Glandular endometrial hyperplasia

Recurrent glandular hyperplasia of the endometrium can cause abnormal uterine bleeding during all periods of the reproductive cycle of the female body. Juvenile uterine bleeding in adolescence, hemorrhage in menopause, as well as in perimenopause and postmenopause in a significant number of cases (up to 60-75%) are due to hyperplastic changes in the mucous membrane of the uterine cavity.

Numerous endocrine studies of recent years, including highly specific radioimmunoassays and immune-enzyme methods for determining hormones in the blood, used in patients with glandular hyperplasia of the endometrium, allow us to unequivocally recognize the etiological role of hyperestrogenism in the development of excessive proliferative changes in the mucous membrane of the uterine cavity.

Estrogens are the main hormonal factor that causes endometrial proliferation. In conditions of reduced effect of progesterone, which is often due to anovulation, estrogens can cause pronounced proliferation of glandular and stromal elements of the endometrium, which quickly acquires morphological signs of hyperplastic changes. In this regard, it should be noted that with the development of methods for determining estrogens in biological fluids, clinical observations of hyperestrogenia, based on morphological studies and functional test data, have received objective quantitative confirmation.

In accordance with modern concepts, both functional (chronic anovulation) and organic changes in the ovaries play a role in the development of hyperestrogenism (hypertrophy of the current tissue, sclerokinoznye changes in the ovaries and much less often feminizing ovarian tumors). In this case, regardless of the reasons for the development of anovulation, the sequence of arising disorders is of the same type.

The main element of these disorders is the development of follicle (follicle) persistence or their atresia, as a result of which the luteal phase of the menstrual cycle also falls out. If ovulation is violated in another way, by the type of atresia, the follicle or group of follicles grow, but, not reaching maturity, are regressed, which leads to a decrease in ovarian estrogen secretion. In response to a decrease in estrogen secretion, gonadotropin pituitary secretion (LH and FSH) is stimulated, which causes the growth of new follicles and a new increase in estrogen secretion. In this way, with atresia of the follicles, there is a wave-like secretion of estrogens that does not reach a high level, but leads to a prolonged, “monotonous” estrogen stimulation of the endometrium. In conditions of reduced antiestrogenic effect of progesterone, hyperplasia of the mucous membrane of the uterus body develops. In this case, there may not be a significant increase in estrogen levels in the blood, but a prolonged effect on the target tissues leads to changes that indicate an increased total effect of estrogen stimulation.

In other words, in order to develop a pronounced proliferation of the endometrium, along with a high estrogen content in the blood, a normal or even decreased levels of estrogen plays a significant role if their indices remain monotonous for a sufficiently long time (time factor). This conclusion is of great importance for explaining the role of relatively low hyperestrogenism when there is no significant increase in the level of estrogens in the blood and at the same time endometrial hyperplasia is determined against this background.

In addition to functional and organic changes in the sex glands that are responsible for the development of hyperestrogenism, recent studies have shown a significant role in the development of excessive estrogenic effects on the endometrium of such, at first glance, “nonspecific” factors like age and obesity.

A detailed study of the pathogenetic role of these disorders in the development of cardiovascular pathology made it possible to substantiate the existence of a stable complex of metabolic and age-associated shifts that provide not only the development of atherosclerosis, but also the disruption of hormonal homeostasis in the reproductive system.

The exact diagnosis of endometrial hyperplasia (ET) under normal conditions is based on a morphological study of the material obtained by scraping the uterine mucosa. At the same time, there are quite a few terms and even classifications of the process for indicating the registered changes. So, simple GE, glandular GE, glandular cystic CE are synonyms, the names of one process. Hyperplasia can be diffusely spread across the uterine cavity or limited to a small area, most often in the region of the uterine fundus. Until recently, there were no methods to diagnose asymptomatic glandular hyperplasia of the endometrium in women who had no menstrual irregularities. And only the emergence of uterine bleeding and the implementation of this diagnostic curettage of the mucous membrane of the uterine cavity made it possible to establish the presence of glandular hyperplasia of the endometrium.

At present, with the development of ultrasound diagnostic methods, it has become possible to detect hyperplastic changes in the mucous uterus by a noninvasive method, using abdominal and vaginal ultrasound sensors (3.5-7.5 MHz). An echosemiotics of hyperplastic changes in myometrium and endometrium has been developed, which allows to conduct preclinical (screening) diagnosis of the disease.

With external examination, the hyperplastic endometrium in the scrap material looks like a thickened and juicy layer of the mucous membrane of the uterine cavity, often with polypoid areas. Scraping is copious, resembling the type of tissue that is obtained when performing curettage on the 26th-28th day of the normal secretory cycle. Another picture is observed with scraping in postmenopause. Scraping of the mucous membrane is usually poor, and morphological examination reveals only small foci of GE in a small number.

According to morphological features, the ET is characterized by proliferation as glands, and stroma, which also provides the appearance of hyperplastic mucosa in the form of a yellowish color of velvety mass, lobate species with polypous structures. Despite the presence of proliferation of both glands and stroma, tissue microscopy reveals mainly clusters glandular structures of the GE. The gland has the appearance of tubular crimped structures, which vary greatly in shape and quantity. Sometimes some glands can be significantly enlarged, forming cystic structures. Secretory activity in such glands, as a rule, is absent, and if it does, then in the form of small and rare foci. Mitoses are present, but according to the amount does not exceed the proliferative type observed in the endometrium. In general, cystic changes in the endometrium (changes resembling the picture of “Swiss cheese”) serve as a sign of its already inactive state, which does not have any potential for proliferative changes.

local_offerevent_note December 18, 2017

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