Barrett's oesophagus

What Barrett's oesophagus is

The oesophagus is lined with a pale, smooth lining that is not built to cope with acid. The stomach is lined with something tougher. In Barrett's oesophagus, after years of acid and other stomach contents washing back up, the lining at the bottom of the oesophagus is replaced by a lining more like the intestine's, which handles acid better. The body has made a sensible local repair. The problem is that this new lining carries a small risk of turning into something dangerous over a long period.

Barrett's causes no symptoms of its own. People do not feel it. It is found at gastroscopy, usually one done for reflux, and sometimes incidentally in someone being scoped for another reason. Up to about 2 per cent of the population may have it, and most of them do not know.

Two things have to be true for the diagnosis. The endoscopist has to see the salmon coloured lining extending up into the oesophagus, and the biopsies have to confirm it. In Australia the diagnosis requires intestinal metaplasia on the biopsies, meaning the characteristic goblet cells. A short tongue of colour with no intestinal metaplasia is not Barrett's oesophagus and does not need surveillance.

How the length is measured, and why it matters

Barrett's is recorded in two numbers, written as something like C2 M4. This is the Prague classification, agreed internationally in 2006 and used in every Australian endoscopy report.

• C is the circumferential extent: how far up the oesophagus the new lining goes all the way around, measured in centimetres above the junction with the stomach
• M is the maximum extent: how far up the longest tongue of it reaches

So C0 M4 means there is no part that goes right around, and the longest tongue reaches 4 cm. C4 M6 means the bottom 4 cm is circumferential, with a tongue going 2 cm higher.

It is worth knowing how precise those numbers really are. When the system was tested, 29 endoscopists scoring the same recordings landed within 2 cm of each other almost every time, but agreed on the exact figure only about a third of the time. So the measurement is dependable as a band rather than to the centimetre, which is why a borderline length is not treated as a hard line, and why your own reports may vary by a centimetre or two between examinations without anything having changed.

Below 1 cm, endoscopists often could not agree on whether Barrett's was there at all. That is the reason a segment under 1 cm is not called Barrett's on appearance alone, and why one with no intestinal metaplasia on the biopsies is not put under surveillance.

Length matters for the risk as well as the record. In a cohort of 1,175 people with Barrett's and no dysplasia followed for an average of five and a half years, each additional centimetre of length carried a 28 per cent higher risk of progressing to high-grade dysplasia or cancer. The average length was 6.1 cm in those who progressed and 3.5 cm in those who did not.

What the risk actually is

The honest answer is that it is a good deal lower than the word precancerous implies, and lower than the figures still printed in a lot of patient material.

The Australian guideline authors put the risk of progression to oesophageal cancer, for Barrett's with no dysplasia, at 1 to 3 per 1,000 patient-years. That is somewhere between 1 in 1,000 and 1 in 300 people per year.

Those numbers come from large population studies. A Danish national cohort followed 11,028 people with Barrett's for a median of 5.2 years and found 66 cancers after the first year, an annual risk of 0.12 per cent. The authors pointed out that this was far below the 0.5 per cent figure that surveillance intervals had been built on. A meta-analysis of 57 studies covering 11,434 people found 0.33 per cent a year, about 1 in 300, falling to 0.19 per cent for short segments.

The same meta-analysis found something worth saying plainly. Among the studies that reported deaths, there were 56 cancers of the oesophagus against 684 deaths from unrelated causes. People with Barrett's oesophagus overwhelmingly die of something else. That is not a reason to ignore it. It is a reason to keep it in proportion, and to put at least as much energy into blood pressure, weight and smoking as into the gastroscopy calendar.

Anything that still quotes 0.5 per cent a year, or 1 in 200, is using numbers that the population studies have superseded.

How often a gastroscopy is needed

Barrett's has its own surveillance schedule, set by the length of the segment and by what the biopsies show. It is not related to the schedule used after bowel polyps, which is a different guideline for a different organ.

• Under 1 cm, no intestinal metaplasia on the biopsiesNone
• Under 3 cm, no dysplasia3 to 5 years
• 3 cm or more, no dysplasia2 to 3 years
• Indefinite for dysplasia6 months
• Low-grade dysplasia, confirmed6 months, or treat
• High-grade dysplasiaTreat
• Early adenocarcinomaTreat

Two notes on that list. Indefinite for dysplasia usually means inflammation is making the cells hard to read, so acid control is optimised first and the gastroscopy is repeated at six months. High-grade dysplasia and early cancer are not followed, they are treated, through the endoscope in a specialist Barrett's service, and surveillance resumes afterwards. A low-grade dysplasia report should be confirmed by a second expert pathologist before either path is chosen, for the reason set out below.

Those intervals come from the Australian clinical practice guidelines produced by the Cancer Council Australia Barrett's Oesophagus Guidelines Working Party, published in 2014 and summarised by the guideline's own authors in the Medical Journal of Australia in 2016. It is worth knowing that Cancer Council now flags that guideline as more than five years old, and there is no Australian replacement. In practice the interval is set for the individual, taking account of length, what the biopsies showed, age and other health, and it is reasonable to ask why yours is what it is.

How that compares with the major guidelines

Four groups read much the same evidence and land in slightly different places. It is worth knowing, because a figure found online often will not match the one on your letter.

Scroll the table sideways to see all four. Sources for each are listed at the foot of this page.

They agree at both ends. Nobody recommends watching a segment under 1 cm, and all four want confirmed dysplasia dealt with at a centre that does this work. In the middle the difference is smaller than it looks. Both American guidelines set a single figure for each length, five years for a short segment and three for a longer one. The 2025 one puts it the other way round, three years by default and five for people at lower risk, with a short segment as its own example of lower risk, which lands in the same place. The Australian and British guidelines give ranges and watch long segments a little more closely, at two to three years.

The real disagreement is over confirmed low-grade dysplasia. The American college prefers treating it. The Australian and British guidelines favour closer surveillance. The 2025 American guideline sits between them and asks for the decision to be made with the patient: if surveillance is chosen, a gastroscopy at six months, again at a year, then yearly, returning to three-yearly if the dysplasia goes away. All of those positions are defensible, which is why the decision is made case by case rather than by a table.

At each gastroscopy the lining is examined carefully, any visible abnormality is sampled or removed, and biopsies are taken in a systematic pattern from all four quadrants at set intervals up the segment. This is called the Seattle protocol, and it is slower than taking a few random biopsies. The spacing depends on the history: every 2 cm where there has never been dysplasia, and every 1 cm where there has. It matters: in a large review of community practice in the United States, the protocol was followed in half of cases, adherence fell as segments got longer and dysplasia was detected significantly less often when it was not followed.

What the evidence for surveillance does and does not show

Surveillance is standard practice in Australia and internationally, and it is how dysplasia and early cancer are found at a point where they can be treated through the endoscope. It is also fair to say that the evidence behind it is thinner than most people assume.

In 2025 the first randomised trial of the practice reported. BOSS recruited 3,453 people with Barrett's across 109 UK centres and randomised them to two-yearly surveillance or to endoscopy only when symptoms called for it, then followed them for a median of 12.8 years. There was no difference in overall survival (333 deaths of 1,733 versus 356 of 1,719, hazard ratio 0.95), no difference in cancer-specific survival and no difference in the stage at which cancers were found. Serious adverse events were rare in both arms, under half a per cent.

That result does not mean surveillance is pointless, and it has not changed Australian practice. What it does mean is that the benefit is smaller than the usual framing suggests, that it is weighted towards people whose Barrett's actually carries risk, and that the interval is a conversation rather than a rule. The Gastroenterological Society of Australia has long advised against repeating the test sooner than three years after two consecutive clear results.

When the biopsies show dysplasia

Dysplasia means the cells have started to change, short of cancer. It is reported in grades, and what happens next depends on the grade and, just as much, on who read the slide.

The second opinion is not a formality

Low-grade dysplasia is the hardest call in this area of pathology. In a Dutch study, 147 people given a low-grade dysplasia diagnosis in community hospitals had their slides re-read by two expert pathologists. Eighty-five per cent were downgraded to no dysplasia or to indefinite for dysplasia. Only 15 per cent had the diagnosis confirmed.

The difference mattered enormously. Those whose low-grade dysplasia was confirmed progressed at 13.4 per cent a year. Those downgraded progressed at 0.49 per cent a year, which is to say at close to the background rate. So a low-grade dysplasia report should be reviewed by a second expert pathologist before anything is decided. That is the Australian guideline's own recommendation and it is standard practice.

What each grade means in practice

• Indefinite for dysplasia usually means inflammation is making the cells hard to read. Acid suppression is optimised and the gastroscopy is repeated, generally at six months.
• Low-grade dysplasia, once confirmed, is followed closely or treated. Pooled across 24 studies and 2,694 people, progression to cancer ran at 0.54 per cent a year, and to cancer or high-grade dysplasia at 1.73 per cent a year. Australian and British guidance has favoured six-monthly surveillance, the American college updated in 2022 favours treating it, and the 2025 American Gastroenterological Association guideline asks for the two to be weighed up with the patient. Where surveillance is chosen it is six-monthly for a year, then yearly, and if the dysplasia resolves the interval goes back to three years. All of those positions are defensible and the choice is made case by case.
• High-grade dysplasia is treated. Progression to cancer in a meta-analysis of 236 people ran at about 6 per cent a year.

How dysplasia is treated

Treatment happens through the endoscope in a specialist Barrett's service, and in most cases it avoids surgery altogether. It has two parts, usually in this order.

• Anything visible is removed by endoscopic resection. Lifting a nodule or a flat lesion off the wall and sending it to pathology does two jobs at once: it takes the lesion away and it establishes how deep the change goes, which is what decides whether endoscopic treatment is enough.
• The remaining flat Barrett's lining is ablated, most often with radiofrequency energy delivered through a balloon or a plate on the end of the endoscope. The treated lining sloughs and normal squamous lining grows back in its place, usually over several sessions.

What the trials showed

Ablation has been tested properly, which is not true of every endoscopic treatment.

In a sham-controlled trial of 127 people with dysplastic Barrett's, dysplasia was completely eradicated at 12 months in 81 per cent of those with high-grade dysplasia treated with ablation against 19 per cent of the sham group, and in 90.5 per cent against 22.7 per cent of those with low-grade dysplasia. Progression to cancer occurred in 1.2 per cent of treated patients against 9.3 per cent of controls.

In a European trial of 136 people with expert-confirmed low-grade dysplasia, progression to high-grade dysplasia or cancer over three years was 1.5 per cent with ablation against 26.5 per cent with surveillance alone. The trial was stopped early. Two things are worth noting about that striking number: everyone in it had their low-grade dysplasia confirmed by expert review first, so the control arm was a genuinely high-risk group and not comparable to an unreviewed community diagnosis, and the ablation arm's result rests on a single patient progressing out of 68.

What it costs the patient

Ablation is not free of consequence. Narrowing of the oesophagus needing stretching occurred in 6 per cent of patients in the first trial and 11.8 per cent in the second, where around one in five had some treatment-related problem. Chest discomfort for a few days afterwards is common. All of it is manageable, and all of it is worth knowing in advance.

Eradication is also not the end. Complete clearance was achieved in 77 to 92 per cent of people in those trials rather than in all of them, and everyone stays under surveillance afterwards, because the lining can come back.

A/Prof Kariyawasam does not perform Barrett's ablation. Dysplasia is referred to a specialist Barrett's service for treatment, and surveillance, the reflux care behind it and ongoing follow-up continue with him.

Who gets it, and who should be looked for

The risk factors for having Barrett's are reasonably consistent across studies: long-standing reflux, being male, older age, carrying weight around the middle, smoking and a close relative with Barrett's or oesophageal cancer. Pooling studies worldwide, men outnumber women by close to two to one. The gap is wider still for oesophageal cancer itself. Carrying weight around the middle roughly doubles the odds, and it does so only partly through reflux: pooled across 17 studies the link held at the same strength in analyses that compared people with similar heartburn. Waist measurement predicts the risk better than body mass index does, so where you carry weight matters more than the number on the scales. Past Helicobacter pylori infection is associated with a lower risk, which surprises people.

Being a woman with Barrett's is a meaningfully different situation from being a man with it. In a cohort of 2,145 people, annual progression to cancer was 0.05 per cent in women against 0.3 per cent in men. The authors of that study went as far as suggesting that surveillance may not be necessary for women at all. No Australian guideline has adopted that position, and surveillance is still offered here, but it is the clearest reason the interval is set for the person in front of you rather than read off a table.

Should everyone with reflux be scoped?

No, and no guideline says so. Australia does not recommend population screening for Barrett's. The British and American guidelines both suggest considering a single gastroscopy in someone with chronic reflux symptoms who also has at least three other risk factors from the list above, with a lower threshold if a first-degree relative has had Barrett's or oesophageal cancer. The American guideline grades its own recommendation as conditional, on very low quality evidence.

In practice, in Australia, this is a decision made between a patient and a specialist rather than by a rule, and the discussion is usually prompted by years of reflux rather than by a calculator.

Treating the reflux underneath

Barrett's is the result of reflux, so the reflux is treated on its own merits. Acid suppression controls symptoms, heals oesophagitis and is usually continued in people with Barrett's. The page on reflux and how it is treated covers the medicines, the long-term safety question and the lifestyle measures that actually have evidence behind them.

What acid suppression and weight loss will not do is make the Barrett's go away. There is no good evidence that treating the reflux, changing the diet or losing weight reverses established Barrett's metaplasia. They are worth doing for the symptoms, for the oesophagitis and for general health, and that is the honest case for them.

Can anything lower the risk of progression?

This has been studied properly once, in a UK trial of 2,557 people with Barrett's followed for a median of 8.9 years, which tested high-dose against low-dose acid suppression, with or without aspirin. The high-dose comparison reached statistical significance on a composite endpoint that combined death from any cause with cancer and high-grade dysplasia. The aspirin comparison did not reach its prespecified significance threshold.

That is a weaker result than the headlines at the time suggested, and it does not support anybody starting high-dose acid suppression or aspirin on their own to prevent cancer. Aspirin carries a real bleeding risk, the doses used in the trial were specific and the treatment ran for years. The American college reviewed the same evidence in 2022 and concluded it could not make a recommendation either way.

Guidance has moved a little since. The American Gastroenterological Association guideline published in 2025 makes a conditional recommendation for daily acid suppression over no treatment in people with Barrett's, and over anti-reflux surgery, to reduce the chance of progression. Conditional is the right word: it means the panel judged the balance to favour it without the evidence being strong. It is an argument for taking the tablet you are already on properly, not for taking more of it. If this comes up, it is a conversation to have with the doctor managing the Barrett's rather than a decision to make at the pharmacy.

Living with the diagnosis

Most people, once the first fortnight has passed, find that Barrett's oesophagus asks very little of them. The practical list is short.

• Keep the gastroscopy appointments, at whatever interval has been set, and know what that interval is and why.
• Keep the reports. The Prague measurement and the biopsy result are what the next endoscopist needs. A patient who can say C0 M4, no dysplasia, 2024 has saved everyone a good deal of time.
• Treat the reflux properly rather than intermittently, and review the dose from time to time.
• Report new symptoms early rather than waiting for the next scheduled test. Food sticking, unexplained weight loss, repeated vomiting, black stools or new pain on swallowing are all reasons to be seen sooner.
• Tell your family, briefly. A first-degree relative with Barrett's or oesophageal cancer is one of the things that lowers the threshold for scoping someone else with long-standing reflux.

The thing most worth holding on to is the arithmetic. The lining has changed, the change is being watched, the great majority of people with it never develop cancer, and the changes that come before cancer can usually be treated without surgery if they are found.

Where Barrett's oesophagus is managed in Sydney

A/Prof Viraj Kariyawasam is a consultant gastroenterologist and hepatologist with an advanced endoscopy fellowship. Barrett's oesophagus, its surveillance and the treatment of dysplasia are assessed at consultation in Norwest, Rouse Hill, Pennant Hills and Macquarie Park.

The gastroscopy and the surveillance biopsies are performed at Norwest Private Hospital, Macquarie University Hospital and Pennant Hills Day Surgery. A referral from your GP is needed for a consultation.