Key takeaways

• Endometrial hyperplasia is a thickening of the womb lining caused by an imbalance between oestrogen and progesterone. It is not cancer, but some forms carry a higher risk of developing into cancer if left unmanaged.
• If you are not on HRT, any bleeding after your periods have stopped for 12 consecutive months must be investigated by your GP or a specialist urgently. Do not wait.
• In women with a womb, combined HRT, oestrogen taken alongside the right progestogen, does not increase the risk of endometrial hyperplasia when prescribed correctly.

Endometrial hyperplasia and menopause: causes, symptoms and treatment

If you have been told your womb lining is thickened, or if you have experienced unexpected bleeding and are trying to understand what it means, this article is for you. Endometrial hyperplasia might sound alarming, but in most cases, it is a manageable and treatable condition. There are specific symptoms that should prompt you to seek clinical assessment without delay.

This guide explains what endometrial hyperplasia is, why the menopause transition raises the risk, what the symptoms mean, and what the UK clinical guidelines recommend for treatment. It also explains the relationship between HRT and endometrial health: a topic that matters directly to anyone with a uterus who is considering or already taking HRT.

Key takeaways

Here's what you need to know:

• Endometrial hyperplasia is a thickening of the womb lining caused by an imbalance between oestrogen and progesterone. It is not cancer, but some forms carry a higher risk of developing into cancer if left unmanaged.
• If you are not on HRT, any bleeding after your periods have stopped for 12 consecutive months must be investigated by your GP or a specialist urgently. Do not wait.
• In women with a womb, combined HRT, oestrogen taken alongside the right progestogen, does not increase the risk of endometrial hyperplasia when prescribed correctly.

What is endometrial hyperplasia, and is it the same as cancer?

The endometrium is the lining of the womb. During each menstrual cycle, it thickens in preparation for a potential pregnancy and then sheds during a period. Endometrial hyperplasia occurs when the lining grows thicker than it should, usually because oestrogen has been stimulating its growth without enough progesterone to counterbalance it.

Endometrial hyperplasia is not cancer. But it is a condition that requires investigation, because some forms carry a risk of progressing to cancer if left unaddressed.

There are two main types, and understanding the difference matters.

Endometrial hyperplasia without atypia:

In this type, the cells in the lining are thickened but look normal under a microscope. This is the more common type. A retrospective study of 315 perimenopausal women published in Clinics and Practice (2025) found that hyperplasia without atypia accounted for 74.6% of cases in this population group. The risk of it developing into cancer is low: fewer than 5 in 100 women with this type develop endometrial cancer over 20 years, and it responds well to treatment.

Atypical endometrial hyperplasia (also called endometrial intraepithelial neoplasia, or EIN):

In this type, the cells show abnormal changes under a microscope. This is a precancerous condition. More than 8 in 100 women with this type of hyperplasia will go on to develop endometrial cancer if it is left untreated. It requires more active management, and in most cases a hysterectomy is recommended.

The distinction between the two types is made by a biopsy. That is why investigation matters: symptoms alone cannot tell you which type you have.

Why menopause raises the risk: the oestrogen-progesterone connection

To understand why endometrial hyperplasia is more common during and around menopause, you need to understand what oestrogen and progesterone each do to the womb lining.

Oestrogen stimulates the womb lining to grow in preparation. Progesterone, produced after ovulation, signals the lining to stop growing and mature in anticipation of a fertilised egg. If the egg remains unfertilised, progesterone levels rapidly drop causing the lining to shed. When oestrogen and progesterone are in balance, the lining thickens and sheds in a regular monthly cycle.

During perimenopause, this balance breaks down in a specific way. As ovarian function becomes irregular, ovulation is frequently skipped. When ovulation does not occur, no progesterone is produced. The result is a cycle of unopposed oestrogenic stimulation: the womb lining thickens but is not regularly shed, and over time this cumulative exposure can lead to hyperplasia.

A 2024 review published in the International Journal of Women's Health by Mukherjee and colleagues describes this perimenopause-specific mechanism clearly: anovulatory cycles (where no egg is released), chronic luteal phase insufficiency (a shortening of the second half of your cycle), and persistent unopposed oestrogenic stimulation during the menopausal transition create the biological environment for pathological endometrial proliferation.

After menopause, the ovaries stop producing both hormones. But oestrogen is not entirely absent. The body continues to produce small amounts through adipose (fat) tissue and the adrenal glands. In women without progesterone to counterbalance it, even this very low level of oestrogen can continue to stimulate the endometrium over time.

The BMS Tools for Clinicians: Progestogens and endometrial protection (updated May 2026) confirms that unopposed oestrogen replacement is associated with a significant increase in endometrial hyperplasia risk that is both dose and time-dependent. This is why progesterone is a non-negotiable component of HRT for any woman with a uterus.

Who is most at risk?

Endometrial hyperplasia can affect any woman with a uterus, but certain factors increase the likelihood.

Obesity: Adipose (fat) tissue converts other hormones into oestrogen, raising circulating oestrogen levels independently of ovarian function. This is one of the strongest modifiable risk factors.

Polyendocrine metabolic ovarian syndrome (PMOS; formally known as PCOS): Women with PMOS frequently experience anovulatory cycles, creating exactly the progesterone-deficiency pattern described above, often from a much younger age.

Late natural menopause: A longer reproductive lifespan means more cumulative oestrogen exposure to the womb.

Oestrogen-only HRT without progesterone: Taking oestrogen without an appropriate progesterone significantly increases the risk of endometrial hyperplasia. This risk is dose- and duration-dependent.

Tamoxifen use: Tamoxifen, commonly used in breast cancer treatment, has a weak oestrogenic effect on the uterus and is associated with increased endometrial hyperplasia risk.

Diabetes and insulin resistance: Insulin resistance increases oestrogen production and may reduce the effectiveness of progesterone signalling.

Family history of endometrial or colon cancer: A family history of Lynch syndrome or other hereditary cancer conditions increases risk.

What are the symptoms, and when should you act urgently?

The most common symptom of endometrial hyperplasia is abnormal uterine bleeding. What this looks like depends on whether you are still having periods.

During perimenopause. Periods may become heavier, longer, or more irregular. Spotting between periods can occur. These changes are very common during perimenopause for reasons that have nothing to do with endometrial hyperplasia, but they can also be a sign of it, and persistent or heavy abnormal bleeding warrants investigation.

After menopause. Any bleeding after your periods have stopped for 12 consecutive months is classified as postmenopausal bleeding. This must be investigated urgently by your GP or a specialist. Do not adopt a wait-and-see approach.

While prompt investigation is essential, the majority of postmenopausal bleeding has a non-cancerous cause. A clinical review published in The Obstetrician and Gynaecologist (Jones et al., 2021) found that 90% of women with endometrial cancer present with postmenopausal bleeding. NICE NG12 (updated September 2020) mandates urgent referral for any woman with postmenopausal bleeding.

The same applies to bleeding that is unusually heavy during perimenopause: bleeding that soaks through protection in under an hour, passes large clots, or significantly interferes with daily life meets the clinical definition of heavy menstrual bleeding and should be assessed promptly.

Voy's menopause service is not a substitute for this investigation. If you have postmenopausal bleeding or heavy bleeding that concerns you, your first step is your GP or a gynaecologist.

How is it diagnosed?

Diagnosis is carried out through the NHS specialist gynaecology pathway. Voy's role is to support women in understanding why investigation matters and to ensure their HRT is appropriately prescribed, not to diagnose endometrial hyperplasia directly.

The standard UK diagnostic pathway involves three steps.

Transvaginal ultrasound (TVUS).

This is the first-line investigation for women with postmenopausal bleeding. The ultrasound assesses the endometrium and measures its thickness. In post-menopausal women, an endometrial thickness of 4mm or more on ultrasound is the threshold at which further investigation is recommended.

Endometrial biopsy.

A tissue sample is taken from the womb lining for laboratory analysis. This is the definitive test for determining whether hyperplasia is present and, critically, whether atypia is involved. The 2024 Cochrane systematic review by Nagar and colleagues supports the British Gynaecological Cancer Society’s recommendation for biopsy for postmenopausal bleeding and an endometrial thickness of 4mm or more.

Hysteroscopy.

In some cases, a hysteroscopy (a camera examination of the womb cavity) is performed to allow direct visualisation and guided biopsy. This provides the most accurate tissue sample.

Treatment options: what the UK guidelines recommend

Treatment depends on which type of hyperplasia is confirmed.

Endometrial hyperplasia without atypia

The definitive UK guidance is RCOG/BSGE Green-top Guideline No. 67 (Gallos, Alazzam and Clark), which recommends the LNG-IUS (levonorgestrel-releasing intrauterine system, also known as the Mirena coil) as the first-line medical treatment for endometrial hyperplasia without atypia. The LNG-IUS delivers progestogen directly inside the uterine cavity, achieves higher regression rates than oral progestogens, and has a more favourable bleeding profile.

Oral progestogens are an alternative when the LNG-IUS is not suitable or acceptable to the patient.

For mild cases, particularly where reversible risk factors such as obesity can be addressed, observation alone may be appropriate in the short term. This is a clinical decision made in discussion with your gynaecologist.

Women on sequential HRT who develop hyperplasia without atypia should be advised by their specialist to have a Mirena coil placed or to switch to continuous HRT (taking progesterone every day), per the RCOG guideline.

Follow-up endometrial surveillance (repeat biopsy at six months) is standard practice to confirm regression.

Atypical endometrial hyperplasia

Atypical hyperplasia is a precancerous condition, and the RCOG guideline recommends hysterectomy (surgical removal of the womb) as the definitive treatment.

“This sounds significant, but it is important to understand the context: hysterectomy at this stage, before cancer has developed, is a curative intervention. It is not a response to cancer. It is a prevention of it.”

Katy Jackson, Clinical Director - Women's Health

For younger women who wish to preserve fertility and who are not yet ready for hysterectomy, high-dose progestogen therapy (usually delivered via the Mirena or oral progestogens) is a fertility-sparing option. This pathway requires careful management by a specialist oncological gynaecology team, with regular biopsy and ultrasound surveillance, and is not appropriate for all women.

Endometrial hyperplasia and HRT: what you need to know

This is the section most directly relevant to women who are considering HRT or already taking it.

Oestrogen-only HRT in women with a womb significantly increases the risk of endometrial hyperplasia. This risk is dose- and duration-dependent. Oestrogen-only HRT is only appropriate for women who have had their womb removed.

Combined HRT, prescribed correctly, does not increase endometrial risk. When oestrogen is taken alongside an appropriate and matched progestogen, the endometrial lining is protected. The progestogen counterbalances the growth-stimulating effect of oestrogen, in exactly the same way your body’s own progesterone does a part of the menstrual cycle.

The type of progestogen regimen matters. The BMS Tools for Clinicians (updated May 2026) distinguishes between two approaches.

Sequential HRT involves taking oestrogen continuously and progestogen for at least 12 to 14 days per month. This produces a monthly withdrawal bleed. It is generally recommended for women in perimenopause who are still having periods. However, women who take sequential HRT for five years or more carry a small increased endometrial cancer risk compared to women not taking HRT. This risk is real but modest, and must be weighed against the significant symptom relief HRT provides.

Continuous HRT involves taking both oestrogen and progestogen every day. It does not produce a regular withdrawal bleed and provides more effective long-term endometrial protection. It is generally recommended for women who are post-menopausal or who have been on sequential HRT for several years.

Any unexpected bleeding while taking HRT should be discussed promptly. Breakthrough (or unscheduled) bleeding in the first three to six months of first starting combined HRT is incredibly common and usually not a cause for concern. Unscheduled bleeding after a dose increase or HRT preparation change is also common for up to three months afterwards. Persistent or unexpected bleeding after this initial period, or any bleeding in a woman on continuous combined HRT who had previously stopped having bleeds, should be assessed by your prescribing specialist without delay.

This is a clinical conversation best had with a specialist who has the time to review your full history. Voy's 45-minute consultations with BMS-trained menopause specialists are specifically structured to cover this kind of nuanced prescribing decision.

What this means if you are considering HRT, or already taking it

For any woman with a uterus, the core principle is straightforward: oestrogen must always be accompanied by an appropriate progestogen. This is not a restriction on HRT. It is how HRT is correctly and safely prescribed.

At Voy, all HRT prescribing for women with a uterus follows this principle. A BMS-trained menopause specialist will assess your individual history, your symptoms, and your preferences to identify the right formulation and regimen. That includes the progestogen component, and it includes discussion of whether sequential or continuous HRT is more appropriate for your stage of the menopause transition.

Across Voy members receiving menopause treatment, 88% felt more hormonally balanced at three months, compared to 62% receiving standard care. 93% reported an improvement in overall quality of life. These outcomes reflect what appropriately prescribed, carefully monitored HRT can achieve.

If you believe you may have experienced unexpected bleeding, please speak to your GP in the first instance. That is the right clinical pathway for investigation. A Voy consultation can follow once concerning causes have been ruled out, or run in parallel to support your understanding of the hormonal picture.

This content is for informational purposes and does not constitute medical advice. If you have postmenopausal bleeding or concerning symptoms, please contact your GP or a specialist urgently. Always consult a healthcare professional before making any changes to your treatment.