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Management

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

The management of Barrett's oesophagus is controversial.

Clinicians should focus on the following issues once Barret’s oesophagus has been diagnosed:

  • control of GORD symptoms with the use of non pharmacological and pharmacological methods
  • long term endoscopic surveillance to identify progression to dysplasia and oesophageal adenocarcinoma
  • establish whether patients with confirmed dysplasia require endoscopic treatment (1)

Symptom control:

  • acid suppression drugs
    • PPIs have the best clinical profile for symptomatic management and are recommended in all cases of Barrett’s oesophagus irrespective of symptoms.
      • proton pump inhibitors (PPIs) use was associated with a 75% reduction in the risk of neoplastic progression
  • lifestyle modifications
    • weight loss, bed head elevation, stop smoking, take small regular meals etc
  • antireflux surgery
    • is not superior to pharmacological acid suppression for the prevention of neoplastic progression of Barrett’s oesophagus
    • should be considered in patients with poor or partial symptomatic response to PPIs (1,2,3)

Endoscopic surveillance

Risk of progression to adenocarcinoma in patients with non-dysplastic Barrett’s oesophagus is approximately 0.33% per annum while in patients with high grade dysplasia this figure is around 10% per annum

Endoscopic monitoring with histopathological assessment of dysplasia is the only current method of surveillance with sufficient evidence to be recommended

  • high-resolution endoscopy (HRE) should be used in Barrett's oesophagus surveillance
  • not recommended in patients with intestinal metaplasia (IM) at the cardia or in those with an irregular Z-line regardless of the presence of IM
  • dysplasia confirmed by two GI pathologists is currently the best tissue biomarker for the assessment of cancer risk
  • surveillance is not recommended if life expectancy is less than 5 years

Endoscopic treatment

Endoscopic eradication therapy should be preferred over continued surveillance in patients with any grade of dysplasia.

  • an independent pathologist should confirm diagnosis of dysplasia before initiating endoscopic therapy
  • immunohistochemical staining for p53 protein overexpression is recommended in the UK in patients with suspected low grade dysplasia

Surgery

  • surgical therapy (oesophagectomy) is considered the treatment of choice
    • for early adenocarcinoma that has extended into submucosa because of the significant risk of lymph node metastasis
    • when endoscopic therapies have failed
  • currently there is no evidence to support one technique of oesophagectomy over another. It is recommended that the procedure is tailored to the particular case and the expertise available in that centre (2)

NICE suggest that (4):

  • Managing Barrett's oesophagus with dysplasia
    • offer endoscopic resection of visible oesophageal lesions as first-line treatment to people with high-grade dysplasia.
    • offer endoscopic ablation of any residual Barrett's oesophagus to people with high-grade dysplasia after treatment with endoscopic resection.
    • offer radiofrequency ablation to people with low-grade oesophageal dysplasia diagnosed from biopsies taken at 2 separate endoscopies. Two gastrointestinal pathologists should confirm the histological diagnosis
    • consider endoscopic surveillance at 6 monthly intervals with dose optimisation of acid-suppressant medication for people diagnosed with indefinite dysplasia of the oesophagus
    • offer endoscopic follow-up to people who have received endoscopic treatment for Barrett's oesophagus with dysplasia

Reference:


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