Adenoid cystitis is caused by prolonged noxious irritation of the bladder and includes cystic and glandular cystitis (CCEG), a mucosal proliferative change common to the normal bladder mucosa, first described by von inbeck in 1887. Proliferative lesions of the normal bladder mucosa initially manifest as von Brunn’s nests, in which normal bladder uroepithelial cells are nested deep into the submucosa and the cells grow in clusters with no internal spaces, which in early years were called proliferative cystitis, and this reactive proliferative change is seen in 85% to 95% of normal subjects. The cause of adenoidal cystitis is not known and is related to chronic irritation caused by chronic infection of the lower urinary tract, obstruction, stones, long-term indwelling catheters, reduced estrogen levels, psychological factors, metabolic reactions, and vitamin deficiencies. The following pathogenesis of adenoid cystitis occurs in the presence of long-term chronic harmful irritation of the bladder: simple hyperplasia of the migrating epithelium → Brunn’s bud → Brunn’s nest → cystic cystitis → adenoid cystitis. The main concern of patients is that adenocystitis is a precancerous lesion that will become bladder cancer (this is also the opinion of some physicians). In fact, this statement has been true since the 1950s when it was suggested that adenoid cystitis might be associated with bladder adenocarcinoma, and later confirmed to be a phenomenon in which the two sometimes coexist. We now recognize that it is the presence of long-term inflammation that is correlated with cancer. It is now believed that only intestinal epithelial metaplasia of the bladder (i.e., intestinal adenocystitis) is precancerous, whereas intestinal adenocystitis is a relatively rare type of adenocystitis, and in severe cases it is also pathologically diagnosed as exuberant adenocystitis (very similar to adenocarcinoma, but a benign lesion), which is multiple in the bladder, large follicular and widely distributed throughout the bladder walls centered on the triangle. Bowel-type adenocystitis is also associated with prolonged inflammatory irritation (especially in neurogenic bladders with long-term indwelling urinary catheters), except that prolonged inflammation irritates the bladder mucosa and puts it at a critical stage of malignancy, and this type of adenocystitis does require transurethral resection of the bladder mass to prevent malignancy. It is now believed by foreign scholars that adenocystitis is not a precancerous lesion, so most patients with adenocystitis have nothing to worry about, especially those who do not have long-term indwelling bladder tubes. There is also an international consensus to actively search for and remove the cause of adenocystitis and to provide anti-inflammatory treatment for patients who have received a diagnosis of adenocystitis, while the method of bladder irrigation chemotherapy for such patients after receiving a diagnosis of adenocystitis has long been abandoned internationally. possibility. The current view is that when a suspicious mucosal lesion of the bladder is found and a diagnosis of adenocystitis is obtained by cystoscopy, the diagnosis of adenocystitis should not be satisfied with the diagnosis of adenocystitis alone, but should focus on the etiology. There are numerous diseases that may lead to inflammatory bladder lesions, such as recurrent urinary tract infections, lower urinary tract obstruction, post-radiotherapy cystitis, interstitial cystitis, or autoimmune disease bladder lesions, all of which need to be screened for and treated in a targeted manner in order for the patient to achieve long-lasting relief of symptoms and local proliferative changes in the bladder mucosa. However, extensive intestinal or exuberant pathological changes should first be treated with transurethral electrodesiccation and regular follow-up cystoscopy to prevent the development of malignant changes.