Endometrial thickening is a common disease currently. Patients with endometrial thickening are mostly young women and women who have just given birth. The causes of endometrial thickening include changes in estrogen and unstable horizontal lines. Because of tumors or long-term anovulation, the endometrium of the uterus accumulates little by little. It is also possible that irregular menstruation and abnormal shedding of the endometrium of the uterus lead to endometrial thickening. Causes 1. The body is stimulated by high levels of estrogen, either endogenously (such as endocrine functional tumors in the ovary or pituitary gland) or exogenously (such as estrogen replacement therapy). 2. Due to the lack of ovulation, the endometrium is in a state of proliferative growth for a long time and lacks periodic secretory phase transformation. 3. Simple hyperplasia is considered to be a physiological response of the endometrium to the body's high estrogen state. The most common cause is anovulatory menstruation, which often occurs in women before menarche or menopause. Pathological changes Based on the differences in cell morphology and the degree of proliferation and differentiation of glandular structures, the classification is as follows: 1. Simple hyperplasia Previously known as mild hyperplasia or cystic hyperplasia, the number of glands increases and some glands expand into small cysts. The epithelium lining the glands is generally simple or pseudostratified, with columnar cells without atypia, and the cell morphology and arrangement are similar to those of the proliferative endometrium. 1% of simple endometrial hyperplasia may progress to endometrial adenocarcinoma. 2. Complex hyperplasia It was previously called adenomatous hyperplasia, in which the glands proliferate significantly, crowding each other and appearing back-to-back. The glandular structure is complex and irregular. Due to the proliferation of glandular epithelial cells, it can grow in a papillary manner into the glandular cavity or in a budding manner into the stroma, without cell atypia. The intimal stroma was significantly reduced. About 3% may develop into adenocarcinoma. 3. Atypical hyperplasia On the basis of complex hyperplasia, there is epithelial cell atypia, disordered cell polarity, increased volume, increased nuclear-cytoplasmic ratio, concentrated nuclear chromatin, prominent nucleoli, and varying numbers of nuclear division images. Severe atypical hyperplasia is sometimes difficult to distinguish from endometrial cancer. If there is stromal infiltration, it is classified as cancer and often requires a comprehensive examination after hysterectomy to confirm the diagnosis. One-third of patients may develop adenocarcinoma. |
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