What does endometrial cystic hyperplasia mean?

Uterine wall cysts are caused by the proliferation and thickening of the uterine wall itself under the action of estrogen. The endometrium falls off and bleeds during menstruation. It is a kind of hyperplasia. This disease can occur at any time and place, causing serious harm to the human body. So what does cystic hyperplasia of the uterine wall mean? What causes endometrial hyperplasia? Let me introduce it to you below.

(1) Simple hyperplasia of the uterine wall: The affected uterus is slightly larger, the endometrium is significantly thickened, and sometimes appears diffusely cystic. The amount of curettage material is large, and may be stained with red, smooth cystic tissue. Microscopically, the lesions are focal, invading the functional layer and dermis of the endometrium. Due to the simultaneous proliferation of the stroma and the glandular ducts, there is no duct congestion. The glandular ducts are of different sizes and have smooth contours (Figure 1). The shape of the glandular epithelial cells is similar to that of the normal late reproductive stage and does not have atypia.

(2) Complex hyperplasia of the uterine wall: The cause of complex hyperplasia is similar to that of simple hyperplasia, but because the disease is localized, it may also be related to the distribution of growth hormone protein kinase in the tissue. A very small number of complex hyperplasia may develop into intestinal metaplasia, which in turn affects the prognosis. Among the 21 reported cases of endometrial hyperplasia in women under 40 years old, 4 were complex hyperplasia. All of them were cured after short-term medication and became pregnant and delivered at full term. Among them, 3 cases still had complex hyperplasia 2 to 3 years after giving birth, and no lesions were found in the follow-up of 9 to 38 years.

The diseased uterine wall may be thickened or thin, or cystic. Unlike simple hyperplasia, the disease is a focal hyperplasia of the glandular duct components without invading the interstitial space. The amount of material collected during curettage may be more or less, and is often contaminated with normal, atrophic or other types of hyperplastic uterine wall. The glandular ducts in the diseased area are congested and may be "back to back", the interstitial space is significantly reduced, the contour of the glandular duct is irregular, or it is serrated, or intraglandular papillae are formed, but there is no atypia of the glandular epithelial cells.

(3) Intestinal metaplasia of the uterine wall: The occurrence of intestinal metaplasia is similar to that of complex hyperplasia, but some cases can slowly develop into cancer. In moderate to severe intestinal metaplasia, the lesion rate is as high as 30% to 50%.

This type of hyperplasia is limited to the glandular ducts of the uterine wall. The atypia of the glandular epithelial cells is the key to diagnosis. The lesions are distributed in focal or multifocal areas. During this period, normal, atrophic or other types of hyperplastic ducts can also be seen. The glandular ducts in the lesion area are increased, and the interstitial space is reduced. The hyperplastic glandular ducts not only have irregular contours, but also have glandular epithelial cell atypia, that is, the polarity of the cell arrangement is disordered or reduced, the cytoplasm is enlarged and rounded, irregular, the nucleolus is prominent, and the cytoplasm is rich and eosinophilic. According to the degree of the lesion, intestinal metaplasia can be divided into mild, moderate and severe degrees. Mild: The contours of the glandular ducts are slightly irregular, and the glandular epithelial cell atypia is mild. Moderate to severe: The contours of the glandular ducts are significantly irregular and branched, with intraluminal budding and papillary structures. The glandular epithelial cell atypia is obvious (see Figure 3). Mild to moderate: The lesion is close to the middle.

2. Causes of the disease

1. Endogenous estrogen

(1) Anovulation: In adolescent girls, perimenopausal women, imbalance in a certain stage of the hypothalamic-pituitary-uterine-ovarian axis, polycystic ovary syndrome, etc., anovulation may occur, causing the uterine wall to be continuously affected by estrogen for a long time, without estrogen resistance, lack of regular metabolic phase transitions, and long-term hyperplasia. Among 41 patients with intestinal metaplasia of the uterine wall under the age of 40, more than 80% of the endometrium had no metabolic phase except for the focal areas of intestinal metaplasia; 70% of the temperature measurements during the ovulation period were monophasic, so most patients did not ovulate.

(2) Obesity: In obese women, androstenedione metabolized by the adrenal glands is converted into estrone by the action of aromatase in adipose tissue. The more adipose tissue there is, the stronger the conversion capacity is, and the higher the level of estrone in the blood is, thus leading to a persistent estrogenic effect.

(3) Endocrine multifunctional tumors: Endocrine multifunctional tumors are rare tumors, but in scientific research statistics, endocrine multifunctional tumors account for 7.5%. The gonadotropin action of the pituitary gland is abnormal. Uterine ovarian granulosa cell tumors are also tumors that continuously metabolize estrogen.