Long-term estrogen stimulation alone is the main cause of endometrial hyperplasia, such as non-ovulation caused by polycystic ovary syndrome, extraglandular transformation of adipose tissue estrogen in obese individuals, combined ovarian tumors with endocrine function, and exogenous estrogen therapy. I. Pathological features of endometrial atypical hyperplasia Endometrial hyperplasia has a certain tendency to become cancerous. 1979, Sherman et al. referred to precancerous endometrial adenocarcinoma as endometrial intraepithelial neoplasia. 1985, Kurman suggested that endometrial hyperplasia should be divided into endometrial simple hyperplasia, endometrial compound hyperplasia, endometrial atypical hyperplasia, including simple atypical hyperplasia, compound atypical hyperplasia, and endometrial atypical hyperplasia. atypical hyperplasia, and compound atypical hyperplasia). Long-term observation confirmed that the cancer rate of endometrial atypical hyperplasia is 23%, the cancer rate of endometrial compound hyperplasia is 3% to 5%, and the cancer rate of endometrial simple hyperplasia becomes 1% to 2%. 1.Simple hyperplasia of endometrium: It refers to mild or moderate focal or diffuse hyperplasia of endometrial glands, with increased and dense glands or unevenly spaced glands, unequal size of glandular cavities, most of which are small and round, and some of which are cystically dilated. The glandular epithelial cells are monolayered or multilayered. The interstitial cells are increased and dense. 2, endometrial hyperplasia: endometrial glands are highly diffuse hyperplasia, most of them are crowded, with complex structure, such as villous branched glands, glandular cavity over glandular cavity or with papillary folds in the glandular cavity. The glandular epithelium was focally or diffusely complexed. The mesenchymal cells are densely proliferated. 3. Endometrial atypical hyperplasia: The endometrial glands are abnormally hyperplastic, with papillary or serrated glands that are abnormally crowded with each other. The glandular epithelial cells are actively proliferating, with increased levels and disorganized arrangement, loss of polarity, large and irregular nuclei, deep staining, and large nucleoli. The glandular epithelium grows in a germinating, branching pattern and protrudes into the glandular lumen to form sub-glandular bodies, which may further extend and fuse to form a bridge pattern within the glandular lumen, and may locally form a sieve-like structure. The interstitium is crowded and atrophied, with only a small amount of connective tissue spacing between the glands. Clinical diagnosis and treatment of endometrial atypical hyperplasia 1. Clinical diagnosis: Patients often have a history of long-term application of estrogen or hormone replacement therapy, or tamoxifen treatment after breast cancer. Some patients may have polycystic ovary syndrome, obesity, etc. Ultrasound examination often indicates endometrial thickening or abnormalities, and attention should be paid to bilateral ovaries for early detection of ovarian tumors with endocrine function. Blood hormone tests often reveal increased estrogen levels, especially in postmenopausal women, who should be alerted to ovarian tumors with endocrine function. Endometrial biopsy pathological examination is the most reliable method to diagnose endometrial lesions. Hysteroscopic endometrial biopsy can detect microscopic lesions, making the diagnosis more comprehensive and reducing the number of missed diagnoses. 2.Treatment: The treatment of endometrial precancerous lesions is mainly decided according to the patient’s age and requirements for fertility, the type of endometrial hyperplasia and the degree of cell heterotypy, the response to endocrine therapy, etc. (1) Endocrine therapy: In patients younger than 40 years old, especially those with simple hyperplasia and compound hyperplasia with fertility requirements, progestin therapy should be applied on the premise of excluding endometrial cancer, and should be closely followed up during treatment. Diagnostic curettage should be performed once every 3 months after progestin therapy is started. This will allow progestin to have its full effect on the endometrium, and also allow timely detection of those who do not respond to progestin therapy so that the treatment plan can be changed in a timely manner. Kurman et al. reported that 25% of patients under 40 years of age delivered at term after progestogen therapy. For patients with mild to moderate endometrial atypia, the commonly used progestins are progesterone, chlormadinone, megestrol acetate, and megestrol acetate. Erythropoietin 10-12mg/d orally, or chlormadinone 2-4mg/d orally, or MPA 100-200mg/d or MA 80mg/d for 3 months, and scraping the uterus after stopping the drug to determine the efficacy by endometrial pathological examination. In recent years, clinical observations have shown that mifepristone therapy often has some effect on patients with endometrial atypical hyperplasia for whom progestin therapy is ineffective. Mifepristone 12.5-25mg/d is commonly used for 3 months to observe the efficacy. Due to the prolonged administration of mifepristone, it can cause liver function damage. Therefore, changes in liver function should be noted in mifepristone treatment. (2) Surgery: For recalcitrant disease that is ineffective with progestin therapy or recurrence after stopping the drug, one should be alert to the possibility of cancer and should not continue progestin therapy blindly, but should perform surgery in time. Surgical treatment includes endometrial resection and hysterectomy. For those who have serious medical comorbidities and cannot tolerate surgery, endometrial resection can be performed under hysteroscopy. It should be noted that the endometrial resection should be comprehensive to prevent missing, especially the endometrium at the opening of the fallopian tubes bilaterally. It should also be noted that the thickness of the endometrium should reach the basal layer, otherwise recurrence cannot be avoided. Patients should be closely followed up after surgery. There have been reports of endometrial cancer after hysteroscopic endometrial resection. For patients with severe endometrial atypical hyperplasia, hysterectomy is advisable because it is difficult to distinguish them from highly differentiated endometrial adenocarcinoma by biopsy specimens alone, and sometimes the two can even coexist. The prognosis of endometrial atypical hyperplasia There is a possibility of recurrence of endometrial precancerous lesions after conservative treatment, especially in patients with endometrial atypical hyperplasia, which has a higher chance of recurrence. It has been reported that the remission rate of highly effective medroxyprogesterone acetate for endometrial atypical hyperplasia is 83%, and the pregnancy rate is 20%-30%, but 75% of patients still have recurrence after pregnancy, and 10%-15% have malignant changes. Therefore, patients with endometrial precancerous lesions should be closely followed up during and after conservative treatment, with special emphasis on monitoring ultrasound and regular scraping to detect recurrence and malignant changes early to avoid delaying treatment.