Barrett's Oesophagus

208 Users are discussing this topic

PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Barrett's Oesophagus written for patients

Synonyms: Barrett's oesophagitis, Barrett's columnar lined oesophagus

Barrett’s oesophagus is defined as an oesophagus in which any portion of the normal distal squamous epithelial lining has been replaced by metaplastic columnar epithelium, which is clearly visible endoscopically (>1 cm) above the gastro-oesophageal junction and confirmed histopathologically from oesophageal biopsies.[1] 

It was first described in 1950 by Barrett, a surgeon.

  • It is often subdivided into short segment (less than 3 cm) or long segment (more than 3 cm).[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 2% of the adult population and in 5% of persons with gastro-oesophageal reflux disease (GORD).[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 (NSAIDS) - by non-selectively blocking COX receptors[5] - and Helicobacter pylori[6] appear to be protective and may be associated with a lower risk of developing oesophageal adenocarcinoma.

NEW - log your activity

  • Notes
    Add notes to any clinical page and create a reflective diary
  • Track
    Automatically track and log every page you have viewed
  • Print
    Print and export a summary to use in your appraisal
Click to find out more »

Risk factors

  • Patients with chronic GORD 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.
  • Hiatus hernia is a risk factor and the size of the hernia is correlated with the length of Barrett's oesophagus.[7]
  • Some studies indicate a higher prevalence of obesity, smoking and alcohol intake.[7]
  • Risk factors for progression to adenocarcinoma include male gender, increasing age, extended segment (>8 cm) disease, intestinal metaplasia, duration of reflux history, early age of onset of GORD, duodeno-gastro-oesophageal reflux, mucosal damage (ulceration and stricture) and family history.[1][4] 
  • 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 Caucasian male with a long history of gastro-oesophageal reflux and, occasionally, dysphagia.[2]
  • Histological corroboration of endoscopically visible columnarisation is the most accurate method of diagnosis.[1] In cases of erosive oesophagitis, it is important to treat the oesophagitis first 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.[2]
  • A patient with a columnar-lined distal oesophagus without confirmed intestinal metaplasia on biopsy must be followed up with further endoscopies and biopsies.
BARRETT'S OESOPHAGITIS

Barrett's oesophagus

The role of surveillance endoscopy is controversial and changing.[1][4] Oesophageal cancers arising in Barrett's oesophagus detected by surveillance are often early and have an excellent prognosis. There is a paucity of randomised controlled trial (RCT) data on the effect of surveillance but studies demonstrate that surveillance results in earlier cancer staging and improved survival. It is recommended that when surveillance is considered appropriate, it should be performed every 2-5 years in the UK, depending on the length of the affected segment and the presence of intestinal metaplasia.[1] 

The management of low-grade dysplasia is unclear although it is recommended that, after two pathologists have confirmed the diagnosis, surveillance be repeated every six months.[1] 

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.[8]  Photodynamic therapy has been largely superceded by radiofrequency ablation, as recommended in the latest BSG guidance.

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.[1][8]

Non-drug

The recommended lifestyle advice is the same as that recommended for patients with GORD:

  • 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 three hours of going to bed.
  • Avoid drugs that affect oesophageal motility (nitrates, anticholinergics, tricyclic antidepressants) or damage the mucosa (NSAIDs, potassium salts, alendronate).

Drug

  • Available data indicate that long-term proton pump inhibitor (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 provide any increased benefit for prevention of oesophageal adenocarcinoma.[2]
  • Recent review of data - the Aspirin Esomeprazole Chemoprevention Trial (AspECT) - indicates that chemoprevention with aspirin may be the most promising approach for reduction of adenocarcinoma risk, previous studies having shown a protective association between NSAIDs and oesophageal cancer.[9]
  • Ablative therapy.[8][10] The goal of ablative therapy is to destroy the Barrett's epithelium to a sufficient depth to eliminate the intestinal metaplasia and allow regrowth of squamous epithelium. A number of modalities have been tried - eg, 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.[11] 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.[12]

Surgical

  • Anti-reflux surgeries (eg, Nissen's fundoplication) have not been shown to prevent the progression of Barrett's oesophagus to oesophageal cancer.[2]
  • Oesophagectomy is, however, often recommended when severe dysplasia is confirmed.[13]
  • 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.[14] The incidence of adenocarcinoma is rising, with current rates in Scotland being the highest reported rates in the world.[4]
  • Although Barrett's oesophagus is the only known precursor to oesophageal adenocarcinoma, most patients with Barrett's oesophagus do not develop cancer.[15]
  • Barrett's oesophagus has a 2-25% risk of mild-severe dysplasia and a lifetime risk of developing adenocarcinoma of 3% in women and 5% in men.[4] 40-50% of those patients with Barrett's oesophagus and severe dysplasia go on to develop oesophageal adenocarcinoma within five years.[12]
  • Barrett's oesophagus is a premalignant condition and increases the risk of oesophageal adenocarcinoma to 30-60 times that of the general population.[16]
  • Most patients will not develop oesophageal cancer and will die of other causes.
  • 5-10% of those with Barrett's oesophagus will develop adenocarcinoma over 10-20 years.[17] 
  • 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.[2]

Endoscopic surveillance for patients with Barrett's oesophagus is described above.

Should patients with heartburn be screened for Barrett's oesophagus?

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 1,000 per annum. The latest British Society of Gastroenterology guidelines recommend that:

  • Screening with endoscopy is not feasible or justified for an unselected population with gastro-oesophageal reflux symptoms.
  • Endoscopic screening can, however, be considered in patients with chronic GORD symptoms and multiple risk factors (at least three of age 50 years or older, white race, male sex, obesity).
  • The threshold of multiple risk factors should, however, be lowered in the presence of a family history including at least one first-degree relative with Barrett's oesophagus or oesophageal adenocarcinoma.[1] 

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.

Further reading & references

  1. Guidelines for the diagnosis and management of Barrett's columnar-lined oesophagus; British Society of Gastroenterology (2013)
  2. Sharma P, McQuaid K, Dent J, et al; A critical review of the diagnosis and management of Barrett's esophagus: the AGA Chicago Workshop. Gastroenterology. 2004 Jul;127(1):310-30.
  3. Flejou JF; Barrett's oesophagus: from metaplasia to dysplasia and cancer. Gut. 2005 Mar;54 Suppl 1:i6-12.
  4. Jankowski J, Barr H, Wang K, et al; Diagnosis and management of Barrett's oesophagus. BMJ. 2010 Sep 10;341:c4551. doi: 10.1136/bmj.c4551.
  5. Fitzgerald RC; Barrett's oesophagus and oesophageal adenocarcinoma: how does acid interfere with cell proliferation and differentiation? Gut. 2005 Mar;54 Suppl 1:i21-6.
  6. Malfertheiner P, Peitz U; The interplay between Helicobacter pylori, gastro-oesophageal reflux disease, and intestinal metaplasia. Gut. 2005 Mar;54 Suppl 1:i13-20.
  7. Avidan B, Sonnenberg A, Schnell TG, et al; Hiatal hernia and acid reflux frequency predict presence and length of Barrett's esophagus. Dig Dis Sci. 2002 Feb;47(2):256-64.
  8. Barrett's oesophagus - ablative therapy; NICE Clinical Guideline (August 2010)
  9. Corley DA, Kerlikowske K, Verma R, et al; Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis. Gastroenterology. 2003 Jan;124(1):47-56.
  10. Photodynamic therapy for Barrett's oesophagus; NICE Interventional Procedures, June 2010
  11. Rees JRE, Lao-Sirieix P, Wong A, Fitzgerald RC. Treatment for Barrett's oesophagus. Cochrane Database of Systematic Reviews 2010, Issue 1. Art. No.: CD004060. DOI: 10.1002/14651858.CD004060.pub2.
  12. Deviere J; Barrett's oesophagus: the new endoscopic modalities have a future. Gut. 2005 Mar;54 Suppl 1:i33-7.
  13. Schuchert MJ, Luketich JD; Management of Barrett's esophagus. Oncology (Williston Park). 2007 Oct;21(11):1382-9, 1392; discussion 1392, 1394, 1396.
  14. Gopal DV, Lieberman DA, Magaret N, et al; Risk factors for dysplasia in patients with Barrett's esophagus (BE): results from a multicenter consortium. Dig Dis Sci. 2003 Aug;48(8):1537-41.
  15. Spechler SJ, Lee E, Ahnen D, et al; Long-term outcome of medical and surgical therapies for gastroesophageal reflux disease: follow-up of a randomized controlled trial. JAMA. 2001 May 9;285(18):2331-8.
  16. Lagergren J; Adenocarcinoma of oesophagus: what exactly is the size of the problem and who is at risk? Gut. 2005 Mar;54 Suppl 1:i1-5.
  17. Dyspepsia - proven GORD; NICE CKS, November 2012 (UK access only)

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
1020 (v24)
Last Checked:
23/01/2014
Next Review:
22/01/2019

Did you find this health information useful?

Yes No

Thank you for your feedback!

Subcribe to the Patient newsletter for healthcare and news updates.

We would love to hear your feedback!

 
 
Patient Access app - find out more Patient facebook page - Like our page