Barrett Esophagus with Dysplasia: Understanding Your Pathology Report

By Jason Wasserman MD PhD FRCPC
July 29, 2026

Dysplasia in Barrett esophagus is a precancerous change in the gland-forming cells that line a segment of Barrett esophagus. Barrett esophagus is a condition in which the normal squamous lining of the lower esophagus has been replaced by glandular cells resembling those of the intestine, usually after years of acid reflux. Dysplasia means those replacement cells have started to look genuinely abnormal under the microscope, in a way that reflects early damage to the genetic material inside them.

Dysplasia is not cancer. The abnormal cells remain inside the glands where they belong and have not broken through into the tissue underneath. That boundary is what separates dysplasia from cancer, and it is the single thing the pathologist looks hardest to confirm. Because the abnormal cells have not invaded, they cannot have spread anywhere, and dysplasia found at this stage is highly treatable.

Your report may describe this finding in several ways: Barrett esophagus with low grade dysplasia, Barrett esophagus with high grade dysplasia, Barrett esophagus indefinite for dysplasia, or glandular dysplasia arising in Barrett esophagus. These describe different points along the same scale, explained below.

One point of confusion is worth clearing up first. The esophagus can develop two entirely separate kinds of dysplasia. The kind described in this article arises from glandular cells in Barrett esophagus and can lead to adenocarcinoma of the esophagus. A different condition, squamous dysplasia of the esophagus, arises from squamous cells, has different causes, and leads to a different cancer. If your report does not mention Barrett esophagus, you may be looking for that article instead. This article will help you understand the findings in your pathology report, what each term means, and why it matters for your care.

What causes dysplasia in Barrett esophagus?

Dysplasia in Barrett esophagus develops because the glandular cells of the Barrett segment continue to accumulate genetic damage over time. The Barrett lining itself formed as a response to years of stomach acid and bile washing back into the esophagus, and those same cells go on dividing under continued irritation. With each division, there is a chance of a copying error, and errors gradually accumulate in the genes that control how cells grow and repair themselves. Dysplasia is the first point at which that accumulated damage becomes visible under the microscope.

Most people with Barrett esophagus never develop dysplasia. Factors that make it more likely include:

A longer Barrett segment — More abnormal lining means more cells at risk. Segments 3 cm or longer carry higher risk than shorter ones.
Longer duration of Barrett esophagus — Risk accumulates with the number of years the lining has been present.
Poorly controlled reflux — Continued acid exposure drives ongoing cell turnover.
Male sex and age over 60 — Both are associated with higher rates of dysplasia.
Central obesity — Weight carried around the abdomen, which both worsens reflux and has effects on cell growth independent of reflux.
Smoking — An independent risk factor for progression within Barrett esophagus.
Family history — A first-degree relative with Barrett esophagus or esophageal adenocarcinoma.

Dysplasia is not caused by anything you did or failed to do after your Barrett esophagus was diagnosed, and it does not mean earlier treatment failed. It is the expected behavior of a lining that has been present for a long time, which is exactly why people with Barrett esophagus are examined periodically.

What are the symptoms of dysplasia in Barrett esophagus?

Dysplasia in Barrett esophagus causes no symptoms of its own. It is a microscopic change in the surface lining; it does not narrow the esophagus, bleed, or cause pain, and it cannot be felt.

Essentially everyone with this diagnosis learns of it from biopsies taken during a surveillance endoscopy for known Barrett esophagus, or during an endoscopy performed to investigate reflux. Any symptoms present come from the underlying reflux rather than from the dysplasia. Because dysplasia is silent, how a person feels is not a way to judge whether it is stable or progressing, which is why periodic endoscopy with biopsies is used instead. New difficulty swallowing or unexplained weight loss are not features of dysplasia and should be reported promptly, since they can signal invasive cancer.

How is the diagnosis made?

Dysplasia in Barrett esophagus is diagnosed only after tissue from the Barrett segment is examined under a microscope by a pathologist. The tissue is obtained during an upper endoscopy, in which a thin flexible tube with a camera is passed through the mouth into the esophagus.

Dysplasia is usually flat and can look identical to the surrounding Barrett lining, so it cannot be found by looking alone. For this reason, the endoscopist takes biopsies in a systematic pattern, four samples around the circumference of the esophagus at every 1 to 2 cm along the whole Barrett segment, so that the segment is mapped rather than spot-checked. High-definition cameras, narrow band imaging, and dyes such as dilute acetic acid are used to make subtle abnormalities easier to see. Any area that is raised, nodular, depressed, or otherwise different from the rest is sampled separately, and if a visible lesion is present, it is generally removed whole by endoscopic resection rather than simply biopsied, because that is the only way to be certain no invasive cancer is hidden within it.

Under the microscope, the pathologist assesses both how the individual cells look and how the glands are arranged. In dysplasia, the nuclei, the compartments holding each cell’s genetic material, become enlarged, dark-staining (a change called hyperchromasia), and irregular in shape. They stack up in layers instead of sitting in a single row, and they lose their normal orientation within the cell. The glands themselves become crowded, irregular, and may branch, bud, or fuse into cribriform patterns with sieve-like spaces. Normally, cells look most abnormal deep in the glands and become progressively more mature toward the surface; loss of that surface maturation is one of the strongest signs of dysplasia.

Throughout, the pathologist is confirming that the abnormal cells remain within the glands and have not broken out into the surrounding tissue of the lamina propria. Once they have, the diagnosis is no longer dysplasia but intramucosal adenocarcinoma.

One thing makes this assessment genuinely difficult. Inflammation, an ulcer, or healing after any injury causes glandular cells to divide rapidly and look abnormal in ways that closely mimic dysplasia. These reactive changes are the main reason a diagnosis is sometimes deferred, and the main reason biopsies are repeated after reflux has been treated.

Grades of dysplasia

Every biopsy from a Barrett segment is placed into one of the following categories, and the category on your report is what determines what happens next. The grades describe how abnormal the glandular cells look and how far the abnormality extends:

Negative for dysplasia — The glandular cells look the way they should in Barrett esophagus. This is the most common and most reassuring result. Your report will simply describe Barrett esophagus, or intestinal metaplasia, without dysplasia.
Indefinite for dysplasia — The cells look abnormal, but the pathologist cannot determine whether this represents true dysplasia or a reaction to inflammation, an ulcer, or recent injury. This is not a diagnosis of dysplasia and it is not a diagnosis of cancer. It means the answer is genuinely uncertain on this sample, most often because inflammation is obscuring the picture. It is usually resolved by treating the reflux intensively for a few months and repeating the biopsies, after which most cases turn out to show no dysplasia.
Low grade dysplasia — The cells are clearly abnormal but the changes are limited. Nuclei are enlarged and dark and stack into layers, but they remain confined to the lower portion of the cells, the glands keep a relatively orderly arrangement, and some maturation toward the surface is often preserved.
High grade dysplasia — The cells look markedly abnormal, approaching the appearance of cancer. Nuclei are large, irregular, and stacked through the full height of the cells, they have lost their normal orientation, and the glands are crowded, branching, or fused into cribriform patterns. Surface maturation is lost. The abnormal cells have still not broken out of the glands, which is what keeps this a diagnosis of dysplasia rather than cancer.

Beyond high grade dysplasia lies intramucosal adenocarcinoma, in which cells have escaped the glands and are growing into the lamina propria while remaining confined to the innermost lining. It is a separate diagnosis, and it is still an early and usually curable one.

Your report may also describe the type of dysplasia as well as the grade. Most Barrett dysplasia is intestinal type, sometimes called adenomatous type, in which the cells resemble those of a colon polyp. A minority is foveolar type, sometimes called gastric type, in which the cells resemble the surface lining of the stomach. Both are graded on the same low grade and high grade scale, and the type does not currently change how the finding is managed.

Why does my diagnosis need to be confirmed by a second pathologist?

Grading dysplasia in Barrett esophagus is one of the more subjective judgments in pathology, and pathologists reviewing the same slides do not always reach the same conclusion. Disagreement is greatest at exactly the points where it matters most: between reactive change, indefinite for dysplasia, and low grade dysplasia. For this reason, guidelines worldwide recommend that any diagnosis of dysplasia in Barrett esophagus be confirmed by a second pathologist with particular expertise in gastrointestinal pathology before treatment is planned.

This is not a formality. When low grade dysplasia diagnosed in a general practice setting is sent for expert review, the majority of cases are reclassified as no dysplasia or as indefinite. And among the cases that are confirmed, the risk of progression rises steeply with the degree of agreement: in one large study, the odds of progressing to high grade dysplasia or cancer were about ten times higher when one expert pathologist confirmed the diagnosis, and about twenty-seven times higher when two agreed.

The practical effect is that confirmation changes the diagnosis itself for many people, and for those whose diagnosis stands, it changes the estimated risk enough to alter the recommended treatment. If your report describes dysplasia and you have not been told whether it was reviewed, it is a reasonable thing to ask. A diagnosis that is revised on review is not an error; it reflects a genuinely difficult distinction being resolved with more expertise.

p53 immunohistochemistry

p53 is a protein that normally helps a cell repair damaged DNA or shut itself down when the damage is too great. The gene that makes it is among the earliest to be damaged as Barrett esophagus progresses toward cancer. Immunohistochemistry, a test that uses antibodies to detect proteins inside cells, can show whether the p53 protein is behaving normally, and the result may appear on your report as an aid to the dysplasia diagnosis.

Normal (wild-type) pattern — Scattered cells show a small amount of p53, which is what healthy tissue looks like. This argues against dysplasia and supports a reactive explanation for abnormal-looking cells.
Overexpression pattern — Strong staining in many cells in a row, caused by a damaged gene producing a protein the cell cannot clear. This supports a diagnosis of dysplasia.
Null pattern — Complete absence of staining in an area where surrounding normal cells do stain. This also reflects a damaged gene and supports dysplasia.

Both the overexpression and null patterns are described as abnormal or aberrant, and an abnormal result is also associated with a somewhat higher chance of progression. p53 is a supporting test rather than a decisive one: an abnormal result does not by itself diagnose dysplasia, and a normal result does not rule it out. British guidelines recommend adding p53 to the assessment of Barrett biopsies, while North American guidelines have not yet endorsed it for predicting who will progress, so practice varies between centers. Other tissue-based risk prediction tests are offered in some centers but are likewise not yet endorsed by North American guidelines. A report that does not mention p53 is not incomplete.

What is the risk that dysplasia will become cancer?

The risk that dysplasia in Barrett esophagus will progress to adenocarcinoma of the esophagus depends on the grade, and for low grade dysplasia it depends heavily on whether the diagnosis was confirmed by an expert pathologist. For comparison, Barrett esophagus without dysplasia progresses at roughly 0.3% per year.

Indefinite for dysplasia — The risk sits between that of no dysplasia and low grade dysplasia. Most cases are reclassified as no dysplasia once inflammation has been treated and biopsies repeated.
Low grade dysplasia — Published rates range enormously, from under 1% to over 13% per year, and that spread is largely explained by who made the diagnosis. Pooled figures that include unconfirmed community diagnoses sit near 0.7% per year. When the diagnosis is confirmed by expert pathologists, rates around 10% per year are reported. In a randomized trial in which every diagnosis was expert-confirmed, about 27% of people who were monitored rather than treated progressed to high grade dysplasia or cancer within 3 years, rising to about 34% by six years.
High grade dysplasia — Roughly 6% to 7% per year without treatment. This is why treatment rather than monitoring is the usual course at this grade.

Other findings associated with higher risk include a longer Barrett segment, an abnormal p53 result, dysplasia that persists on repeated biopsies rather than coming and going, dysplasia found at more than one level of the segment, a visible nodule or raised area, continued uncontrolled reflux, and ongoing smoking.

It is worth holding two things together here. These percentages are meaningfully higher than for Barrett esophagus alone, which is why the finding is taken seriously. At the same time, dysplasia is found while the abnormal cells are still confined to the surface lining, where they cannot have spread, and where treatment is highly effective. Finding dysplasia is what surveillance is for.

What happens after this diagnosis?

Once dysplasia in Barrett esophagus is reported, the first step is usually confirmation of the diagnosis by a second pathologist with gastrointestinal expertise, since this can change both the diagnosis and the recommended treatment. Alongside that, reflux control with a daily acid-suppressing medication, usually a proton pump inhibitor, is part of care at every grade. What follows depends on the confirmed grade:

Indefinite for dysplasia — Intensified acid suppression for three to six months, followed by repeat endoscopy and biopsies so the tissue can be reassessed once inflammation has settled.
Low grade dysplasia — If confirmed, current guidelines favor endoscopic eradication therapy over monitoring. In the randomized trial mentioned above, treating roughly three or four people prevented one from progressing to high grade dysplasia or cancer. Surveillance every 12 months remains an accepted alternative, and the choice takes into account other health conditions and the person’s own priorities.
High grade dysplasia — Endoscopic eradication therapy is the standard approach, and monitoring alone is not generally recommended.

Endoscopic eradication therapy has two parts. Any visible lesion is first removed whole by endoscopic mucosal resection, both to treat it and to let the pathologist confirm that no invasive cancer is hidden within it. For Barrett-related lesions, endoscopic mucosal resection is generally preferred, with the more involved technique of endoscopic submucosal dissection reserved for larger lesions, lesions that do not lift properly, or those suspected of deeper invasion. The remaining flat Barrett lining is then destroyed by ablation, most often radiofrequency ablation, which uses controlled heat so that healthy squamous lining can grow back in its place. Several sessions are usually needed.

Surgery to remove part of the esophagus is now rarely needed for dysplasia alone, and is considered only in unusual circumstances such as very extensive disease or when endoscopic treatment has not succeeded.

Endoscopy continues at intervals for years after successful treatment. Complete clearance of Barrett esophagus is achieved in around 90% of people and holds up over long follow-up, but the lining returns in roughly 1 in 10, usually as small islands or tongues that can be treated again. Referral to a center with particular expertise in Barrett esophagus is common, especially where the diagnosis is uncertain, the segment is long, or a visible lesion is present.

Questions to ask your doctor

What grade of dysplasia was found in my biopsies?
Was my diagnosis confirmed by a second pathologist with gastrointestinal expertise?
If my report says indefinite for dysplasia, what does that mean, and when should the biopsies be repeated?
Could inflammation or an ulcer explain the changes seen in my biopsy?
Was dysplasia found at one level of my Barrett segment or at several?
Was a visible lesion or nodule seen during my endoscopy, and was it removed whole?
How long is my Barrett segment, and does that change my risk?
Was p53 testing performed on my biopsy, and what did it show?
Based on my report, what is my estimated risk of progressing to cancer?
Is endoscopic treatment recommended in my case, or is monitoring a reasonable option?
If I have ablation, how many sessions will I likely need, and what are the risks?
Should I be referred to a center that specializes in Barrett esophagus?
How often will I need endoscopy after treatment, and for how long?
What should I do about reflux control, and will I need medication long term?