Endometrial hyperplastic processes are possibleany age, but their frequency is significantly increased for the period of perimenopause. The increased incidence of endometrial hyperplasia associated with both an increase in life expectancy and the unfavorable ecological situation, the increasing number of chronic physical illness and depression of immunity in women.
The mechanism of the disease
The endometrium is the target organ for sexhormones because of the presence therein of specific receptors. Balanced hormonal effects through the cytoplasmic and nuclear receptors provides a physiological cyclical transformation of the uterine lining. Violation of hormonal status may lead to changes in cell growth and differentiation of cells of the endometrium and lead to the development of hyperplastic processes.
The leading role in the pathogenesis of hyperplasticthe endometrium is given an absolute or relative increase in estrogen levels, lack of or inadequate antiestrogen influence of progesterone. Reasons hyperestrogenism:
- anovulation due to persistence or atresia follicles
- hyperplastic processes in the ovaries or the Gorm-noprodutsiruyuschie ovarian tumor (stromal hyperplasia, tekomatoz, granulosa tumor, theca cell tumor, etc.)
- violation of gonadotropic pituitary function
- adrenal hyperplasia
- misuse of hormones (estrogens, anti-estrogens)
However, endometrial hyperplasiacan develop undisturbed and hormonal ratios. In the development of pathological processes leading role for tissue disorders reception. Infectious and inflammatory changes in the endometrium can lead to the development of endometrial hyperplastic processes 30% of patients.
In the pathogenesis of endometrial hyperplastic processes occupy an important place as an exchange-endocrine disorders:
- changes in fat metabolism
- metabolic hormones in the pathology of the hepatobiliary system and the gastrointestinal tract
- low immunity
- thyroid dysfunction
Options for the development of endometrial hyperplasia
I'M IN. Bohman has put forward the concept of the two pathogenic variants of endometrial hyperplastic processes. The first variant is characterized by the diversity and depth of hyperestrogenism in conjunction with impaired lipid and carbohydrate metabolism, and manifested in anovulatory uterine bleeding, infertility, late menopause, ovarian hyperplasia, combined with feminizing ovarian tumors and polycystic ovary syndrome. Often there are uterine fibroids and diffuse hyperplasia of the endometrium, against which there are polyps, lesions of atypical endometrial hyperplasia and cancer. Metabolic disorders leading to obesity, hyperlipidemia and diabetes.
In the second embodiment, said pathogenicendocrine and metabolic disturbances are blurred or non-existent; ovarian stromal fibrosis combined with normal structure or atrophy of the endometrium, with the advent of polyps, focal hyperplasia (including atypical) and endometrial cancer.
complex system found in recent yearsfactors involved in cellular regulation and enhanced presentation of intracellular and intercellular interactions in the processes of hormone-dependent tissues. Thus, it was found that in the regulation of cell proliferation activity of the endometrium with estrogens are involved along a number of biologically active compounds (, polypeptide growth factors, cytokines, arachidonic acid metabolites) as well as immune system. In the regulation of tissue homeostasis and pathogenesis of proliferative diseases important role to play not only enhance cell proliferation, but also a violation of the regulation of cell death (apoptosis). Resistance endometrial cells to programmed cell death (apoptosis), resulting in the accumulation of modified and excessively proliferiruyushih cells, which is characteristic of neoplastic changes of the endometrium. Hyperplastic changes are usually subjected to a functional layer of the endometrium, much less - basal.
Thus, pathological transformation of the endometrium - a complex biological process affecting all parts of the neurohumoral regulation of the female organism.