Adenomyosis is the presence of endometrial glands and mesenchyme in the myometrium, accompanied by compensatory hypertrophy and hyperplasia of the surrounding myometrial cells. It used to be referred to as intrinsic endometriosis, while non-myometrial endometriosis was referred to as extrinsic endometriosis to show the difference. ”The etiology of this disease is still unclear, but in 1908 Cullen suggested that basal endometrial invasion was the cause of most adenomyosis. It was found that all cavernous organs in the body have a submucosa, with the exception of the uterus. The main role of the submucosa is to prevent the growth of glands into the myometrium, while maintaining growth toward the cavity. Therefore, most researchers now believe that adenomyosis is the result of the proliferation of endometrial cells in the basal layer and their invasion into the myometrium. There are four theories about the factors that cause the hyperplasia of the basal lamina and interstitium: (1) genetically related; (2) injury, such as curettage and cesarean delivery; (3) hyperestrogenemia; and (4) viral infection. Of these, the relationship between hyperestrogenemia and adenomyosis is particularly striking. Experiments and studies have shown that estrogen and/or progesterone plus prolactin may be required for the development of adenomyosis and that bromocriptine may block the development of adenomyosis. More recent studies suggest that both in situ and ectopic endometrium of women with adenomyosis synthesize estrogens, which may influence the growth of adenomyosis; aromatase and estrone sulfate enzyme activities are significantly increased in the myometrium of women with adenomyosis compared to controls. ”Pathology” 1. Macroscopic examination: The uterus is mostly homogeneously enlarged and spherical, usually not exceeding the size of the uterus at 12 weeks gestation. There are two types of myometrial lesions: diffuse and limited. Generally, the growth is diffuse and involves the posterior wall, so the posterior wall is often thicker than the anterior wall. Dissection of the uterine wall reveals marked thickening and hardening of the myometrium, and thick bundles of muscle fibers and microcystic cavities are seen in the myometrium, with occasional stale blood in the cavity. In a few cases, the endometrium grows in a restricted manner in the myometrium forming nodules or masses, resembling intermyometrial myoma, called adenomyoma. The section lacks the obvious and regular myofiber swirling structure of uterine fibroids, and there is no surrounding envelope and no obvious demarcation with the surrounding myometrium, so it is difficult to peel it out from the myometrium. Microscopic examination: endometrial glands and interstitium in an island-like distribution within the myometrium are the microscopic features of this disease. The exact depth of invasion for the diagnosis of adenomyosis remains somewhat controversial, as l0-30% of the uterus resected for other diseases had endometrial tissue in the myometrium on serial sectioning. Since ectopic endometrial cells are endometrium of the basal layer and are insensitive to ovarian hormones, especially progesterone, ectopic glands are often in the proliferative phase, and localized changes in the secretory phase are occasionally seen. ”The clinical manifestations of adenomyosis usually occur in menstruating women over 40 years of age. The main clinical manifestations are increased menstrual flow and prolonged periods (40%-50%), and progressive dysmenorrhea that gradually increases (25%). The pain often starts a week before the onset of menstruation and ends at the end of menstruation. In addition, some patients may have unexplained midmenstrual vaginal bleeding and loss of libido. About 35% of patients do not have any clinical symptoms. Gynecological examination may reveal a uniformly enlarged uterus or a limited nodular bulge, which is hard and painful, especially during menstruation. 15% to 40% of patients have endometriosis, so the uterus is sometimes less mobile. About half of the patients have a combination of uterine fibroids, which makes preoperative diagnosis difficult. ”The initial diagnosis can be made based on typical symptoms and signs, but histopathological examination is required to confirm the diagnosis, and imaging such as B-mode ultrasound and CT may be helpful. This disease should be differentiated from uterine fibroids and endometriosis. ”Treatment” should depend on the patient’s age, fertility requirements and symptoms. 1.Medication: There is no effective drug to cure this disease. For milder symptoms, symptomatic treatment such as NSAIDs and oral contraceptives are available. GnRHa can relieve pain or disappear and reduce the size of the uterus, but the symptoms will return and the uterus will enlarge after stopping the drug. 2.Surgical treatment: those with severe symptoms, older age and no fertility requirements or those with ineffective medication can be treated with total hysterectomy, whether the ovaries are preserved depends on the presence of ovarian lesions and the patient’s age. For young patients with adenomyoma or those with fertility requirements, focal resection can be performed on a trial basis, but it is easy to recur after surgery. Trans-laparoscopic anterior sacral neurectomy and sacral neurectomy can also treat dysmenorrhea, and the pain disappears or is relieved in about 80% of patients after surgery.