Adenomatosis and adenomyosis, the names of these two diseases sound almost the same, but in reality they are two completely different pathologies. The only thing that unites them is the organ that they affect to one degree or another.
For example, adenomyosis is a form of endometriosis in which the endometrium grows into the submucosal and muscular layer of the uterus. Adenomatosis is a special condition of the uterus that precedes the development of a cancerous tumor. Both diseases require immediate treatment.
With adenomyosis, active growth of endometrial tissue occurs, but it is considered benign, although in this case the cells penetrate into the structures of other tissues. This process is accompanied by inflammation of the myometrium. Adenomyosis is also called internal uterine endometriosis.
And at the same time, doctors say that endometriosis and adenomyosis are not exactly the same thing. There are some differences between these two conditions that make it possible to distinguish adenomyosis as a separate pathology, and not just a special form of endometriosis.
The first difference is that, spreading to other organs and tissues, the endometrium continues to exist, obeying the same laws as the endometrium located in the uterus.
Source: vrachmatki.ru
The process of penetration of the endometrium into the myometrium is accompanied by severe inflammation, which can ultimately lead to the destruction of uterine tissue and transition to adenomatosis, which is the same precancerous condition.
Adenomyosis can take one of three forms: diffuse, nodular and mixed. For example, with the diffuse form, pockets of endometrial tissue are formed, which can penetrate into the myometrium to varying depths.
In advanced forms, fistulas leading into the pelvis are formed in place of such pockets. In the nodular form of adenomyosis, the proliferation of predominantly glandular epithelium occurs.
In this case, a large number of fluid-filled nodes form. In the first case, when pockets form, adenomyosis spreads throughout the uterus. In the nodular form, the foci of endometrial tissue have a clear demarcation. In this case, treating the pathology is much easier.
Adenomatosis
A completely different picture is observed with adenomatosis. In this case, there is an uncontrollable growth of cells that form the endometrium. With the same adenomyosis, endometrial cells have a high degree of predisposition to degeneration.
In this case, doctors have to deal with endometrial hyperplasia. With this pathology, glandular and diffuse forms are also distinguished. In the diffuse form, hyperplasia covers the entire mucous membrane of the uterus. In this case, the disease progresses much more slowly than with the glandular form and less often turns into cancer.
In the diffuse form, accelerated division of cells occurs, and at the same time their structure almost completely changes. With glandular hyperplasia, the uterus thickens and increases in size. A feature of this form of adenomatosis is the disappearance of a clear distinction between the layers, which is present in a healthy uterus.
Causes
The reasons why the endometrium begins to grow into the adjacent layers of the uterus during adenomyosis are still unknown, although the study of this pathology has been going on for a long time. This pathology can be detected in women of different age categories. But more and more doctors are inclined to believe that the growth of the endometrium is due to changes in hormonal levels, while the patient almost always has a severely weakened immune system.
Less commonly mentioned among the causes of adenomyosis are hereditary predisposition, pathological changes in the menstrual cycle, excess weight and problems arising from difficult childbirth. In each specific case of disease, doctors will have to conduct a thorough examination to determine the causes of this pathology.
Adenomatosis primarily occurs when the hormonal balance changes towards an increase in estrogen. Under the influence of this hormone, the menstrual cycle fails, uterine bleeding appears, and infertility develops. With adenomatosis, doctors first of all look for atypical cells in order to thus assess the ability of tissues to degenerate.
Symptoms
With adenomyosis, there is a greater increase in bleeding during menstruation, as well as an increase in its duration, although cases of uterine bleeding between menstruation also occur. With both the first and second diseases, anemia can develop. Only with adenomatosis its appearance is explained by bleeding that occurs during the intermenstrual period.
Anemia leads to weakness and drowsiness. A lack of hemoglobin in the blood is accompanied by pallor of the skin and mucous membranes. For the same reason, performance decreases.
With adenomyosis, spotting appears a few days before menstruation, and the same discharge may occur after menstruation ends. With adenomyosis, pain syndrome is pronounced. The pain intensifies significantly before menstruation and completely disappears after its completion. All symptoms of adenomyosis begin to appear in the later stages of the disease, when the pathological process has sufficiently spread throughout the uterus.
Adenomatosis is much more difficult to detect than adenomyosis. In this case, a full comprehensive examination of the patient will have to be carried out. The symptoms that occur with this pathology are indirect in nature and require confirmation when making a diagnosis.
Among the symptoms of adenomatosis, the first thing noted is the appearance of nagging pain in the lower abdomen. This pathology is characterized by the appearance of bloody discharge between menstruation. But such discharge is a symptom of many pathologies associated with the uterus. Therefore, their presence is clearly not enough to make a diagnosis.
The same can be said about an irregular monthly cycle. An additional cause for concern may be the presence of excess weight, hair growth in places uncharacteristic for the female body.
Another indirect sign of adenomatosis may be an increase in insulin levels in the blood. Therefore, an accurate diagnosis is established after ultrasound and histology of the endometrium. At the same time, doctors determine the existing thickness of the uterine mucosa and identify the type of hyperplasia. Additionally, blood sugar levels are checked.
Treatment
The main drugs in the treatment of adenomatosis are gestagens and oral combined contraceptives. But not in all cases, conservative treatment gives the desired effect. Then surgical removal of the hyperplastic epithelium is performed.
Treatment of adenomyosis should also take into account the causes of its occurrence. Treatment should also prevent recurrence of the pathology. Therapy begins after receiving ultrasound results, as well as checking the mucous membrane for the presence of atypical cells.
Adenomyosis very quickly becomes chronic, so treatment tactics must be well thought out. The choice of drugs depends on the form of adenomyosis and the degree of spread of foci of pathology. Hormonal drugs are selected for treatment. In severe cases, surgical treatment is performed.
Description:
Familial polyendocrine adenomatosis (FPEA) is a disease characterized by the development of tumors in two or more endocrine glands, most often in the islets of Langerhans of the pancreas and the parathyroid gland (source - chief cells).
Symptoms:
There are 3 types of SPEA:
- Type I (Wörmer syndrome, 131100, 1C13, MEN1, R gene):: parathyroid glands, islets of Langerhans of the pancreas and pituitary gland are involved
- occurs in approximately 90% of patients (a quarter of them have hyperplasia of all parathyroid glands)
- Tumors of the islet tissue of the pancreas are found in 80% of patients (usually gastrinoma, glucagonoma or insulinoma)
- observed in 65% of cases
- Stomach ulcers caused by pancreatic gastrinoma.
- Type II (Sipple syndrome, #171400, 10qll.2, RET oncogene, , R): the disease should be suspected in any relative of the patient who has medullary
- Medullary thyroid carcinoma is found in all patients
- observed in approximately 40% of patients. The tumors are usually bilateral and sometimes malignant. In most cases, symptoms of pheochromocytoma occur later than signs of thyroid cancer
- Hyperplasia of the parathyroid glands appears in 60% of patients.
- Type III (#162300, 10qll.2, oncogene RET, R)) is regarded as a variant of type II (sometimes referred to as type lib, then Sipple syndrome is designated as type IIa)
- As with SPEA type II, medullary thyroid gland and pheochromocytoma develop. The most characteristic signs: skeletal deformities and multiple mucous membranes
- SPEA III manifests itself at a younger age (usually up to 20 years) and is much more aggressive; early diagnosis is necessary.
Causes:
The disease has a hereditary etiology.
Treatment:
For treatment the following is prescribed:
SPEA I
The first step is to eliminate the hyperparathyroid state. As a result, gastrin secretion may be reduced, which favors the healing of stomach ulcers. Subtotal parathyroidectomy is necessary because the disease usually involves hyperplasia of all four glands. If hypergastrinemia does not respond to treatment, the gastrin-producing tumor must be removed. If the pancreatic tumor cannot be removed, and the use of H2 blockers does not lead to healing of the ulcers, gastrectomy or gastrectomy is performed. Pituitary tumors are removed by transsphenoidal hypophysectomy.
SPEA II
Medullary thyroid carcinoma (treatment is effective at the precancer stage [C-cell hyperplasia], total thyroidectomy is indicated). Pheochromocytoma or hyperplasia of the adrenal medulla: first of all, they are treated (before thyroidectomy), otherwise, when performing surgery on the thyroid gland, a hypertensive crisis is possible. Hyperparathyroidism can be cured by total thyroidectomy.
SPEA III. Treatment is similar to type II. Because type III is particularly aggressive, early and definitive treatment is necessary.
Atypical endometrial hyperplasia (AHE) can be considered as a borderline state between simple hyperplasia and initial well-differentiated endometrial adenocarcinoma. It is often very difficult for a pathologist to carry out differential diagnosis of these hyperplastic changes on material from curettage of the uterine mucosa.
It is no coincidence that the diagnosis of adenocarcinoma, originally established from scrapings of the uterine mucosa, was actually found to be AGE.
Historically, therapeutic approaches to the treatment of AGE have undergone significant evolution, which can be divided into four stages. At the first stage Clinicians were of the opinion that it was possible to monitor these patients, limiting themselves to symptomatic therapy.
This stage can be described as a “hands-off” tactic. To some extent, this approach was justified by observations of a long period of stable AGE without signs of disease progression. But the most important thing that objectively determined this “non-intervention” approach was the lack of effective hormonal drugs that could prevent the proliferation of the endometrial epithelium.
Second phase characterized by a radical approach to treatment tactics, when the treatment of patients with AGE of any age was standard and hysterectomy was performed, which was often supplemented by oophorectomy. At the same time, AGEs were often not found in the removed specimen, which cast doubt on the advisability of the operation, especially in patients of reproductive age.
Third stage indicated by the appearance in clinical practice of highly active synthetic progestins and combined estrogen-progestin (contraceptive) drugs. At this stage, hormone therapy for AGE became widespread. At the same time, it was believed that the operation fades into the background, being appropriate mainly if hormonal treatment fails.
Fourth stage characterized by individualized use of hormone therapy and surgery depending on the patient’s age and the morphological form of AGE. Individualization of treatment tactics is especially indicated in the reproductive period, when treatment is designed to preserve not only the organ, but also menstrual and generative functions.
Treatment of AGE
When planning treatment for patients with AGE It is important to remember that atypical changes determined in the endometrial scraping material can only serve as a background to pre-existing endometrial adenocarcinoma. Thus, when studying surgical microslides, AGE was combined with adenocarcinoma in 12% of cases (before 40 years of age) and up to 40% (after 50 years of age).
Clarification of the diagnosis is facilitated by performing hysteroscopy (hysterography) and targeted biopsy.
An adequate treatment method for atypical endometrial hyperplasia at any age is therapy.
Treatment with progestins
Treatment with progestins is aimed at preventing the transition of atypical hyperplasia to invasive cancer, increasing structural and cellular differentiation, secretory transformation and desquamation of the endometrium, with the subsequent development of atrophic changes in the mucous membrane of the uterine cavity.
Recent studies have shown the ability of tamoxifen to increase the sensitivity of the endometrium to progestins, due to its ability to increase the synthesis of cytoplasmic receptors for progestins (Vishnevsky A. S., et al., 1993). These data made it possible to justify the need to include tamoxifen in the progestin therapy regimen for AFL at the first stage of treatment.
Scheme of combined progestin therapy.
A two-stage regimen of combined progestin therapy seems to be the most effective.
- At the first stage, lasting 6 months, a progestin is administered continuously (oxyprogesterone capronate 500 mg 3 times a week, intramuscularly, or Medroxyprogesterone acetate (Provera) 250 mg per day, orally, in combination with tamoxifen at a dose of 20 mg per day, throughout the first stage of treatment) in order to eliminate atypical changes in the epithelium of the glands, reduce the proliferative activity of cells and transition the mucous membrane of the uterine cavity to a state of atrophy. Clinically, this manifests itself in the cessation of bleeding and the establishment of persistent amenorrhea for the entire period of treatment. After a two-month course of treatment (total dose of OPC 12.0 g, Provera - 14.0 g), a control diagnostic curettage of the uterine cavity mucosa is necessary. If elements of atypical hyperplasia are preserved in the scraping, then a conclusion is made about insufficient sensitivity to progestins and the issue of indications for surgical treatment is discussed. If the elements of AGE have regressed, then progestin therapy continues further, up to 6 months: OPC 500 mg 2 times a week - 3rd and 4th months, and 500 mg once a week - 5th and 6th months.
Provera is prescribed respectively at 250 mg 3 times a week for the 3rd and 4th months and 250 mg 2 times a week for the 5th and 6th months. The dose of Tamoxifen remains the same - 20 mg per day.
As a result of this approach to the treatment of AGE, it is possible to achieve cure in 80–85% of patients, resulting in complete regression of AGE, secretory transformation, and then atrophy of the mucous membrane. At the second stage of treatment, after histologically proven regression of AGE in patients in the reproductive period (up to 46 years), the main task is the formation of a correct menstrual cycle.
For this purpose: - the patient, from the 5th day of a menstrual-like reaction, which can occur 8-10 days after the last administration of progestin, is transferred to cyclic treatment with combined (estrogen-progestin) contraceptive drugs prescribed according to the contraceptive regimen for 4-6 cycles. In this case, preference is given to second-generation drugs with high progestin activity (Microgynon, Rigevidon). In patients over 46 years of age (46–55 years), steroid contraceptives are prescribed on a continuous basis (1 tablet per day) for 3–4 months, which leads to to maintain persistent amenorrhea.
- In young people Those interested in pregnancy, at the second stage of treatment, the use of ovulation stimulants (clomiphene citrate, Gn-Rg analogues) is indicated. The onset of pregnancy during this treatment with its natural gestagenic effect on the uterine mucosa prevents the possibility of relapse of AGE. withdrawal of progestins.
For polycystic ovary syndrome in young patients, after achieving cure for AGE, it is advisable to perform wedge resection of the ovaries in order to restore ovulatory menstrual cycles and prevent relapse of the disease.
Recently, convincing clinical evidence has been obtained that antiestrogen Tamoxifen can significantly increase the sensitivity of endometrial cancer to progestins. Therefore, in some exceptional cases ( the young age of the patient or the presence of a high risk of surgical treatment in a patient with aggravated somatic pathology in perimenopause), with persistent AGE after the first two months of treatment, it is possible to continue progestin therapy in combination with Tamoxifen (20 mg per day, orally) for the next two (third and fourth) months of treatment. If by the fourth month of treatment, histological examination of scrapings of the mucous membrane does not detect AGE, then hormone therapy continues for the fifth and sixth months. If elements of AGE persist, then the issue of surgical treatment is reconsidered.
Consequently, depending on the age of the patient, hormone therapy at the second stage is modified, but has the sole goal of curing AGE, and therefore should be long-term (10–12 months). If there is no effect of treatment as a result of three months of hormone therapy, extirpation of the uterus and appendages is indicated (in young women under 35 years of age it is possible to preserve the ovaries).
Long-term (5-year) results of treatment of patients with AGE were traced in the work of Ya. V. Bokhman, L. V. Arsenova and A. A. Nikonov (1992), carried out in the oncogynecological department of the Research Institute of Oncology of the Ministry of Health of the RSFSR, in which many important aspects were considered treatment and evaluation of the effectiveness of hormone therapy for AGE. The authors' experience is based on observation of 220 patients with AGE. Of this number, 104 had structural atypia (average age 43.9 years), and 116 had cellular AGE (average age 47.2 years). As the authors note, “structural atypia is characterized by a close focal or diffuse arrangement of glands, with narrow layers of stroma between them. In histological sections, the pronounced tortuosity of the glands and their tree-like branching are manifested by the bizarre shape of their combinations, budding of the epithelium, the formation of false papillae and cribriform structures.”
Cellular atypia“most often combined with structural and divided into weak, moderate and severe. Microscopic examination reveals large glandular epithelial cells with cellular and nuclear atypia. The epithelium lining the glands is multirowed and multilayered with a violation of the polarity of the cells. The nuclei are defined as hypochromic (with moderate atypia) or hyperchromic (with severe).
The multi-row arrangement of nuclei and coarse-grained chromatin, eosinophilic coloring of the cytoplasm increase with the severity of atypia. With a combination of severe structural and cellular atypia, so-called false papillae are determined, devoid of stroma and consisting of a jumble of epithelial cells.” This detailed description of the morphological picture of AGE very convincingly demonstrates the exceptional difficulty that the pathologist faces in making a differential diagnosis of AGE and well-differentiated endometrial adenocarcinoma.
Based on the authors' material, it is shown that AGE in reproductive age often occurs against the background of glandular hyperplasia (79.5%), in postmenopause - atrophy (68.4%). In operated patients, a significant number of observations revealed ovarian stromal hyperplasia (70.0%) and follicular cysts (45.0%). These data can be considered as a morphological marker of hyperestrogenism and an indirect indicator of its role in the genesis of the disease.
Five-year results of hormone therapy for AGE depending on the morphological form of the disease are presented in Table. 6.2 (Bohman Ya.V. et al., 1992).
Long-term (5-year) results of progestin therapy in patients with AGE depending on the morphological form of the disease
Note: I - clinical effect and morphological normalization of the endometrium; II - morphological normalization of the endometrium in the absence of clinical effect; III - lack of clinical and morphological effect.
As can be seen from the presented results of treatment of AGE, adequately administered progestin therapy is an effective treatment method that ensures stable recovery (77.6% of 5-year cures), and in young patients - preservation of reproductive function. Of the 86 patients of reproductive age monitored by the authors, pregnancy occurred in 17 (19.8%).
The main reason for the lack of effectiveness of hormonal treatment AGEs are organic changes in the myometrium and ovaries. First of all, it should be noted the adverse effect of concomitant uterine fibroids, especially if the submucosal location of the nodes is determined. For intramural fibroids, the administration of progestins may also be ineffective.
This is explained by a decrease in myometrial tone with prolonged administration of large doses of progestins, which is morphologically manifested by tissue edema and clinically by bleeding. Another reason for the ineffectiveness of progestin therapy for AGE may be organic changes in the ovaries (thecoma, stromal hyperplasia, theca-follicular cysts). Therefore, if hormone therapy is unsuccessful, one should look for organic changes in the uterus and ovaries and broaden the indications for surgical treatment.
The criteria for assessing the effectiveness of progestin therapy are a two-month period (8 weeks) of its implementation and an adequate dose of progestin. If after this time of treatment and receiving the specified dose of progestin, elements of AGE remain and (or) episodic bleeding continues, then hormone therapy should be considered ineffective and the issue of surgical treatment must be addressed.
Treatment of patients with AGE at any age, it should begin with the prescription of progestins if there is confidence in the absence of endometrial adenocarcinoma (confirmed by hysterography or hysteroscopy), concomitant uterine fibroids or ovarian tumors. In case of successful treatment in young women, this approach allows preserving menstrual function and the possibility of motherhood. In older patients, hormonal treatment avoids the risk of surgery, which can be significant given the large volume of surgery and concomitant diseases.
In general, it should be noted the high effectiveness of progestin therapy methods in the treatment of patients with endometrial hyperplastic processes complicated by menometrorrhagia. In most clinical situations, progestin therapy not only saves patients from uterine bleeding and the need for surgical intervention, but also helps to normalize the uterine mucosa, which, in essence, can be considered as the prevention of endometrial cancer.
In other words, with the help of progestin therapy, the main task of medical rehabilitation of patients with endometrial hyperplastic processes is realized - the preservation of the organ and its normal function.
Progestin therapy for glandular endometrial hyperplasia in peri- and postmenopause, complicated by uterine bleeding, is justified by the same considerations as the therapy of these conditions in the reproductive period.
In these patients it is important to exclude oncopathology of the endometrium and hormone-producing ovarian tumors . After separate diagnostic curettage of the mucous membrane of the uterine cavity and ultrasound of the uterus and its appendages, at the second stage the issue of choosing a drug and treatment regimen is decided.
If amenorrhea lasts less than a year and acyclic uterine bleeding occurs after this period, the administration of estrogen-progestin combinations of a sequential type (Klimonorm, Klimen, Femoston 1/10, 2/10), lasting 6–8 cycles, should be considered adequate therapy.
If uterine bleeding occurs against the background of prolonged amenorrhea for more than 1 year, after examination, it is recommended to prescribe “pure” progestins (Provera, Norkolut, Livial), in a constant regimen, for 3–4 months. The introduction of the Mirena IUD is very effective..
Helps to adequately select a treatment regimen and drug for this group of patients (in the sense of recommending a “cyclical” or “continuous” drug regimen) determination of the level of gonadotropic activity by the FSH content in (Table 6.3).
Selection of a drug for progestin therapy for metrorrhagia in peri- and postmenopause depending on the level of gonadotropic activity (FSH)
If the FSH value is less than 15 IU/l, we can assume that the “menopausal mechanism” has not yet formed in this patient, the late reproductive period remains, and a cyclic regimen would be an adequate hormone therapy for her. When determining high FSH values (more than 15-20 IU/l), it can be assumed that the “menopausal mechanism” has already formed, and an adequate treatment regimen for this patient would be to take “pure” progestins on a constant basis.
Endometrial adenomatosis is called atypical (focal or diffuse) endometrial hyperplasia, which is essentially a precancerous condition.
A precancerous process is a certain pathology that, with varying degrees of probability, can turn into cancer. The precancerous hyperplastic process has the possibility of reverse development; only 10% actually turns into oncology. Uterine adenomatosis should be taken very seriously by doctors.
Description of the disease
Hormonal dysfunction is directly related to hyperplastic processes in the endometrium. In this case, uterine bleeding and infertility often occur. They appear for the reason that hyperestrogenism occurs. An excess amount of estrogens in the endometrium leads to quantitative and qualitative structural changes, which provokes growth and thickening of its internal structures. This is how cervical adenomatosis occurs.
There are several types of hyperplastic processes, depending on the type of cells that implement these processes in the body:
Glandular hyperplasia;
Diffuse hyperplasia;
Focal hyperplasia.
Let's look at each of them in more detail.
Glandular hyperplasia
When the glandular structures increase, glandular hyperplasia of the endometrium develops. Sometimes this leads to cystic-enlarged formations in the lumens of the glands, then glandular-cystic hyperplasia is diagnosed. Atypical cells appear and grow in the endometrium, which is characteristic of adenomatosis.
It is important to understand that when brain function is impaired, especially if the hypothalamus is affected, as well as weakened immunity, cancer occurs in the case of glandular hyperplasia. And regardless of age.
Diffuse hyperplasia
In some cases, the spread of hyperplastic processes occurs over the entire surface of the endometrium, then specialists identify diffuse hyperplasia. That is, a diffuse hyperplastic process leads to diffuse adenomatosis.
Focal hyperplasia
In addition, there is a focal form of hyperplasia. The proliferation of endometrioid tissue occurs in a limited area. Then this growth disappears into the uterine cavity, becoming similar to a polyp. Focal adenomatosis is a polyp that contains atypical cells.
Uterine adenomatosis is treated mainly surgically. The further prognosis is determined by several factors:
The age of the patient;
The nature of hormonal disorders;
Concomitant neuroendocrine diseases;
State of immunity.
Some women are interested in the question of what is the difference between uterine adenomatosis and endometrial adenomatosis? After all, this is the same atypical process. The term “adenomatosis of the uterus” is not entirely correct, since atypia affects only the inner layer, which is the endometrium. And in the uterus itself there are several layers.
Fibrosis and adenomatosis
Fibrous adenomatosis does not exist as a diagnosis. Fibrosis is a pathology in which connective tissue grows, adenomatosis - glandular tissue grows. The pathology can also have a mixed nature, which will be called fibrocystic hyperplasia.
Adenomatosis can occur not only in the uterus. It happens in the mammary glands, but in essence these pathological processes are completely different. Adenomatosis of the mammary glands is Reclus' disease, when benign formation of small cysts occurs. We looked at cervical adenomatosis. What it is has become clearer.
What are the causes of endometrial adenomatosis?
The causes of atypical cellular transformation are the same factors that provoke hyperplastic processes in the endometrium. The exact causes of adenomatosis are not known. Of course, provoking factors are constantly being studied, but today it is impossible to say for sure that this is the trigger for the atypical process in the endometrium. But the more different unfavorable conditions there are, the greater the likelihood of developing pathology.
The first place among all provoking factors of endometrial adenomatosis is occupied by hormonal imbalance. The neurohumoral regulation of the entire human body is disrupted. Estrogens and gestagens are involved in physiological cyclic changes in the uterus. First of all, thanks to estrogens, the internal mucous layer increases. But the job of gestagens is to promptly stop the growth of the endometrium and cause its rejection.
With an excessive amount of estrogen, the growth of the endometrium occurs uncontrollably. Hyperestrogenism can happen for various reasons:
The hormonal function of the ovaries is disrupted;
Anovulation occurs;
The cycle becomes single-phase;
Endometrial hyperplasia occurs.
With polycystic ovary syndrome, anovulation is chronic. This is also a kind of provoking factor for the development of hyperplasia. If a woman takes hormonal drugs uncontrollably, her hormonal levels may suffer from this. This will trigger the hyperplastic process in the endometrium.
If there is both hyperestrogenism and neuroendocrine disorders in the body, the likelihood of developing adenomatosis increases. An obese woman with hypertension is 10 times more likely to get endometrial cancer than one with normal weight and blood pressure.
For what other reasons can hyperestrogenism develop? Often, diseases of the liver and biliary tract lead to this pathology, since it is the liver that utilizes estrogens.
So, uncontrolled growth of the inner layer of the uterus occurs, which leads to the formation of atypical cells. This is endometrial adenomatosis. What is the treatment for a diagnosis of cervical adenomatosis? More on this later.
Signs of endometrial adenomatosis
As a rule, there are no obvious symptoms of adenomatosis, since atypical cells can only be detected in a laboratory way. First, a hyperplastic process is detected, after which it is necessary to clarify its nature.
There are some symptoms of hyperplasia that you definitely need to pay attention to:
The nature of bleeding has changed - menstruation becomes heavy, blood appears outside the cycle;
Painful sensations in the lower abdomen and lower back before and during menstruation;
Manifestation of metabolic syndrome - excess weight, excessive male pattern hair, increased insulin levels in the blood;
Fertility is impaired - it is impossible to conceive and bear a child;
Presence of mastopathy;
Inflammation of the genitourinary system;
Pain during sexual intercourse, bleeding after it.
Is uterine adenomatosis detected on ultrasound?
Using ultrasound scanning, the thickness and structure of the endometrium is determined. does a good job with this research. What kind of hyperplastic process is observed - focal or diffuse - will be shown by this scan. As a result, if diffuse hyperplasia is detected, then the presence of diffuse adenomatosis can be assumed. It is impossible to visualize it using a sensor, since there are no distinctive features.
Focal adenomatosis of the uterus is easy to detect because it is visualized as a polyp. Although the nature of the cellular changes will also not be revealed. Atypia cannot be traced by ultrasound scanning.
A scraping of the uterine mucosa is made, after which this material is sent for histological examination. This diagnostic method is very important for adenomatosis. The composition of the cell, its structural changes, as well as to what extent and severity it is atypical are studied. If atypia is not detected, then this indicates a benign course of hyperplasia.
Often, surgical curettage of the uterine cavity is performed, and then the resulting material is examined. Hysteroscopy can help with this for visual control during total evacuation of the uterine mucosa.
Uterine adenomatosis: treatment
The presence of adenomatosis in a woman can cause infertility, but even with successful conception, premature termination of pregnancy can occur due to the disease.
Treatment primarily consists of mechanically removing the altered endometrium. Thus, the source of pathological changes is surgically eliminated, and a scraping is obtained for histological examination. When the results are obtained, the treatment plan is determined based on this.
Hormone therapy and surgery are prescribed on an individual basis. If the girl is young, then specialists limit themselves to treatment with hormonal drugs. The patient, who is close to menopause, undergoes a radical surgical operation along with hormone therapy - removal of the uterus and appendages. This significantly reduces the likelihood of adenomatosis turning into cancer. You can save a woman's life.
It is important to understand that early diagnosis of adenomatosis is most desirable, in this case the risk of cancer is minimal. Therefore, it is necessary to regularly visit a gynecologist, undergo a comprehensive examination, and take all necessary tests. We examined in this article adenomatosis of the endometrium of the uterus. Take care of your health!
Focal endometrial proliferation in the form of glandular hyperplasia, polyposis and adenomatosis are precancerous conditions. Under the condition of exposure to exo- and endogenous carcinogenic factors, a tumor forms against their background.
In menstruating women, precancerous conditions of the endometrium are most often manifested by menstrual irregularities such as menopause and metrorrhagia, spotting and bleeding during menopause.
A gynecological examination usually does not detect any deviations from normal anatomical relationships; Sometimes with adenomatosis there is a slight increase in the body of the uterus, mainly in the anteroposterior size, and thickening of its walls.
Differential diagnosis of precancerous conditions of the uterine body carried out using cytological examination of smears from the uterine cavity (aspiration using a Brown syringe), hysterography and histological examination of scrapings from the uterine cavity (M. T. Kunitsa, 1966).
During a cytological examination of a smear from the uterine cavity in cases of endometrial hyperplasia and adenomatosis, isolated endometrial cells and groups of them are determined throughout the menstrual cycle and in menopause. In this case, significant fluctuations in the size of cells and various changes in the nuclei are noted. The nuclei are often hyperchromatic, sometimes enlarged to gigantic sizes. There are cells with two nuclei and atypical mitoses.
With endometrial polyposis, many isolated cells and groups of cells with significant polymorphism are determined. However, changes in the cell nucleus are minor and not as varied as with endometrial cancer.
The associated inflammatory process against the background of precancerous conditions of the endometrium contributes to significant deviations in the cellular structure, which complicates the diagnosis. In such cases, it is necessary to perform hysterography and histological examination of purposefully made scrapings.
With hysterography (under control in 2 projections - anteroposterior and lateral) with the introduction of 2-4 ml of iodolipol or diodon in women with hyperplasia and adenomatosis, the pictures reveal an uneven surface of the mucous membrane, the edges of the contrast shadow are jagged, pitted, and the shadow itself is heterogeneous. With endometrial polyposis, you can determine the size of the polyp and its location. In some cases, it is possible to establish the presence of a solitary polyp or several tumors.
The morphological characteristics of precancerous conditions of the endometrium are determined as a result of histological examination. Glandular and glandular-cystic hyperplasia of the endometrium is characterized by thickening of the mucous membrane, often with polypous growths, and an increase in the number of sharply tortuous and dilated glands. Polyps are covered with single-layer glandular epithelium, contain dilated cavities, and the endometrial stroma is swollen. In adenomatosis, the epithelium of the glands is multirowed and forms papillary growths; the changes are predominantly focal in nature. Adenomatosis is often combined with glandular endometrial hyperplasia.
Treatment for precancerous conditions of the endometrium should begin with curettage of all the walls of the uterine cavity.
Histological confirmation of the hyperplastic process in the endometrium is the basis for hormone therapy. Endometrial hyperplasia is the result of absolute or relative hyperextrogenism and insufficiency of corpus luteum function. Therefore, the use of progestins in the treatment of precancerous conditions of the endometrium is justified. Experience with the use of synthetic progestins and, in particular, oxyprogesterone capronate indicates a good effect of progestin therapy in patients with glandular, glandular polyposis, cystic and adenomatous endometrial hyperplasia.
The choice of a single and course dose of oxyprogesterone capronate is determined by the patient’s age, the nature and severity of morphological changes in the endometrium. Thus, in women of childbearing age with glandular endometrial hyperplasia, it is sufficient to administer 1 ml of 12.5% oxyprogesterone capronate once a month on the 12th or 14th day of the menstrual cycle; the course of treatment lasts 5-6 months.
For endometrial hyperplasia with polyposis, cystic or adenomatous nature during childbearing age, the dose of the drug should be increased: 1 or 2 ml of a 12.5% solution is administered intramuscularly 2 times a month (on the 12th and 19th or 14th and 21st day of the menstrual cycle depending on the length of the cycle). Women during menopause and menopause, depending on the nature of endometrial dysplasia, are administered 1-2 ml of a 12.5% or 25% solution of oxyprogesterone capronate 1 or 2 times a week for 5-6 months, then the dose is gradually reduced (by half every 2 months ).
As a result of treatment, secretory and then atrophic changes in the glands occur. In women of reproductive age, the normal menstrual cycle is restored, and during the menopausal and menopausal periods, a cessation of bleeding is noted. In some cases, mainly in menopause, the use of androgens is possible.
Treatment of precancerous conditions of the endometrium is one of the important measures in prevention
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