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In some cases, endometrial hyperplasia may progress to endometrial carcinoma, although most cases are benign and respond well to treatment.
Symptoms
In the majority of cases, endometrial hyperplasia develops as a result of persistently elevated estrogen levels combined with insufficient levels of hormones such as progesterone, which normally counteract the proliferative effects of estrogen.
The main symptom is abnormal vaginal bleeding, although in some cases the condition may be almost asymptomatic.
The most common signs of endometrial hyperplasia include:
• vaginal bleeding between menstrual periods or after menopause,
• heavy menstrual bleeding,
• menstrual periods lasting longer than usual,
• pain during sexual intercourse,
• amenorrhea (absence of menstruation),
• anovulatory cycles (menstrual cycles without ovulation).
Diagnosis
The diagnosis of “endometrial hyperplasia” is usually established based on these symptoms. Diagnostic methods include:
• Transvaginal ultrasound: allows visualization of the endometrial lining. Suspicion arises when the endometrium appears excessively thickened, in which case histological examination is required for confirmation and differentiation of hyperplasia types.
• Endometrial aspiration biopsy using flexible aspiration cannulas (aspiration curettage): enables sampling of endometrial tissue.
• Hysteroscopy: allows direct visualization of the uterine cavity and its mucosa, with the possibility of biopsy if necessary.
Types of Hyperplasia
Following diagnosis, the type of endometrial hyperplasia can be determined. The main types include:
• Simple hyperplasia: characterized by active proliferation of endometrial cells. It may regress spontaneously or with medical treatment and carries a low risk of malignant transformation (approximately 1% risk of endometrial carcinoma).
• Complex hyperplasia: excessive proliferation of endometrial cells with structural changes in the glandular component and a higher malignant potential than the simple type (risk below 5%). Non-atypical hyperplasia involves normal cells and glands that are increased in number and size. When cellular changes predisposing to malignancy occur, the condition is termed atypical hyperplasia (either simple or complex).
• Atypical endometrial hyperplasia: characterized by cellular atypia and architectural glandular abnormalities without stromal invasion. It has a high potential for malignant transformation and is considered a precancerous lesion (risk 25–30%).
The average time for progression from non-atypical hyperplasia to carcinoma is about 10 years, while for atypical hyperplasia it is approximately 4 years. It tends to develop into endometrial adenocarcinoma more frequently in postmenopausal women, with the peak incidence around age 60. Endometrial carcinoma is found in 12–42% of women diagnosed with atypical endometrial hyperplasia.
Causes
Endometrial hyperplasia results from chronic, prolonged estrogen exposure and is therefore more common in women with chronic anovulation or obesity.
Risk factors include:
• obesity,
• polycystic ovary syndrome,
• nulliparity,
• early menarche,
• late menopause,
• estrogen-only hormone therapy,
• estrogen-secreting tumors,
• smoking,
• diabetes mellitus,
• thyroid dysfunction,
• family history of uterine, ovarian, or colorectal cancer.
Genetic conditions such as Lynch syndrome also increase the risk of endometrial carcinoma and therefore of endometrial hyperplasia.
In all cases, it represents a response to prolonged estrogenic stimulation insufficiently balanced by progesterone. Endometrial hyperplasia is rare in women under 30 years old, its incidence increases after age 45, and peaks between 50 and 54 years.
Treatment
Therapy primarily depends on the histological diagnosis (type of hyperplasia and associated malignant potential), the presence or absence of symptoms, the patient’s age, and reproductive plans.
For endometrial hyperplasia without atypia, management focuses on correcting hyperestrogenic states, for example by weight reduction in obese patients. Benign hyperplasia can often be managed conservatively through observation with periodic ultrasound and/or histological control, without immediate progesterone therapy.
In women with typical hyperplasia, treatment may include hormonal therapy to provide additional progesterone, which helps normalize the estrogen-progesterone ratio and prevent excessive endometrial proliferation.
Women with atypical hyperplasia are at increased risk of uterine cancer and may require more radical management. The most common option is hysterectomy (surgical removal of the uterus). However, women wishing to preserve fertility may consider alternative options.
A frequent alternative to hysterectomy is intensive hormonal therapy: for women desiring pregnancy, treatment typically begins with oral contraceptives or progesterone-based therapy, under close medical supervision (initially every 3 months, then annually) to monitor progression.
Prevention
Can endometrial hyperplasia be prevented?
Postmenopausal women are more prone to developing this condition due to changes in hormonal balance and menstrual cycles. Although endometrial hyperplasia cannot be entirely prevented, it is closely associated with obesity. Increased adipose tissue elevates endogenous estrogen production — a known risk factor.
Therefore, all patients with benign endometrial hyperplasia are advised to adopt a healthier lifestyle and achieve weight reduction. Additional preventive measures should be discussed with the attending physician.
Symptoms
In the majority of cases, endometrial hyperplasia develops as a result of persistently elevated estrogen levels combined with insufficient levels of hormones such as progesterone, which normally counteract the proliferative effects of estrogen.
The main symptom is abnormal vaginal bleeding, although in some cases the condition may be almost asymptomatic.
The most common signs of endometrial hyperplasia include:
• vaginal bleeding between menstrual periods or after menopause,
• heavy menstrual bleeding,
• menstrual periods lasting longer than usual,
• pain during sexual intercourse,
• amenorrhea (absence of menstruation),
• anovulatory cycles (menstrual cycles without ovulation).
Diagnosis
The diagnosis of “endometrial hyperplasia” is usually established based on these symptoms. Diagnostic methods include:
• Transvaginal ultrasound: allows visualization of the endometrial lining. Suspicion arises when the endometrium appears excessively thickened, in which case histological examination is required for confirmation and differentiation of hyperplasia types.
• Endometrial aspiration biopsy using flexible aspiration cannulas (aspiration curettage): enables sampling of endometrial tissue.
• Hysteroscopy: allows direct visualization of the uterine cavity and its mucosa, with the possibility of biopsy if necessary.
Types of Hyperplasia
Following diagnosis, the type of endometrial hyperplasia can be determined. The main types include:
• Simple hyperplasia: characterized by active proliferation of endometrial cells. It may regress spontaneously or with medical treatment and carries a low risk of malignant transformation (approximately 1% risk of endometrial carcinoma).
• Complex hyperplasia: excessive proliferation of endometrial cells with structural changes in the glandular component and a higher malignant potential than the simple type (risk below 5%). Non-atypical hyperplasia involves normal cells and glands that are increased in number and size. When cellular changes predisposing to malignancy occur, the condition is termed atypical hyperplasia (either simple or complex).
• Atypical endometrial hyperplasia: characterized by cellular atypia and architectural glandular abnormalities without stromal invasion. It has a high potential for malignant transformation and is considered a precancerous lesion (risk 25–30%).
The average time for progression from non-atypical hyperplasia to carcinoma is about 10 years, while for atypical hyperplasia it is approximately 4 years. It tends to develop into endometrial adenocarcinoma more frequently in postmenopausal women, with the peak incidence around age 60. Endometrial carcinoma is found in 12–42% of women diagnosed with atypical endometrial hyperplasia.
Causes
Endometrial hyperplasia results from chronic, prolonged estrogen exposure and is therefore more common in women with chronic anovulation or obesity.
Risk factors include:
• obesity,
• polycystic ovary syndrome,
• nulliparity,
• early menarche,
• late menopause,
• estrogen-only hormone therapy,
• estrogen-secreting tumors,
• smoking,
• diabetes mellitus,
• thyroid dysfunction,
• family history of uterine, ovarian, or colorectal cancer.
Genetic conditions such as Lynch syndrome also increase the risk of endometrial carcinoma and therefore of endometrial hyperplasia.
In all cases, it represents a response to prolonged estrogenic stimulation insufficiently balanced by progesterone. Endometrial hyperplasia is rare in women under 30 years old, its incidence increases after age 45, and peaks between 50 and 54 years.
Treatment
Therapy primarily depends on the histological diagnosis (type of hyperplasia and associated malignant potential), the presence or absence of symptoms, the patient’s age, and reproductive plans.
For endometrial hyperplasia without atypia, management focuses on correcting hyperestrogenic states, for example by weight reduction in obese patients. Benign hyperplasia can often be managed conservatively through observation with periodic ultrasound and/or histological control, without immediate progesterone therapy.
In women with typical hyperplasia, treatment may include hormonal therapy to provide additional progesterone, which helps normalize the estrogen-progesterone ratio and prevent excessive endometrial proliferation.
Women with atypical hyperplasia are at increased risk of uterine cancer and may require more radical management. The most common option is hysterectomy (surgical removal of the uterus). However, women wishing to preserve fertility may consider alternative options.
A frequent alternative to hysterectomy is intensive hormonal therapy: for women desiring pregnancy, treatment typically begins with oral contraceptives or progesterone-based therapy, under close medical supervision (initially every 3 months, then annually) to monitor progression.
Prevention
Can endometrial hyperplasia be prevented?
Postmenopausal women are more prone to developing this condition due to changes in hormonal balance and menstrual cycles. Although endometrial hyperplasia cannot be entirely prevented, it is closely associated with obesity. Increased adipose tissue elevates endogenous estrogen production — a known risk factor.
Therefore, all patients with benign endometrial hyperplasia are advised to adopt a healthier lifestyle and achieve weight reduction. Additional preventive measures should be discussed with the attending physician.
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