Atypical endometrial hyperplasia is a pathological overgrowth of the inner layer of the uterus with the appearance of atypical cells. It is provoked by an excess of estrogens and a lack of progesterone. It is considered as a precancerous disease. It can develop at any age, but it is more often detected after 45 years. It is accompanied by menstrual irregularities and uterine bleeding (menorrhagia, metrorrhagia). The diagnosis is established on the basis of complaints, anamnesis and data from additional studies. Treatment – hormone therapy, curettage or ablation of the mucous membrane.
N85.1 Adenomatous endometrial hyperplasia
Atypical endometrial hyperplasia is an increased proliferation of the endometrium, accompanied by a change in cell morphology. There are no data on the prevalence. Pathology is more often detected in women aged 45-55 years. Prolonged recurrent hyperplasia during menopause and menopause is considered as a precancerous disease. The probability of malignant degeneration, depending on the form of the disease, ranges from 8 to 29%. Atypical endometrial hyperplasia is often combined with other diseases of the reproductive system. Treatment tactics are determined depending on the age of the patient, her desire to have children, the presence or absence of concomitant genital and extragenital pathology. The treatment is carried out by specialists in the field of clinical gynecology and oncology.
The development of this disease is caused by an increase in estrogen levels, a decrease in progesterone levels and the presence or absence of ovulation. Estrogens and progesterone are involved in the regulation of cyclic changes in the endometrium. In the first phase of the menstrual cycle, estrogens provide cell proliferation. In the second phase, progesterone suppresses proliferation and stimulates secretion. In the absence of ovulation, relative or absolute hyperestrogenemia, the secretion phase either does not occur, or does not manifest itself clearly enough. The cells of the functional layer of the endometrium continue to grow, hyperplasia occurs.
Predisposing factors for the development of atypical endometrial hyperplasia are:
- age-related changes in the level of sex hormones;
- early onset of menstruation;
- late onset of menopause;
- diseases and conditions accompanied by anovulation and ovarian dysfunction (polycystic ovary syndrome, hormone-producing ovarian tumors);
- somatic pathologies: obesity, hypertension, diabetes mellitus and other diseases of the endocrine system;
- inflammatory diseases and congenital anomalies of the reproductive system;
- multiple abortions and diagnostic curettage;
- hereditary predisposition;
- taking estrogen-containing drugs and tamoxifen.
Atypical endometrial hyperplasia is characterized by a pathological proliferation of the functional layer of the uterine mucosa, while the glandular tissue of the epithelium undergoes more pronounced changes compared to the elements of the stroma. In the process of histological examination, an increase in the number of glands and swelling of the stroma is revealed. The glands are located close to each other. The vessels are arranged unevenly. Epithelial cells with hyperchromic nuclei. Numerous pathological mitoses are determined.
Depending on the location of glandular cells, there are two forms of atypical endometrial hyperplasia: simple and adenomatous. With a simple form, there is an increase in the number and excessive proliferation of cells without changing the structure of the mucous membrane. With an adenomatous form, special structures are formed from glandular cells that are absent in the endometrium of a healthy uterus. These structures can be located throughout the endometrium (diffuse form) or form separate foci (focal form). In addition, areas of adenomatous hyperplasia can be found in the area of uterine polyps.
The main symptom of this disease is uterine bleeding. In most patients, such bleeding occurs against the background of a delay in menstruation for a period of 1-3 months. Less often (as a rule, in the absence of obesity and obvious endocrine pathology), regular cycles are observed with a duration of menorrhagia of more than 7 days. Approximately a quarter of patients with atypical endometrial hyperplasia have anovulatory uterine bleeding. In 5-10% of cases, metrorrhagia is diagnosed. There may be scant spotting in the middle of the menstrual cycle or in the absence of menstruation.
More than half of the patients are diagnosed with obesity. In 70-75% of cases, excess weight is combined with virilization symptoms: male-type hair loss, coarsening of the voice, enlargement of the clitoris, etc. At normal body weight, signs of virilization are observed in 30% of patients. All categories of patients with atypical endometrial hyperplasia often suffer from chronic inflammatory diseases of the reproductive system, miscarriage, secondary infertility, endometriosis, adenomyosis and mastopathy, however, in patients without obesity, these pathological conditions are detected twice as often.
The diagnosis is established on the basis of complaints, anamnesis data and the results of instrumental studies. During the survey, the gynecologist finds out the age of the menarche, determines the duration of the cycle, the duration and abundance of menstruation, clarifies whether there were cycle delays and spotting. Then the doctor performs a gynecological examination and prescribes a transvaginal ultrasound to assess the condition of the endometrium (its structure, thickness, uniformity) and identify pathological changes in the ovaries (signs of a tumor, cyst or POS).
The accuracy of the diagnosis of hyperplastic processes during ultrasound is 60-70%, however, it is usually not possible to confirm or refute endometrial atypia using ultrasound. The patient is referred for ultrasound on the 5-7 day of the cycle. With prolonged bleeding, ultrasound is prescribed regardless of the phase of the cycle. Normally, at childbearing age, the thickness of the uterine mucosa is no more than 7 mm, with postmenopause lasting less than 5 years – no more than 5 mm, with postmenopause lasting more than 5 years – no more than 4 mm. The increase in thickness, the heterogeneity of the structure and the presence of echogenic inclusions make it possible to suspect endometrial hyperplasia.
In some cases, aspiration biopsy is performed after ultrasound, followed by histological or cytological examination of the aspirate. This procedure belongs to the category of screening tests and is performed on an outpatient basis. However, the gold standard for the diagnosis of atypical endometrial hyperplasia is hysteroscopy and separate diagnostic curettage. The informative value of the study is more than 90%.
If there is a suspicion of POS and metabolic syndrome, blood tests are prescribed to determine the level of progesterone, testosterone, estradiol, LDH, PSG, adrenal and thyroid hormones. Mammography is performed. With frequent relapses, laparoscopy is performed with biopsy or wedge-shaped resection of the ovaries and subsequent histological examination of the material.
Atypical endometrial hyperplasia is differentiated from other diseases that provoke uterine bleeding:
- submucosal fibroma of the uterus;
- malignant tumors of the uterine mucosa (adenocarcinoma, cancer of the uterine body).
Treatment of this pathology can be both conservative and operative, carried out on an outpatient basis or in a hospital. Indications for planned hospitalization in the reproductive age are bleeding and spotting, in postmenopause – bleeding, prolonged watery or purulent discharge. Emergency hospitalization is indicated for heavy bleeding. The tactics of treatment of atypical endometrial hyperplasia is determined taking into account the age of the patient, her desire to have children, the presence of somatic diseases and diseases of the reproductive system (especially adenomyosis or fibroids), the form of atypical endometrial hyperplasia and the number of relapses.
- Stopping the bleeding. In the presence of metrorrhagia or menorrhagia, measures are taken at the first stage to stop bleeding and replenish blood loss. Perform endometrial scraping, prescribe oxytocin and cold on the lower abdomen. Iron preparations are used. If necessary, blood and blood substitutes are transfused. Infusion therapy is performed using isotonic solution, glucose solution, gelatinol or dextran to restore the water-electrolyte balance and improve the rheological properties of blood.
- Pharmacotherapy. Patients with atypical endometrial hyperplasia undergo hormone therapy for 3-6 months aimed at suppressing the proliferation of the mucous membrane. Subsequently, hormonal drugs are prescribed to restore the two-phase menstrual cycle or achieve a stable menopause. Hormone therapy is carried out against the background of taking vitamins, hyposensitizing drugs and hepatoprotectors.
- Surgical treatment. As indications for surgical treatment, all cases of atypical endometrial hyperplasia in the post-menopausal period are considered, as well as the presence of contraindications to hormone therapy, the lack of effect from conservative therapy and relapses of the disease in women of reproductive age. Abalation of the endometrium is performed – a minimally invasive surgical intervention, the purpose of which is to destroy or remove the entire thickness of the mucous membrane. The operation is performed hysteroscopically using high-frequency currents.
Dispensary observation after conservative treatment is carried out for 5 years, after surgery – for 6 months.
The prognosis for atypical endometrial hyperplasia depends on age, the tendency of the disease to relapse, the presence of concomitant genital and extragenital pathology. Complete recovery with preservation of reproductive function, recovery with loss of reproductive function or rebirth into a malignant tumor of the endometrium is possible. In the latter case, a hysterectomy or a pangisterectomy (removal of the uterus together with an adnexectomy) will be required. Prognostically unfavorable are combinations of atypical endometrial hyperplasia with any metabolic disorders and diseases of the endocrine system, especially at the age of over 45 years. The risk of malignant degeneration in the simple form of the disease is 8%, with adenomatous – 29%.