What are the causes of uterine fibroids? Can uterine fibroids cause uterine hypertrophy?

Uterine fibroids are a common benign gynecological tumor, and their etiology is still unclear. However, according to a large number of clinical observations and experimental results, fibroids are a tumor that depends on estrogen for growth. For example, it is common in women of childbearing age, and it is common in the age of 30 to 50 years old, especially in high estrogen environments such as pregnancy and exogenous high estrogen, and fibroids gradually decrease after menopause. Patients with fibroids are often accompanied by ovarian congestion, swelling, and endometrial hyperplasia, indicating that this is related to excessive estrogen stimulation.

In fact, the estrogen dependence of fibroids also includes receptors. In recent years, with the relevant research on uterine fibroids and endocrine, fibroid tissue has been confirmed to have estrogen receptors (ER) and progesterone receptors (pR), and its density exceeds that of the surrounding normal muscle tissue. ER and pR change with the menstrual cycle. It is reported that the application of exogenous hormones and clomiphene will increase the number of uterine fibroids. Inhibiting or reducing the level of sex hormones can prevent the growth of fibroids, reduce fibroids, and improve clinical symptoms, indicating that fibroids are sex hormone-dependent tumors.

The use of antagonistic hormone drugs can treat fibroids, but there is no obvious difference in the sex hormones in the blood of patients with fibroids and women without fibroids. This shows that the occurrence of fibroids is related to the hormonal environment of patients with fibroids, rather than to the abnormal local endocrine environment. For example, the estrogen concentration in fibroids is higher than that in uterine muscles; the endometrial hyperplasia rate near fibroids is higher. The same is true for receptors. E2R (estradiol receptor) and pR in fibroids are higher than those in uterine muscles.

From the perspective of histogenesis, uterine fibroid cells have long been thought to be derived from smooth muscle cells of the uterine muscle and vascular wall, such as immature myoblasts, but the latter have no clear concept histologically.

Tissue studies have found that small uterine fibroids that have not grown for a long time are not only rich in smooth muscle cells with mature myofilaments, but also contain immature smooth muscle cells seen in the fetal uterus. This suggests that the occurrence of human uterine fibroids may come from the differentiation process of undifferentiated mesenchymal cells to smooth muscle cells. Multiple uterine fibroids may be due to the origin cells of multiple furnaces in the myometrium. This undifferentiated mesenchymal cell is the original cell of the fibroid and is a multi-differentiated cell in the embryonic stage. It has biological media that depend on estrogen for proliferation, progesterone for differentiation and hypertrophy.

After entering sexual maturity, the remaining undifferentiated mesenchymal cells and immature smooth muscle cells undergo a long-term and repeated process of proliferation, differentiation and hypertrophy under the action of the estrogen and progesterone cycle before the formation of myoma.