Atypical Endometrial Hyperplasia: Understanding Your Pathology Report

Section Editor: Kianoosh Keyhanian MD FRCPC
September 2, 2026

Atypical endometrial hyperplasia (AEH) is a precancerous condition of the lining of the uterus, which is called the endometrium. In this condition, the glands that make up the lining become crowded and irregular, and the cells lining them look abnormal. The word atypical refers to that abnormal appearance of the cells.

AEH is not cancer. It is called precancerous because, without treatment, it can develop over time into endometrioid carcinoma, the most common cancer of the uterus.

This diagnosis raises two questions, and they are worth keeping separate. The first is whether a cancer is already present somewhere in the uterus that the biopsy did not reach. The second is the risk of cancer developing in the future if the condition is not treated. Both are answered below, along with the treatment options.

Atypical endometrial hyperplasia

Why does this condition have two names?

Your report may call this atypical endometrial hyperplasia, or it may call it endometrioid intraepithelial neoplasia, usually shortened to EIN. Some reports give both. These are two names for the same diagnosis, and neither is more serious than the other.

The two names come from two ways of describing the same tissue. “Atypical hyperplasia” is the older term and describes what the pathologist sees: too many glands, with abnormal-looking cells. “Endometrioid intraepithelial neoplasia” is the newer term and describes what the tissue is: a defined area of abnormal cells that can develop into cancer. The World Health Organization classification now uses EIN, but many laboratories still report atypical hyperplasia, and some use both terms.

What matters is that treatment and follow-up are the same, no matter which term appears on your report.

What causes atypical endometrial hyperplasia?

AEH develops when the lining of the uterus is exposed to estrogen over a long period without enough progesterone to balance it. Estrogen makes the lining grow. Progesterone, which is produced only after ovulation, matures the lining and prepares it to shed. When ovulation does not happen regularly, the lining stays under the influence of estrogen and keeps growing. Over time, the glands become crowded, and the cells begin to change.

Several situations produce this imbalance.

Irregular or absent ovulation — Common in polycystic ovary syndrome and in the years approaching menopause.
Excess body weight — Fat tissue converts other hormones into estrogen, raising the amount reaching the lining. This is the most common contributing factor after menopause.
Estrogen-only hormone therapy — Taken by someone who still has a uterus, this produces exactly this imbalance.
Tamoxifen — A medication used in breast cancer treatment. It blocks estrogen in the breast but acts like estrogen in the uterus.
Diabetes and high blood pressure — Both are associated with a higher risk, partly through their link with body weight.

AEH is most often diagnosed between the ages of 50 and 55, around and after menopause, though it occurs at any age once periods have begun.

A small number of cases occur in people with an inherited cancer syndrome. The main one is Lynch syndrome. Cancer of the uterus is the most common Lynch-related cancer in women, and it often appears at a younger age than usual. If your diagnosis came at a young age, or there is a strong family history of uterine or bowel cancer, your doctor may suggest genetic counseling.

What are the symptoms?

The most common symptom is abnormal bleeding from the uterus, and it is usually what leads to the biopsy.

Heavy or prolonged periods — Bleeding heavier or lasting longer than usual for you.
Bleeding between periods — Spotting or bleeding when a period is not expected.
Irregular cycles — Unpredictable timing, or long gaps followed by heavy bleeding.
Bleeding after menopause — Should always be assessed promptly, whatever the eventual cause.

Abnormal bleeding has many possible causes, most of which are not serious, which is why a tissue sample is taken to determine what is behind it.

How is the diagnosis made?

A pathologist examines tissue from the lining under a microscope to make the diagnosis. The sample is obtained in one of two ways.

Endometrial biopsy — A brief clinic procedure in which a thin flexible tube is passed through the cervix to collect a small piece of tissue. No anesthetic is usually needed.
Dilation and curettage — A short procedure under anesthetic in which tissue is scraped from the lining. This collects more tissue than a biopsy.

AEH does not usually form a visible mass. An ultrasound may show a thickened lining, and hysteroscopy may show the affected area as a raised or polyp-shaped patch, but neither test can make the diagnosis. The affected area is often localized rather than involving the whole lining, which matters for the reason described further below.

What does atypical endometrial hyperplasia look like under the microscope?

AEH is an area of the lining of the uterus in which crowded glands are lined by cells that look abnormal. Under the microscope, the pathologist looks for the following features.

Crowded, irregular glands — The glands sit close together and vary in shape, with less of the supporting tissue, called stroma, that normally separates them.
Abnormal-looking cells — The glandular cells have larger, darker, or more irregular nuclei than normal. This finding separates AEH from endometrial hyperplasia without atypia, where the glands are crowded, but the cells look normal.
A distinct area — The abnormal glands form a defined region that looks different from the lining around it.
A minimum size — The abnormal area has to reach a certain size, usually about 1 mm across, before the diagnosis is made.
No invasion — The glands stay within the lining and do not grow into the muscle wall. Invasion would make the diagnosis cancer rather than AEH.

Immunohistochemistry

Immunohistochemistry is a laboratory test that uses antibodies to detect specific proteins inside cells. It is not needed in every case, but it can help when the appearance is not clear-cut.

PTEN. Often lost. PTEN normally acts as a brake on cell growth, and losing it is one of the earliest changes in this condition.
PAX2. Often lost. PAX2 is normally present in endometrial glands, and its loss in an abnormal area helps separate this condition from a normal lining.
Mismatch repair proteins. Usually retained. These four proteins, MLH1, PMS2, MSH2, and MSH6, repair errors in DNA. When one or more is lost, further testing may follow to determine whether the cause is Lynch syndrome or a change that arose in the tissue itself.

Neither PTEN nor PAX2 loss alone is enough to make the diagnosis, and neither is present in every case. These stains support what the pathologist sees rather than replacing it.

Could there already be a cancer in my uterus?

This is the more immediate question. AEH is usually diagnosed on a small sample of the lining, and a cancer can be present in an area the sample did not reach. Among people diagnosed with AEH on biopsy who then have a hysterectomy, somewhere between 30 and 50 out of every 100 are found to have a cancer already present.

That number sounds alarming and needs context. These cancers are almost always found at an early stage and confined to the uterus, because the bleeding that led to the biopsy brought them to attention early. Being found this way is a good outcome, not a bad one.

The practical consequence concerns treatment choice. If you are considering keeping your uterus, your doctor will want to look more thoroughly first. Hysteroscopy, which uses a camera to inspect the lining directly and take targeted samples, is the most accurate way to do this. Imaging alone cannot rule out a small cancer.

What is the risk of cancer developing over time?

This is the second question, and it concerns the future rather than now. Without treatment, roughly 8 out of every 100 people with this diagnosis develop cancer of the uterus within about four years. The figure rises to roughly 28 out of every 100 by 20 years.

The comparison with the milder condition is useful. Endometrial hyperplasia without atypia carries a risk of fewer than 5 in 100 over the same 20 years. Atypia raises the risk roughly sixfold, which is why this condition is treated rather than watched.

Treatment substantially reduces the risk. Most people diagnosed with AEH and treated appropriately never develop cancer of the uterus.

How is atypical endometrial hyperplasia treated?

Treatment depends on your age, whether you have completed your family, and whether surgery is suitable for you.

Hysterectomy — Removal of the uterus is the definitive treatment, and it is usually recommended for those who have completed childbearing or who have gone through menopause. It both removes any hidden cancer and prevents new disease. The whole uterus, including the cervix, is removed, since leaving the cervix behind is not appropriate for this diagnosis.
Removing the tubes and ovaries — The fallopian tubes are usually removed at the same time. Whether the ovaries are removed depends on your age. After menopause, they are commonly removed; before menopause, keeping them is often preferred, since removing them brings on menopause early.
Progestin therapy — For those who wish to preserve fertility or cannot have surgery. Progestin is a synthetic form of progesterone, given as tablets or through a hormonal IUD. The evidence favors the IUD, which achieves a higher rate of the abnormal cells returning to normal than tablets alone.
Follow-up biopsies — An essential part of non-surgical treatment rather than an optional extra. Repeat sampling confirms that the abnormal cells have gone and checks that they have not returned.
Addressing the cause — Reviewing estrogen-only hormone therapy, managing polycystic ovary syndrome, or weight reduction where relevant.

One treatment is specifically not recommended. Endometrial ablation, a procedure that destroys the lining, should not be used for this condition. It leaves abnormal tissue behind and makes future bleeding much harder to assess.

If you are hoping to become pregnant, raise this early. Among people treated with progestin rather than surgery, reported pregnancy rates range from roughly 26 to 41 out of every 100. Most teams recommend proceeding with pregnancy once the lining has returned to normal, and discussing hysterectomy afterward.

What other findings may be described in the report?

Your report may describe other features of the lining alongside the AEH.

Hyperplasia without atypia — The lining outside the abnormal area may show crowded glands with normal-looking cells. This is reported separately.
Endometrial polyp — AEH sometimes arises within an endometrial polyp. When the polyp is removed whole, this may be favorable, since the abnormal tissue may have come out with it.
Sample adequacy — A note that the sample was scant or fragmented. This matters here, because a limited sample is less able to exclude a cancer elsewhere in the lining.
Metaplasia — Areas where the lining cells take on a different but still normal appearance. Common and not precancerous.
Findings in a hysterectomy specimen — If the uterus was removed, the report states whether cancer was found, and if so its type, grade, and how deeply it extended into the wall.

Questions to ask your doctor

Does my report use atypical hyperplasia, EIN, or both, and does it matter?
What features in my biopsy confirmed this diagnosis?
Was the sample adequate, or should it be repeated?
How likely is it that a cancer is already present?
Should I have a hysteroscopy before deciding on treatment?
Do you recommend a hysterectomy, or can I try progestin treatment first?
If I use progestin, would tablets or a hormonal IUD be better for me?
How often will I need follow-up biopsies, and for how long?
If I have a hysterectomy, will my ovaries be removed, and why?
What is my risk of developing cancer of the uterus in the future?
Should I be tested for Lynch syndrome, and does this affect my family?
Can I still become pregnant, and when would that be safe?
What can I do to reduce the chance of this coming back?