Uterine Fibroids

What is Uterine Fibroids?

Uterine fibroids are a benign hormone-dependent tumor in women of reproductive age (mainly 30-45 years). Uterine fibroids up to 30% of gynecological diseases.

Causes of Uterine Fibroids

The modern view of the development of uterine fibroids is based on hormonal theory. Impaired excretion and metabolic conversion of estrogen, as well as the ratio of estrogen fractions (the predominance of estrone and estradiol in follicular, and estriol in the luteal phase) lead to morphological changes in myometrium. 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 their hypertrophy 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 the fibroids, in addition, progesterone affects fibroid growth by inducing growth factors. In the tissue, the myoma of the estradiol and progesterone receptors is greater than in the 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 estrogen in uterine tissue of the uterus 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 chronic foci of infection; pronounced changes in hemodynamics of the pelvis, 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 action of estrogen and progesterone.

Myomas are heterogeneous in structure. In terms of tissue composition, the nodes are divided into fibroids, fibroids, angiomyomas, and adenomyomas.

According to morphogenetic features, there are 3 main forms:

  • simple fibroids, developing the type of benign muscle hyperplasia;
  • proliferating fibroids with morphogenetic criteria for a true benign tumor. Every 4th patient with uterine fibroids proliferating with the rapid growth of myomatous nodes. Pathological mitoses in proliferating myomas do not exceed 25%;
  • predysarcomas – a stage on the path of true malignancy.

Predsarcoma includes multiple foci of proliferation of myogenic elements with atypia, heterogeneity of cell nuclei; the number of pathological mitoses reaches 75%. However, true malignancy of fibroids occurs in less than 1% of clinical observations.

Depending on the localization and growth of myoma nodes, submucous (submucosal) myomatous nodes that grow into the uterine cavity and deform it (see the section “Intrauterine pathology”) and subserous (subperitoneal) nodes are isolated. Myomatous nodes grow in the direction of the abdominal cavity. If the myoma node splits the leaves of the wide uterine ligament as it grows. It is called the intraligamentous myoma node. Interstitial (intermuscular) myomatous nodes grow from the middle layer of the myometrium and are located deep in the myometrium.