chemoprevention in Barrett’s?

The majority of adenocarcinoma is thought to arise from Barrett’s. Experimental and epidemiological data suggest use of NSAID’s may reduce risk of cancer in Barrett’s patients. ASPECT trial, due to report in 2011, is looking at the long-term chemoprevention effect of esomeprazole with or without aspirin.

Discuss the role of ablative therapy in Barrett’s oesophagus?

Ablative therapy is an option in the presence of dysplasia. Thermal or photochemical energy is used to ablate abnormal tissue, but most studies are not randomized or controlled, involve relatively few patients, and have short durations of follow-up

EMR has been used for high grade dysplasia shows low complication rate, but so far studies have short follow –up (up to 36 months)
NICE is currently consulting on ablative therapies in Barrett’s oesophagus and is due to report in July 2010.

Pic1 Barrett’s oesophagus
Pic1 Barrett’s oesophagus


  1. Caygill CP et al. Characteristics and regional variations of patients with Barrett’s oesophagus in the UK. Eur J Gastroenterol Hepatol 2003; 15: 1217–22
  2. Corley DA et al. Surveillance and survival in Barrett’s adenocarcinomas: a population-based study. Gastroenterology 2002; 122: 633–40
  3. Fountoulakis A et al. Effect of surveillance of Barrett’s oesophagus on the clinical outcome of oesophageal cancer. Br J Surg 2004; 91: 997–1003
  4. Fitzgerald RC et al. Rigorous surveillance protocol increases detection of curable cancers associated with Barrett’s esophagus. Dig Dis Sci 2001; 46: 1892–8
  5. Lagergren J et al. Utility of endoscopic screening for upper gastrointestinal adenocarcinoma. JAMA 2000; 284: 961–2
  6. Macdonald CE et al. Final results from 10 year cohort of patients undergoing surveillance for Barrett’s oesophagus: observational study. BMJ 2000; 321: 1252–5
  7. Somerville M, Garside R , Pitt M et al., Surveillance of Barrett’s oesophagus: is it worthwhile?, Eur J Cancer 44 (2008), pp. 588–599
  8. Garside R et al. Surveillance of Barrett’s oesophagus: exploring the uncertainty through systematic review, expert workshop and economic modelling. Health Technology Assess 2006; 10: 1–158.
  9. British Society of Gastroenterology guidelines for the diagnosis and management of Barrett’s columnar-lined oesophagus

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