Uterine fibroids – benign hormone-dependent myometrium tumor, occurs in women of reproductive age (the peak incidence is 40 years). Uterine fibroids up to 30% of gynecological diseases.
Etiology and pathogenesis. Modern ideas about the development of uterine fibroids are based on hormonal theory. Impaired excretion and metabolic conversion of estrogens, as well as the ratio of estrogen fractions (the predominance of estrone and estradiol to follicular, and estriol in the luteal phase) lead to morphological changes in myometry. The mass of myometrium can increase as a result of hyperplasia of smooth muscle cells, which is initiated by estrogens, and hypertrophy of these cells. Along with estrogen the growth of fibroids stimulates progesterone.
Hypertrophy of smooth muscle cells with uterine myoma is similar to that during pregnancy and can occur only when the combined effects of relatively high concentrations of estradiol and progesterone. In the luteal phase, progesterone increases the mitotic activity of fibroids, in addition, it affects the growth of fibroids by inducing growth factors. There are more estradiol and progesterone receptors in myoma tissue than in unchanged myometrium. Disruption of sexual steroid metabolism in myomatous nodes causes autocrine stimulation of cells with the participation of so-called growth factors. Mediators of the action of estrogens in uterine fibroid tissue are insulin-like growth factors I and II.
Along with the hormonal aspects of the pathogenesis of uterine fibroids, an important role is played by changes in the body’s immune reactivity, especially in the presence of chronic foci of infection, pronounced changes in pelvic hemodynamics, as well as hereditary predisposition. Growth zones of fibroids are formed around inflammatory infiltrates and endometrial foci in the myometrium. Phenotypic transformation of smooth muscle cells and degenerative changes in conditions of impaired microcirculation play a significant role in increasing fibroids. The rudiments of myoma nodes can form at the embryonic stage. The growth of progenitor cells continues for many years against the background of a pronounced ovarian activity under the influence of estrogen and progesterone. Myomas are heterogeneous in structure. Depending on the ratio of muscle and connective tissue, the nodes are divided into fibroids, fibroids and fibroids.
According to morphogenetic features, simple fibroids develop, developing according to the type of benign muscle hyperplasia, and proliferating fibroids with the morphogenetic criteria of a true benign tumor. Every 4th patient with uterine myoma proliferating, with the rapid growth of myomatous nodes. The number of pathological mitoses in proliferating myomas does not exceed 25%.
Suspicion of uterine sarcoma appears when more than 70% of pathological mitoses are detected in the process of histological examination, as well as in the determination of myogenic elements with atypia and heterogeneity of cell nuclei. Malignancy of fibroids in sarcoma occurs in less than 1% of clinical observations. With its submucous location, the risk of malignancy is higher.
Depending on location and growth, submucous (submucous) myomatous nodes grow into the uterine cavity and deform it, and subserous (subperitoneal) nodes grow towards the abdominal cavity. If the myoma node splits the leaves of the broad uterine ligament as it grows, it is called intraligamentary. Interstitial (intermuscular) myomatous nodes grow from the middle layer of the myometrium and are located deep in the myometrium.
Submucous myomatous nodes may have a different topographic location. Depending on the location, width of the base of the myoma node and the size of the intramural component, the following types of submucous myomas are distinguished:
0 type – submucous nodes on the leg, without intramural component;
Type 1 – submucous nodes on a broad base with an intramural component of less than 50%;
Type II – myomatous nodes with an intramural component of 50% or more.
For subserous fibroids, there is a similar classification:
0 type – subserous node on the leg, without intramural component;
Type 1 – the intramural component is less than 50% of the volume of the node, most of it is subserous;
Type II – the intramural component represents more than 50% of the myomatous volume node, subserous component expressed little.
Clinical symptoms and diagnosis. Submucous fibroids are characterized by prolonged, heavy menstruation with clots (menorrhagia), which can continue during the intermenstrual period (metrorrhagia). Uterine bleeding leads to the development of anemia. Along with uterine bleeding, there are pulling and cramping abdominal pain. As a result of contractions of the uterus with type 0 submucous fibroids, spontaneous expulsion of the myoma node can occur. When the myomatous node is born, the pains are intense and cramping. Submucous uterine fibroids are often accompanied by infertility and miscarriage.
Separate subserous myomatous nodes of small size may not be clinically manifest for a long time, but as they increase, there are signs of malnutrition of the tumor, the likelihood of the legs of the myoma node increases. Patients may complain of discomfort in the lower abdomen, intermittent pulling or sharp pains. Pain may radiate to the lumbar region, leg, perineum. When the torsion of the myoma node is completed or the vast area of necrosis develops, the pain becomes intense, symptoms of peritoneal irritation and general clinical signs of “acute abdomen” appear.
Interstitial-subserous myomatous nodes are less susceptible to destructive processes due to malnutrition, do not manifest clinically for a long time and can reach a diameter of 10–25 cm or more. Patients are worried about the feeling of heaviness and discomfort in the lower abdomen, its increase. The pain syndrome is associated with stretching of the visceral peritoneum of the uterus, the pressure of myoma nodes on the pelvic plexus. In violation of blood circulation in large myomatous nodes, the pain is acute. Depending on the localization of the subserous nodes, dysfunction of neighboring organs is possible. The growth of myoma node anteriorly contributes to the development of dysuric phenomena: patients complain of frequent urination, incomplete emptying of the bladder, imperative urination, acute urinary retention. · The cervical myoma node at the back of the uterus leads to pressure on the rectum and violates defecation. Subserous nodes located on the side wall of the uterus in the lower and middle third, when large, change the topography of the ureter, can lead to disruption of passage of urine on the affected side, the occurrence of a hydroureter and the formation of hydronephrosis. Subserous myoma nodes rarely cause menstrual dysfunction. However, in case of multiple subserous myomatous nodes, myometrial contractility may be impaired and menometrorrhagia may appear.
Interstitial myoma nodes lead to an increase in the uterus and can significantly affect the contractility of the myometrium. Patients have complaints about obschnye long periods, less often – intermenstrual bleeding from the genital tract. However, there is no direct relationship between the size of the uterus and the appearance of uterine bleeding. Anemia in patients with uterine myoma may be due to chronic blood loss and acute uterine bleeding. Without disturbances of the menstrual cycle, anemia may be due to the deposition of blood in the uterus enlarged by myomatous nodes. Patients with large uterine fibroids (more than 20 weeks of gestation) may experience a syndrome caused by compression of the inferior vena cava, which manifests as a heartbeat and shortness of breath in the prone position. Patients may complain of pain, an increase in the abdomen, there may be acute urinary retention, hydronephrosis. With a combination of interstitial, submucous and subserous nodes, the clinical picture is more diverse than with isolated myomatous nodes.