This fairly common condition that affects the lower oesophagus is named after the Australian-born British chest surgeon, Norman Barrett, who first described it in the early 1950s. The implications of Barrett’s mucosa however, were not fully understood until much later. What is it? The lining (mucosa) of the oesophagus is quite different from that of the stomach and intestine and is called ‘squamous’ as opposed to ‘intestinal’. It looks quite different both at endoscopy and under the microscope and has completely different characteristics. There is a fairly sharp cut-off in the lower oesophagus at the level of the lower oesophageal valve where the paler squamous mucosa gives way to the much pinker gastric (or intestinal-type) mucosa. However in Barrett’s oesophagus the squamous mucosa undergoes a transformation (metaplasia) to look a lot more like the intestinal mucosa. This can extend up into the oesophagus as ‘tongues’ of Barrett’s mucosa or even line a fairly large area of oesophagus in severe cases.
Why does it happen? Nobody really knows for sure, but it seems likely that persistent refluxing of acid (acid reflux or GORD) from the stomach into the lower oesophagus over a long period of time activates a change in the nature of the squamous lining which starts to look a lot much more like intestinal lining, probably as a protective measure against acid attack. This can occur in 5-15% of chronic refluxers. This change if properly controlled (by genes and the immune system etc), is called metaplasia and is harmless, but just occasionally this change goes wrong and the cells start to look abnormal under the microscope (dysplasia). Taken to the worst case scenario, these dysplastic cells can become cancerous. There has been a lot of debate about the incidence of cancer in Barrett’s but the most recent (2011) large population study from Denmark, found an incidence of only 1.2 per 1000 patient years.
What can be done about it? Of course, the biggest anxiety about Barrett’s is the potential for developing cancerous cells. There is limited evidence that reducing the amount of acid washing over the Barrett’s may reduce the risk of dysplasia and even cause the Barrett’s to partially regress. This is most easily achieved by long-term treatment with acid suppressing medication and the best drugs for this are the Proton pump inhibitors (PPIs), such as omeprazole, lansoprazole, pantoprazole or esomeprazole. Anti-reflux surgery may also be considered. Other than this, the only other option is to closely monitor and observe the Barrett’s for signs of dysplasia or malignant change. This is best achieved by endoscopy (gastroscopy) with multiple biopsies.
In the UK, based on health economics, it is recommended that patients with Barrett’s should have an endoscopy with biopsies every 3 years. If dysplasia is observed then the endoscopies are performed much more frequently and even surgery with removal of the lower oesophagus (oesophagectomy) are considered. Malignant change always requires removal although there are newer endoscopic techniques (radiofrequency ablation) that may be offered for very early cancers rather than full-blown oesophagectomy. Most recent evidence suggests that short-segment Barrett’s <3cms in length can probably be renamed as ‘cardial metaplasia’ and represents a very low risk for developing cancer and does not need to be followed up. Written by Dr M J Webberley, Consultant Gastroenterologist, August 2015