Conditions · Obstetrics and gynecology
Endometrial hyperplasia !
Endometrial hyperplasia is an overgrowth of the lining of the uterus, usually from too much oestrogen. Some forms can turn into cancer.
Updated 2026-11-01
Structures involved
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Why it happens
- Hyperplasia: physiologic and pathologic
- Precancerous conditions: when chronic inflammation, metaplasia or hyperplasia raise the risk
- Actions of estrogen and progesterone
- Aromatase (CYP19A1)
- Uterus and the endometrial cycle
What it is
Abnormal thickening of the endometrium caused by proliferation of glands out of proportion to stroma. It is classified by the presence or absence of cellular atypia; the atypical form is a precursor of endometrioid endometrial cancer.
Who gets it
Most often diagnosed in women in their 40s and 50s and after menopause. The rise of obesity and type 2 diabetes in Colombia and Latin America increases the number of women exposed to unopposed oestrogen, the main driver of this condition.
Causes
- Unopposed oestrogen: oestrogen stimulation without enough progesterone to balance it
- Chronic anovulation (polycystic ovary syndrome, perimenopause)
- Peripheral conversion of androgens to oestrogen in adipose tissue (obesity)
- Oestrogen-only hormone therapy in a woman with a uterus
- Tamoxifen (partial oestrogen agonist on the endometrium)
- Oestrogen-secreting ovarian tumours (granulosa cell tumour)
Risk factors
- Obesity
- Polycystic ovary syndrome
- Age over 35 and the menopausal transition
- Nulliparity, early menarche or late menopause
- Diabetes and hypertension
- Lynch syndrome (hereditary nonpolyposis colorectal cancer)
Pathophysiology
Oestrogen drives proliferation of the endometrial glands; progesterone normally converts the lining to a secretory state and triggers its shedding. When oestrogen acts for long periods without progesterone, the glands keep multiplying and crowd the stroma. With time, clonal genetic changes (for example loss of PTEN) can produce atypical cells, the step that links hyperplasia to endometrioid carcinoma.
Classification
- Hyperplasia without atypia (benign)
- Atypical hyperplasia / endometrioid intraepithelial neoplasia (premalignant)
Symptoms and signs
- Heavy, prolonged or irregular menstrual bleeding
- Bleeding between periods
- Any vaginal bleeding after menopause
- Sometimes no symptoms (found on imaging or biopsy)
Diagnosis
- Clinical
- Suspected in a woman with abnormal uterine bleeding and risk factors for unopposed oestrogen, especially a postmenopausal woman with any bleeding. Diagnosis is histological.
- Tests
- Endometrial biopsy (office aspiration sampling) is the key test; hysteroscopy with directed biopsy or dilatation and curettage when sampling is insufficient or symptoms persist. Haemoglobin if bleeding is heavy; pregnancy test in women of reproductive age.
- Imaging
- Transvaginal ultrasound measures endometrial thickness; in a postmenopausal woman with bleeding, a thin endometrium makes cancer unlikely and a thick one calls for sampling.
Differential diagnosis
- Endometrial carcinoma
- Endometrial polyp
- Submucous fibroid
- Atrophic endometrium (common cause of postmenopausal bleeding)
- Pregnancy-related bleeding
- Cervical lesion
Goal of treatment
Stop the abnormal bleeding, reverse the hyperplasia, and prevent or detect early progression to cancer, choosing between hormonal treatment and surgery according to atypia, age and fertility wishes.
Treatment
- Medical
- Hyperplasia without atypia: progestin therapy, either oral or delivered by a levonorgestrel-releasing intrauterine device, which acts directly on the endometrium.
- Lifestyle
- Correcting risk factors, mainly weight loss, and stopping oestrogen-only therapy where present.
- Surgical
- Atypical hyperplasia: total hysterectomy is the standard treatment because of the risk of coexisting or future cancer; endometrial ablation is not appropriate.
- Follow-up
- Repeat endometrial sampling at intervals during hormonal treatment, and fertility-sparing progestin therapy with close histological follow-up for selected young women with atypia.
Complications
- Progression to endometrioid endometrial carcinoma
- Coexisting carcinoma found at hysterectomy for atypia
- Iron-deficiency anaemia from heavy bleeding
- Recurrence after hormonal treatment
Prognosis
Hyperplasia without atypia usually regresses with progestins and rarely becomes cancer. Atypical hyperplasia carries a substantial risk of coexisting or later carcinoma, which is why hysterectomy is preferred; when it is treated, the outlook is excellent.
Prevention
- Adding a progestogen to oestrogen therapy in women with a uterus
- Healthy weight
- Regular progestin withdrawal or hormonal contraception in chronic anovulation
- Prompt evaluation of postmenopausal bleeding
Test yourself
Think of the answer, then tap the question to see it.
What hormonal state is the main cause of endometrial hyperplasia?
Unopposed oestrogen: oestrogen stimulation without enough progesterone, as in obesity, anovulation or oestrogen-only therapy.
Which histological feature determines the risk of progression to cancer?
Cellular atypia; atypical hyperplasia is a precursor of endometrioid endometrial carcinoma.
What is the key test in a postmenopausal woman with bleeding and a thick endometrium?
Endometrial biopsy (tissue sampling) to exclude hyperplasia and cancer.
What is the standard treatment of atypical hyperplasia in a woman who has completed childbearing?
Total hysterectomy.
Related conditions
- Endometrial cancer
- Abnormal uterine bleeding
- Polycystic ovary syndrome
- Obesity
- Menopause and climacteric syndrome
- Type 2 diabetes mellitus
- Uterine fibroids (leiomyomas)
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Endometrial Hyperplasia (Cleveland Clinic, 2024).
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